General Information of the m6A Regulator (ID: REG00025)
Regulator Name YTH domain-containing family protein 3 (YTHDF3)
Synonyms
DF3
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Gene Name YTHDF3
Sequence
MSATSVDQRPKGQGNKVSVQNGSIHQKDAVNDDDFEPYLSSQTNQSNSYPPMSDPYMPSY
YAPSIGFPYSLGEAAWSTAGDQPMPYLTTYGQMSNGEHHYIPDGVFSQPGALGNTPPFLG
QHGFNFFPGNADFSTWGTSGSQGQSTQSSAYSSSYGYPPSSLGRAITDGQAGFGNDTLSK
VPGISSIEQGMTGLKIGGDLTAAVTKTVGTALSSSGMTSIATNSVPPVSSAAPKPTSWAA
IARKPAKPQPKLKPKGNVGIGGSAVPPPPIKHNMNIGTWDEKGSVVKAPPTQPVLPPQTI
IQQPQPLIQPPPLVQSQLPQQQPQPPQPQQQQGPQPQAQPHQVQPQQQQLQNRWVAPRNR
GAGFNQNNGAGSENFGLGVVPVSASPSSVEVHPVLEKLKAINNYNPKDFDWNLKNGRVFI
IKSYSEDDIHRSIKYSIWCSTEHGNKRLDAAYRSLNGKGPLYLLFSVNGSGHFCGVAEMK
SVVDYNAYAGVWSQDKWKGKFEVKWIFVKDVPNNQLRHIRLENNDNKPVTNSRDTQEVPL
EKAKQVLKIIATFKHTTSIFDDFAHYEKRQEEEEAMRRERNRNKQ
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Family YTHDF family; YTHDF3 subfamily
Function
Specifically recognizes and binds N6-methyladenosine (m6A)-containing RNAs, and regulates their stability. M6A is a modification present at internal sites of mRNAs and some non-coding RNAs and plays a role in mRNA stability and processing. Acts as a regulator of mRNA stability by promoting degradation of m6A-containing mRNAs via interaction with the CCR4-NOT complex or PAN3. The YTHDF paralogs (YTHDF1, YTHDF2 and YTHDF3) share m6A-containing mRNAs targets and act redundantly to mediate mRNA degradation and cellular differentiation. Acts as a negative regulator of type I interferon response by down-regulating interferon-stimulated genes (ISGs) expression: acts by binding to FOXO3 mRNAs (By similarity). Binds to FOXO3 mRNAs independently of METTL3-mediated m6A modification (By similarity). Can also act as a regulator of mRNA stability in cooperation with YTHDF2 by binding to m6A-containing mRNA and promoting their degradation. Recognizes and binds m6A-containing circular RNAs (circRNAs); circRNAs are generated through back-splicing of pre-mRNAs, a non-canonical splicing process promoted by dsRNA structures across circularizing exons. Promotes formation of phase-separated membraneless compartments, such as P-bodies or stress granules, by undergoing liquid-liquid phase separation upon binding to mRNAs containing multiple m6A-modified residues: polymethylated mRNAs act as a multivalent scaffold for the binding of YTHDF proteins, juxtaposing their disordered regions and thereby leading to phase separation. The resulting mRNA-YTHDF complexes then partition into different endogenous phase-separated membraneless compartments, such as P-bodies, stress granules or neuronal RNA granules. May also recognize and bind N1-methyladenosine (m1A)-containing mRNAs: inhibits trophoblast invasion by binding to m1A-methylated transcripts of IGF1R, promoting their degradation; Has some antiviral activity against HIV-1 virus: incorporated into HIV-1 particles in a nucleocapsid-dependent manner and reduces viral infectivity in the next cycle of infection . May interfere with this early step of the viral life cycle by binding to N6-methyladenosine (m6A) modified sites on the HIV-1 RNA genome.
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Gene ID 253943
Uniprot ID
YTHD3_HUMAN
Regulator Type WRITER ERASER READER
Mechanism Diagram Click to View the Original Diagram
Target Genes Click to View Potential Target Genes of This Regulator
Full List of Target Gene(s) of This m6A Regulator and Corresponding Disease/Drug Response(s)
YTHDF3 can regulate the m6A methylation of following target genes, and result in corresponding disease/drug response(s). You can browse corresponding disease or drug response(s) resulted from the regulation of certain target gene.
Browse Target Gene related Disease
Browse Target Gene related Drug
Gap junction alpha-1 protein (GJA1)
Representative RNA-seq result indicating the expression of this target gene regulated by YTHDF3
Cell Line Mouse embryonic fibroblasts Mus musculus
Treatment: shYthdf3 embryonic fibroblasts
Control: shLuc embryonic fibroblasts
GSE156437
Regulation
logFC: -7.79E-01
p-value: 7.79E-03
More Results Click to View More RNA-seq Results
Breast cancer [ICD-11: 2C60]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response of This Target Gene [1]
Responsed Disease Breast cancer [ICD-11: 2C60]
Target Regulation Up regulation
Cell Process Cell metastasis
In-vitro Model
MDA-MB-231Br (After brain metastases of MDA-MB-361 breast adenocarcinoma cells)
MDA-MB-231 Breast adenocarcinoma Homo sapiens CVCL_0062
MDA-IBC-3 Breast inflammatory carcinoma Homo sapiens CVCL_HC47
JIMT-1Br3 (After brain metastases of JIMT-1 breast cancer cells)
JIMT-1 Breast ductal carcinoma Homo sapiens CVCL_2077
HEK293-FT Normal Homo sapiens CVCL_6911
HCC1954Br (After brain metastases of HCC1954 breast cancer cells)
HCC1954 Breast ductal carcinoma Homo sapiens CVCL_1259
bEnd.3 Cerebrovascular endothelioma cells from mice Mus musculus CVCL_0170
BEAS-2B Normal Homo sapiens CVCL_0168
4T1Br (After brain metastases of 4T1 mouse breast cancer cells)
4T1 Normal Mus musculus CVCL_0125
In-vivo Model For the in vivo brain and bone extravasation and seeding assays, cancer cells labeled with CMFDA C2925 (Thermo fisher scientific) or GFP were injected intracardially into the nude mice. Cell number and injection procedure were described in "Animal Experiments". For the in vivo lung extravasation and seeding assays, cancer cells labeled with GFP (2.5 × 105 cells/mouse) were injected into the tail vein of nude mice. At 24 or 48 hrs later, the mice were sacrificed.
Response Summary Mechanistically, YTHDF3 enhances the translation of m6A-enriched transcripts for ST6GALNAC5, Gap junction alpha-1 protein (GJA1), and EGFR, all associated with breast cancer brain metastasis. This work uncovers an essential role of YTHDF3 in controlling the interaction between cancer cells and brain microenvironment, thereby inducing brain metastatic competence.
Catenin beta-1 (CTNNB1/Beta-catenin)
Representative RIP-seq result supporting the interaction between the target gene and YTHDF3
Cell Line Hela Homo sapiens
Regulation logFC: 1.43E+00 GSE86214
Melanoma [ICD-11: 2C30]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response of This Target Gene [2]
Responsed Disease Melanoma of uvea [ICD-11: 2D0Y]
Target Regulation Up regulation
Response Summary YTHDF3 enhances Catenin beta-1 (CTNNB1/Beta-catenin) translation through recognizing and binding the m6A peaks on CTNNB1 mRNA.m6A reading protein YTHDF3 promotes the translation of the target transcript CTNNB1, contributing to ocular melanoma propagation and migration through m6A methylation.
Epidermal growth factor receptor (EGFR)
Representative RIP-seq result supporting the interaction between the target gene and YTHDF3
Cell Line Hela Homo sapiens
Regulation logFC: 2.94E+00 GSE86214
Breast cancer [ICD-11: 2C60]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response of This Target Gene [1]
Responsed Disease Breast cancer [ICD-11: 2C60]
Target Regulation Up regulation
Cell Process Cell metastasis
In-vitro Model
MDA-MB-231Br (After brain metastases of MDA-MB-361 breast adenocarcinoma cells)
MDA-MB-231 Breast adenocarcinoma Homo sapiens CVCL_0062
MDA-IBC-3 Breast inflammatory carcinoma Homo sapiens CVCL_HC47
JIMT-1Br3 (After brain metastases of JIMT-1 breast cancer cells)
JIMT-1 Breast ductal carcinoma Homo sapiens CVCL_2077
HEK293-FT Normal Homo sapiens CVCL_6911
HCC1954Br (After brain metastases of HCC1954 breast cancer cells)
HCC1954 Breast ductal carcinoma Homo sapiens CVCL_1259
bEnd.3 Cerebrovascular endothelioma cells from mice Mus musculus CVCL_0170
BEAS-2B Normal Homo sapiens CVCL_0168
4T1Br (After brain metastases of 4T1 mouse breast cancer cells)
4T1 Normal Mus musculus CVCL_0125
In-vivo Model For the in vivo brain and bone extravasation and seeding assays, cancer cells labeled with CMFDA C2925 (Thermo fisher scientific) or GFP were injected intracardially into the nude mice. Cell number and injection procedure were described in "Animal Experiments". For the in vivo lung extravasation and seeding assays, cancer cells labeled with GFP (2.5 × 105 cells/mouse) were injected into the tail vein of nude mice. At 24 or 48 hrs later, the mice were sacrificed.
Response Summary Mechanistically, YTHDF3 enhances the translation of m6A-enriched transcripts for ST6GALNAC5, GJA1, and Epidermal growth factor receptor (EGFR), all associated with breast cancer brain metastasis. This work uncovers an essential role of YTHDF3 in controlling the interaction between cancer cells and brain microenvironment, thereby inducing brain metastatic competence.
Forkhead box protein M1 (FOXM1)
Representative RIP-seq result supporting the interaction between the target gene and YTHDF3
Cell Line Hela Homo sapiens
Regulation logFC: 1.19E+00 GSE86214
Neoplasms of haematopoietic or lymphoid tissues [ICD-11: 2B3Z]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response of This Target Gene [3]
Responsed Disease Neoplasms of haematopoietic or lymphoid tissues [ICD-11: 2B3Z]
Target Regulation Up regulation
Pathway Response mRNA surveillance pathway hsa03015), RNA degradation
Cell Process RNA stability
Response Summary m6A reader Ythdf3 protects hematopoietic stem cell integrity under stress by promoting the translation of Forkhead box protein M1 (FOXM1) and Asxl1 transcripts.
Forkhead box protein O3 (FOXO3)
Representative RIP-seq result supporting the interaction between the target gene and YTHDF3
Cell Line Hela Homo sapiens
Regulation logFC: 2.93E+00 GSE86214
Inflammatory response [ICD-11: MG46]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response of This Target Gene [4]
Responsed Disease Inflammatory response [ICD-11: MG46]
Target Regulation Up regulation
Pathway Response FoxO signaling pathway hsa04068
In-vivo Model YTHDF3-/- mice were generated using the CRISPR-Cas9 system.
Response Summary YTHDF3 as a negative regulator of antiviral immunity through the translational promotion of Forkhead box protein O3 (FOXO3) mRNA under homeostatic conditions, adding insight into the networks of RNA-binding protein-RNA interactions in homeostatically maintaining host antiviral immune function and preventing inflammatory response.
Integrin alpha-6 (ITGA6)
Representative RIP-seq result supporting the interaction between the target gene and YTHDF3
Cell Line Hela Homo sapiens
Regulation logFC: 1.67E+00 GSE86214
Liver cancer [ICD-11: 2C12]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response of This Target Gene [5]
Responsed Disease Hepatocellular carcinoma [ICD-11: 2C12.02]
Cell Process Cell proliferation
Cell migration
Cell invasion
Cell apoptosis
In-vitro Model
HEK293T Normal Homo sapiens CVCL_0063
Hep 3B2.1-7 Childhood hepatocellular carcinoma Homo sapiens CVCL_0326
SMMC-7721 Endocervical adenocarcinoma Homo sapiens CVCL_0534
In-vivo Model HCC cells (5 × 106 cells/mouse) that had been transfected with oe-NC + sh-NC, oe-KDM5B + sh-NC, or oe-KDM5B + sh-ITGA6, or treated with NS, GSK-467 (a selective inhibitor of KDM5B) + oe-NC or GSK-467 + oe-ITGA6 were then subcutaneously implanted into the back of mice.
Response Summary KDM5B regulates the YTHDF3/ITGA6 axis by inhibiting the expression of miR-448 to promote the occurrence of hepatocellular carcinoma. miR-448 could target YTHDF3 and inhibit the YTHDF3/Integrin alpha-6 (ITGA6) axis, thereby inhibiting the occurrence of HCC.
Bladder cancer [ICD-11: 2C94]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response of This Target Gene [6]
Responsed Disease Bladder cancer [ICD-11: 2C94]
Pathway Response Cell adhesion molecules hsa04514
Cell Process Cell adhesion
Cell migration
Cell invasion
In-vitro Model
5637 Bladder carcinoma Homo sapiens CVCL_0126
HEK293T Normal Homo sapiens CVCL_0063
J82 Bladder carcinoma Homo sapiens CVCL_0359
SV-HUC-1 Normal Homo sapiens CVCL_3798
T24 Bladder carcinoma Homo sapiens CVCL_0554
UM-UC-3 Bladder carcinoma Homo sapiens CVCL_1783
In-vivo Model For the subcutaneous implantation model, 1 × 107 cells were subcutaneously implanted into 5-week-old BALB/cJNju-Foxn1nu/Nju nude mice.
Response Summary m6A writer METTL3 and eraser ALKBH5 altered cell adhesion by regulating Integrin alpha-6 (ITGA6) expression in bladder cancer cells. m6A is highly enriched within the ITGA6 transcripts, and increased m6A methylations of the ITGA6 mRNA 3'UTR promotes the translation of ITGA6 mRNA via binding of the m6A readers YTHDF1 and YTHDF3. Inhibition of ITGA6 results in decreased growth and progression of bladder cancer cells in vitro and in vivo.
Polycomb group protein ASXL1 (Asxl1)
Representative RIP-seq result supporting the interaction between the target gene and YTHDF3
Cell Line Hela Homo sapiens
Regulation logFC: 2.55E+00 GSE86214
Neoplasms of haematopoietic or lymphoid tissues [ICD-11: 2B3Z]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response of This Target Gene [3]
Responsed Disease Neoplasms of haematopoietic or lymphoid tissues [ICD-11: 2B3Z]
Target Regulation Up regulation
Pathway Response mRNA surveillance pathway hsa03015), RNA degradation
Cell Process RNA stability
Response Summary m6A reader Ythdf3 protects hematopoietic stem cell integrity under stress by promoting the translation of Foxm1 and Polycomb group protein ASXL1 (Asxl1) transcripts.
Transcriptional coactivator YAP1 (YAP1)
Representative RIP-seq result supporting the interaction between the target gene and YTHDF3
Cell Line Hela Homo sapiens
Regulation logFC: 1.33E+00 GSE86214
Lung cancer [ICD-11: 2C25]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response of This Target Gene [7]
Responsed Disease Non-small-cell lung carcinoma [ICD-11: 2C25.Y]
Responsed Drug Cisplatin Approved
Target Regulation Up regulation
Pathway Response Hippo signaling pathway hsa04390
Cell Process Metabolic
In-vitro Model
A-549 Lung adenocarcinoma Homo sapiens CVCL_0023
Calu-6 Lung adenocarcinoma Homo sapiens CVCL_0236
NCI-H1299 Lung large cell carcinoma Homo sapiens CVCL_0060
NCI-H520 Lung squamous cell carcinoma Homo sapiens CVCL_1566
In-vivo Model Mice were injected with 5 × 106 lung cancer cells with stably expression of relevant plasmids and randomly divided into two groups (five mice per group) after the diameter of the xenografted tumors had reached approximately 5 mm in diameter. Xenografted mice were then administrated with PBS or DDP (3 mg/kg per day) for three times a week, and tumor volume were measured every second day.
Response Summary METTL3, YTHDF3, YTHDF1, and eIF3b directly promoted YAP translation through an interaction with the translation initiation machinery. METTL3 knockdown inhibits tumor growth and enhances sensitivity to DDP in vivo.m6A mRNA methylation initiated by METTL3 directly promotes YAP translation and increases YAP activity by regulating the MALAT1-miR-1914-3p-Transcriptional coactivator YAP1 (YAP1) axis to induce Non-small cell lung cancer drug resistance and metastasis.
Zinc finger E-box-binding homeobox 1 (ZEB1)
Representative RIP-seq result supporting the interaction between the target gene and YTHDF3
Cell Line Hela Homo sapiens
Regulation logFC: 1.92E+00 GSE86214
Liver cancer [ICD-11: 2C12]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response of This Target Gene [8]
Responsed Disease Hepatocellular carcinoma [ICD-11: 2C12.02]
Target Regulation Up regulation
Pathway Response RNA degradation hsa03018
Cell Process RNA stability
In-vitro Model
BEL-7402 Endocervical adenocarcinoma Homo sapiens CVCL_5492
BEL-7404 Endocervical adenocarcinoma Homo sapiens CVCL_6568
Hep-G2 Hepatoblastoma Homo sapiens CVCL_0027
Huh-7 Adult hepatocellular carcinoma Homo sapiens CVCL_0336
L-02 Endocervical adenocarcinoma Homo sapiens CVCL_6926
SMMC-7721 Endocervical adenocarcinoma Homo sapiens CVCL_0534
In-vivo Model 1 × 107 Bel-7404 cells in 200 uL PBS were injected into the right flank of nude mice.
Response Summary circ_KIAA1429 could accelerate HCC advancement, maintained the expression of Zeb1 through the mechanism of m6A-YTHDF3-Zinc finger E-box-binding homeobox 1 (ZEB1) in hepatocellular carcinoma.
Breast cancer [ICD-11: 2C60]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response of This Target Gene [9]
Responsed Disease Breast cancer [ICD-11: 2C60]
Target Regulation Up regulation
Cell Process Cell migration
Cell invasion
Epithelial-mesenchymal transition
In-vitro Model
MDA-MB-231 Breast adenocarcinoma Homo sapiens CVCL_0062
Hs 578T Invasive breast carcinoma Homo sapiens CVCL_0332
HCC1937 Breast ductal carcinoma Homo sapiens CVCL_0290
BT-549 Invasive breast carcinoma Homo sapiens CVCL_1092
Response Summary YTHDF3 positively regulated cell migration, invasion, and EMT in triple-negative breast cancer cells. Moreover, Zinc finger E-box-binding homeobox 1 (ZEB1) was identified as a key downstream target for YTHDF3 and YTHDF3 could enhance ZEB1 mRNA stability in an m6A-dependent manner.
Metastasis associated lung adenocarcinoma transcript 1 (MALAT1)
Representative RIP-seq result supporting the interaction between the target gene and YTHDF3
Cell Line Hela Homo sapiens
Regulation logFC: 1.66E+00 GSE86214
Lung cancer [ICD-11: 2C25]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response of This Target Gene [7]
Responsed Disease Non-small-cell lung carcinoma [ICD-11: 2C25.Y]
Responsed Drug Cisplatin Approved
Target Regulation Up regulation
Pathway Response Hippo signaling pathway hsa04390
Cell Process Metabolic
In-vitro Model
A-549 Lung adenocarcinoma Homo sapiens CVCL_0023
Calu-6 Lung adenocarcinoma Homo sapiens CVCL_0236
NCI-H1299 Lung large cell carcinoma Homo sapiens CVCL_0060
NCI-H520 Lung squamous cell carcinoma Homo sapiens CVCL_1566
In-vivo Model Mice were injected with 5 × 106 lung cancer cells with stably expression of relevant plasmids and randomly divided into two groups (five mice per group) after the diameter of the xenografted tumors had reached approximately 5 mm in diameter. Xenografted mice were then administrated with PBS or DDP (3 mg/kg per day) for three times a week, and tumor volume were measured every second day.
Response Summary METTL3, YTHDF3, YTHDF1, and eIF3b directly promoted YAP translation through an interaction with the translation initiation machinery. METTL3 knockdown inhibits tumor growth and enhances sensitivity to DDP in vivo.m6A mRNA methylation initiated by METTL3 directly promotes YAP translation and increases YAP activity by regulating the Metastasis associated lung adenocarcinoma transcript 1 (MALAT1)-miR-1914-3p-YAP axis to induce Non-small cell lung cancer drug resistance and metastasis.
GD1 alpha synthase (ST6GALNAC5)
Breast cancer [ICD-11: 2C60]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response of This Target Gene [1]
Responsed Disease Breast cancer [ICD-11: 2C60]
Target Regulation Up regulation
Cell Process Cell metastasis
In-vitro Model
MDA-MB-231Br (After brain metastases of MDA-MB-361 breast adenocarcinoma cells)
MDA-MB-231 Breast adenocarcinoma Homo sapiens CVCL_0062
MDA-IBC-3 Breast inflammatory carcinoma Homo sapiens CVCL_HC47
JIMT-1Br3 (After brain metastases of JIMT-1 breast cancer cells)
JIMT-1 Breast ductal carcinoma Homo sapiens CVCL_2077
HEK293-FT Normal Homo sapiens CVCL_6911
HCC1954Br (After brain metastases of HCC1954 breast cancer cells)
HCC1954 Breast ductal carcinoma Homo sapiens CVCL_1259
bEnd.3 Cerebrovascular endothelioma cells from mice Mus musculus CVCL_0170
BEAS-2B Normal Homo sapiens CVCL_0168
4T1Br (After brain metastases of 4T1 mouse breast cancer cells)
4T1 Normal Mus musculus CVCL_0125
In-vivo Model For the in vivo brain and bone extravasation and seeding assays, cancer cells labeled with CMFDA C2925 (Thermo fisher scientific) or GFP were injected intracardially into the nude mice. Cell number and injection procedure were described in "Animal Experiments". For the in vivo lung extravasation and seeding assays, cancer cells labeled with GFP (2.5 × 105 cells/mouse) were injected into the tail vein of nude mice. At 24 or 48 hrs later, the mice were sacrificed.
Response Summary Mechanistically, YTHDF3 enhances the translation of m6A-enriched transcripts for GD1 alpha synthase (ST6GALNAC5), GJA1, and EGFR, all associated with breast cancer brain metastasis. This work uncovers an essential role of YTHDF3 in controlling the interaction between cancer cells and brain microenvironment, thereby inducing brain metastatic competence.
Interleukin-1 beta (IL1B)
Gangrene or necrosis of lung [ICD-11: CA43]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response of This Target Gene [10]
Responsed Disease Gangrene or necrosis of lung [ICD-11: CA43]
Target Regulation Up regulation
Pathway Response MAPK signaling pathway hsa04010
PI3K-Akt signaling pathway hsa04151
Cell Process Biological regulation
Cell apoptosis
In-vitro Model
BEAS-2B Normal Homo sapiens CVCL_0168
In-vivo Model After being anesthetized with urethane (i.p.), SD rats were endotracheally intubated and ventilated using an animal ventilator under the conditions: respiratory rate of 70 breaths/min, tidal volume of 20 ml/kg, and inspiratory/expiratory ratio of 1:1.
Response Summary N6-methyladenosine (m6A) methylation modification is implicated in the pathogenesis of lung ischemia-reperfusion injury. YTHDF3 or IGF2BP2 knockdown inhibited hypoxia/reoxygenation-activated p38, ERK1/2, AKT, and NF-Kappa-B pathways in BEAS-2B cells, and inhibited p-p65, Interleukin-1 beta (IL1B) and TNF-alpha secretion.
Mitogen-activated protein kinase 1 (MAPK/ERK2/MAPK1)
Gangrene or necrosis of lung [ICD-11: CA43]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response of This Target Gene [10]
Responsed Disease Gangrene or necrosis of lung [ICD-11: CA43]
Target Regulation Up regulation
Pathway Response MAPK signaling pathway hsa04010
PI3K-Akt signaling pathway hsa04151
Apoptosis hsa04210
Cell Process Biological regulation
Cell apoptosis
In-vitro Model
BEAS-2B Normal Homo sapiens CVCL_0168
In-vivo Model After being anesthetized with urethane (i.p.), SD rats were endotracheally intubated and ventilated using an animal ventilator under the conditions: respiratory rate of 70 breaths/min, tidal volume of 20 ml/kg, and inspiratory/expiratory ratio of 1:1.
Response Summary N6-methyladenosine (m6A) methylation modification is implicated in the pathogenesis of lung ischemia-reperfusion injury. YTHDF3 or IGF2BP2 knockdown inhibited hypoxia/reoxygenation-activated p38, Mitogen-activated protein kinase 1 (MAPK/ERK2/MAPK1), AKT, and NF-Kappa-B pathways in BEAS-2B cells, and inhibited p-p65, IL-1-beta and TNF-alpha secretion.
Mitogen-activated protein kinase 14 (p38/MAPK14)
Gangrene or necrosis of lung [ICD-11: CA43]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response of This Target Gene [10]
Responsed Disease Gangrene or necrosis of lung [ICD-11: CA43]
Target Regulation Up regulation
Pathway Response MAPK signaling pathway hsa04010
PI3K-Akt signaling pathway hsa04151
Cell Process Biological regulation
Cell apoptosis
In-vitro Model
BEAS-2B Normal Homo sapiens CVCL_0168
In-vivo Model After being anesthetized with urethane (i.p.), SD rats were endotracheally intubated and ventilated using an animal ventilator under the conditions: respiratory rate of 70 breaths/min, tidal volume of 20 ml/kg, and inspiratory/expiratory ratio of 1:1.
Response Summary N6-methyladenosine (m6A) methylation modification is implicated in the pathogenesis of lung ischemia-reperfusion injury. YTHDF3 or IGF2BP2 knockdown inhibited hypoxia/reoxygenation-activated Mitogen-activated protein kinase 14 (p38/MAPK14), ERK1/2, AKT, and NF-Kappa-B pathways in BEAS-2B cells, and inhibited p-p65, IL-1-beta and TNF-alpha secretion.
RAC-alpha serine/threonine-protein kinase (AKT1)
Gangrene or necrosis of lung [ICD-11: CA43]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response of This Target Gene [10]
Responsed Disease Gangrene or necrosis of lung [ICD-11: CA43]
Target Regulation Up regulation
Pathway Response MAPK signaling pathway hsa04010
PI3K-Akt signaling pathway hsa04151
Apoptosis hsa04210
Cell Process Biological regulation
Cell apoptosis
In-vitro Model
BEAS-2B Normal Homo sapiens CVCL_0168
In-vivo Model After being anesthetized with urethane (i.p.), SD rats were endotracheally intubated and ventilated using an animal ventilator under the conditions: respiratory rate of 70 breaths/min, tidal volume of 20 ml/kg, and inspiratory/expiratory ratio of 1:1.
Response Summary N6-methyladenosine (m6A) methylation modification is implicated in the pathogenesis of lung ischemia-reperfusion injury. YTHDF3 or IGF2BP2 knockdown inhibited hypoxia/reoxygenation-activated p38, ERK1/2, RAC-alpha serine/threonine-protein kinase (AKT1), and NF-Kappa-B pathways in BEAS-2B cells, and inhibited p-p65, IL-1-beta and TNF-alpha secretion.
Transcription factor p65 (RELA)
Gangrene or necrosis of lung [ICD-11: CA43]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response of This Target Gene [10]
Responsed Disease Gangrene or necrosis of lung [ICD-11: CA43]
Target Regulation Up regulation
Pathway Response MAPK signaling pathway hsa04010
PI3K-Akt signaling pathway hsa04151
Apoptosis hsa04210
Cell Process Biological regulation
Cell apoptosis
In-vitro Model
BEAS-2B Normal Homo sapiens CVCL_0168
In-vivo Model After being anesthetized with urethane (i.p.), SD rats were endotracheally intubated and ventilated using an animal ventilator under the conditions: respiratory rate of 70 breaths/min, tidal volume of 20 ml/kg, and inspiratory/expiratory ratio of 1:1.
Response Summary N6-methyladenosine (m6A) methylation modification is implicated in the pathogenesis of lung ischemia-reperfusion injury. YTHDF3 or IGF2BP2 knockdown inhibited hypoxia/reoxygenation-activated p38, ERK1/2, AKT, and NF-Kappa-B pathways in BEAS-2B cells, and inhibited Transcription factor p65 (RELA), IL-1-beta and TNF-alpha secretion.
Tumor necrosis factor (TNF/TNF-alpha)
Gangrene or necrosis of lung [ICD-11: CA43]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response of This Target Gene [10]
Responsed Disease Gangrene or necrosis of lung [ICD-11: CA43]
Target Regulation Up regulation
Pathway Response MAPK signaling pathway hsa04010
PI3K-Akt signaling pathway hsa04151
Apoptosis hsa04210
Cell Process Biological regulation
Cell apoptosis
In-vitro Model
BEAS-2B Normal Homo sapiens CVCL_0168
In-vivo Model After being anesthetized with urethane (i.p.), SD rats were endotracheally intubated and ventilated using an animal ventilator under the conditions: respiratory rate of 70 breaths/min, tidal volume of 20 ml/kg, and inspiratory/expiratory ratio of 1:1.
Response Summary N6-methyladenosine (m6A) methylation modification is implicated in the pathogenesis of lung ischemia-reperfusion injury. YTHDF3 or IGF2BP2 knockdown inhibited hypoxia/reoxygenation-activated p38, ERK1/2, AKT, and NF-Kappa-B pathways in BEAS-2B cells, and inhibited p-p65, IL-1-beta and Tumor necrosis factor (TNF/TNF-alpha) secretion.
Tyrosine-protein kinase EIF2AK2 (eIF2AK2/p68)
Colorectal cancer [ICD-11: 2B91]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response of This Target Gene [11]
Responsed Disease Colorectal cancer [ICD-11: 2B91]
In-vitro Model
HCT 116 Colon carcinoma Homo sapiens CVCL_0291
HCT 8 Colon adenocarcinoma Homo sapiens CVCL_2478
Caco-2 Colon adenocarcinoma Homo sapiens CVCL_0025
RKO Colon carcinoma Homo sapiens CVCL_0504
HCoEpiC (Healthy colon epithelial HCoEpiC cells)
FHC Normal Homo sapiens CVCL_3688
Response Summary YTHDF3 was highly expressed in oxaliplatin-resistant (OXAR) CRC tissues and cells. YTHDF3 as a novel hallmark and revealed the molecular mechanism of YTHDF3 on gene translation via coordination with Tyrosine-protein kinase EIF2AK2 (eIF2AK2/p68) in OXAR CRC cells.
Growth arrest specific 5 (GAS5)
Colorectal cancer [ICD-11: 2B91]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response of This Target Gene [12]
Responsed Disease Colorectal cancer [ICD-11: 2B91]
Target Regulation Down regulation
Pathway Response Hippo signaling pathway hsa04390
Cell Process Ubiquitination degradation
In-vitro Model
DLD-1 Colon adenocarcinoma Homo sapiens CVCL_0248
HCT 116 Colon carcinoma Homo sapiens CVCL_0291
HT29 Colon cancer Mus musculus CVCL_A8EZ
LoVo Colon adenocarcinoma Homo sapiens CVCL_0399
LS174T Colon adenocarcinoma Homo sapiens CVCL_1384
RKO Colon carcinoma Homo sapiens CVCL_0504
SW480 Colon adenocarcinoma Homo sapiens CVCL_0546
SW620 Colon adenocarcinoma Homo sapiens CVCL_0547
Response Summary A new mechanism for m6A-induced decay of Growth arrest specific 5 (GAS5) on YAP signaling in progression of Colorectal cancer which offers a promising approach for CRC treatment. LncRNA GAS5 expressions is negatively correlated with YAP and YTHDF3 protein levels in tumors from CRC patients.
hsa-miR-1914-3p
Lung cancer [ICD-11: 2C25]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response of This Target Gene [7]
Responsed Disease Non-small-cell lung carcinoma [ICD-11: 2C25.Y]
Responsed Drug Cisplatin Approved
Target Regulation Up regulation
Pathway Response Hippo signaling pathway hsa04390
Cell Process Metabolic
In-vitro Model
A-549 Lung adenocarcinoma Homo sapiens CVCL_0023
Calu-6 Lung adenocarcinoma Homo sapiens CVCL_0236
NCI-H1299 Lung large cell carcinoma Homo sapiens CVCL_0060
NCI-H520 Lung squamous cell carcinoma Homo sapiens CVCL_1566
In-vivo Model Mice were injected with 5 × 106 lung cancer cells with stably expression of relevant plasmids and randomly divided into two groups (five mice per group) after the diameter of the xenografted tumors had reached approximately 5 mm in diameter. Xenografted mice were then administrated with PBS or DDP (3 mg/kg per day) for three times a week, and tumor volume were measured every second day.
Response Summary METTL3, YTHDF3, YTHDF1, and eIF3b directly promoted YAP translation through an interaction with the translation initiation machinery. METTL3 knockdown inhibits tumor growth and enhances sensitivity to DDP in vivo.m6A mRNA methylation initiated by METTL3 directly promotes YAP translation and increases YAP activity by regulating the MALAT1-hsa-miR-1914-3p-YAP axis to induce Non-small cell lung cancer drug resistance and metastasis.
hsa-miR-5586-5p
Pancreatic cancer [ICD-11: 2C10]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response of This Target Gene [13]
Responsed Disease Pancreatic cancer [ICD-11: 2C10]
Pathway Response Glycolysis / Gluconeogenesis hsa00010
Cell Process Glycolysis
In-vitro Model
SW1990 Pancreatic adenocarcinoma Homo sapiens CVCL_1723
PANC-1 Pancreatic ductal adenocarcinoma Homo sapiens CVCL_0480
HPDE Normal Homo sapiens CVCL_4376
BxPC-3 Pancreatic ductal adenocarcinoma Homo sapiens CVCL_0186
AsPC-1 Pancreatic ductal adenocarcinoma Homo sapiens CVCL_0152
Response Summary Theses results implicate a negative feedback of m6A reader YTHDF3 and glycolytic lncRNA DICER1-AS1 is involved in glycolysis and tumorigenesis of pancreatic cancer. YTHDF3 and lncRNA DICER1-AS1 promotes glycolysis of pancreatic cancer through inhibiting maturation of hsa-miR-5586-5p.
Unspecific Target Gene
Testicular cancer [ICD-11: 2C80]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response of This Target Gene [14]
Responsed Disease Testicular cancer [ICD-11: 2C80]
Cell Process Transcription
Response Summary Abundance of m6A and expression of VIRMA/YTHDF3 were different among Testicular Germ Cell Tumors subtypes, with higher levels in SEs, suggesting a contribution to SE phenotype maintenance.
Aortic aneurysm or dissection [ICD-11: BD50]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response of This Target Gene [15]
Responsed Disease Abdominal aortic aneurysm [ICD-11: BD50.4]
Cell Process Inflammatory infiltrates
Neovascularization
In-vitro Model
PBMCs (Human peripheral blood mononuclear cells (PBMCs) are isolated from peripheral blood and identified as any blood cell with a round nucleus)
SMCs (Aneurysmal smooth muscle cells)
Response Summary YTHDF3 represented an even greater risk of rupture. Regarding the cellular location, METTL14 seemed to be associated with inflammatory infiltrates and neovascularization. Furthermore, a strong correlation was seen between FTO and aneurysmal smooth muscle cells (SMCs), YTHDF3, and macrophage infiltrate. The results also reveal the important roles of m6A modulators, including YTHDF3, FTO, and METTL14, in the pathogenesis of human human abdominal aortic aneurysm(AAA) and provide a new view on m6A modification in AAA.
Asthma [ICD-11: CA23]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response of This Target Gene [16]
Responsed Disease Asthma [ICD-11: CA23]
In-vivo Model Modelled two groups of female 6-week-old BALB/C mice: severe asthma group and blank control group (n = 3 per group). They had the same feeding conditions and growth environment. Immunization solution: Dissolve 20 mg ovalbumin (OVA) in 1 ml normal saline (NS), after OVA is completely dissolved, dilute 0.4-10 ml and mix well, then it was mixed with the same volume of liquid aluminium adjuvant and placed on a shaking table at 4℃ for 30 min. Challenge solution: Add 0.5 g OVA into 10 ml NS, fully dissolve it, and shake it on a shaking table at 4℃ for 30 min. Immunization: Mice were injected intraperitoneally on days 0 and 12, each with 0.2 ml; the control group was treated with equal volume of normal saline. Challenge: On days 18-23, the mice were atomized by ultrasound in a closed container at a dose of 10 ml once a day for 20 min. Lung tissue was taken 24 h after the last atomization and immediately stored in liquid nitrogen.
Response Summary m6A(YTHDF3 and YTHDC1) modification plays a key role in severe asthma, and is able to guide the future strategy of immunotherapy.
Liver disease [ICD-11: DB9Z]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response of This Target Gene [17]
Responsed Disease Liver disease [ICD-11: DB9Z]
Pathway Response PPAR signaling pathway hsa03320
Cell Process Fatty degeneration
In-vivo Model A total of 24 male mice were randomly allocated to LFD (low-fat diet), LFDR (low-fat diet + resveratrol), HFD (high-fat diet), and HFDR (high-fat diet + resveratrol) groups for 12 weeks (n = 6/group).
Response Summary The beneficial effect of resveratrol on lipid metabolism disorder under HFD is due to a decrease of m6A RNA methylation and an increase of PPARalpha mRNA, providing mechanistic insights into the function of resveratrol in alleviating the disturbance of lipid metabolism in mice. The resveratrol in HFD increased the transcript levels of methyltransferase like 3 (METTL3), alkB homolog 5 (ALKBH5), fat mass and obesity associated protein (FTO), and YTH domain family 2 (YTHDF2), whereas it decreased the level of YTH domain family 3 (YTHDF3) and m6A abundance in mice liver.
Transcriptional coactivator YAP1 (YAP1)
Representative RIP-seq result supporting the interaction between the target gene and YTHDF3
Cell Line Hela Homo sapiens
Regulation logFC: 1.33E+00 GSE86214
Cisplatin [Approved]
In total 1 item(s) under this drug
Experiment 1 Reporting the m6A-centered Drug Response of This Target Gene [7]
Responsed Disease Non-small-cell lung carcinoma ICD-11: 2C25.Y
Target Regulation Up regulation
Pathway Response Hippo signaling pathway hsa04390
Cell Process Metabolic
In-vitro Model A-549 Lung adenocarcinoma Homo sapiens CVCL_0023
Calu-6 Lung adenocarcinoma Homo sapiens CVCL_0236
NCI-H1299 Lung large cell carcinoma Homo sapiens CVCL_0060
NCI-H520 Lung squamous cell carcinoma Homo sapiens CVCL_1566
In-vivo Model Mice were injected with 5 × 106 lung cancer cells with stably expression of relevant plasmids and randomly divided into two groups (five mice per group) after the diameter of the xenografted tumors had reached approximately 5 mm in diameter. Xenografted mice were then administrated with PBS or DDP (3 mg/kg per day) for three times a week, and tumor volume were measured every second day.
Response Summary METTL3, YTHDF3, YTHDF1, and eIF3b directly promoted YAP translation through an interaction with the translation initiation machinery. METTL3 knockdown inhibits tumor growth and enhances sensitivity to DDP in vivo.m6A mRNA methylation initiated by METTL3 directly promotes YAP translation and increases YAP activity by regulating the MALAT1-miR-1914-3p-Transcriptional coactivator YAP1 (YAP1) axis to induce Non-small cell lung cancer drug resistance and metastasis.
Metastasis associated lung adenocarcinoma transcript 1 (MALAT1)
Representative RIP-seq result supporting the interaction between the target gene and YTHDF3
Cell Line Hela Homo sapiens
Regulation logFC: 1.66E+00 GSE86214
Cisplatin [Approved]
In total 1 item(s) under this drug
Experiment 1 Reporting the m6A-centered Drug Response of This Target Gene [7]
Responsed Disease Non-small-cell lung carcinoma ICD-11: 2C25.Y
Target Regulation Up regulation
Pathway Response Hippo signaling pathway hsa04390
Cell Process Metabolic
In-vitro Model A-549 Lung adenocarcinoma Homo sapiens CVCL_0023
Calu-6 Lung adenocarcinoma Homo sapiens CVCL_0236
NCI-H1299 Lung large cell carcinoma Homo sapiens CVCL_0060
NCI-H520 Lung squamous cell carcinoma Homo sapiens CVCL_1566
In-vivo Model Mice were injected with 5 × 106 lung cancer cells with stably expression of relevant plasmids and randomly divided into two groups (five mice per group) after the diameter of the xenografted tumors had reached approximately 5 mm in diameter. Xenografted mice were then administrated with PBS or DDP (3 mg/kg per day) for three times a week, and tumor volume were measured every second day.
Response Summary METTL3, YTHDF3, YTHDF1, and eIF3b directly promoted YAP translation through an interaction with the translation initiation machinery. METTL3 knockdown inhibits tumor growth and enhances sensitivity to DDP in vivo.m6A mRNA methylation initiated by METTL3 directly promotes YAP translation and increases YAP activity by regulating the Metastasis associated lung adenocarcinoma transcript 1 (MALAT1)-miR-1914-3p-YAP axis to induce Non-small cell lung cancer drug resistance and metastasis.
hsa-miR-1914-3p
Cisplatin [Approved]
In total 1 item(s) under this drug
Experiment 1 Reporting the m6A-centered Drug Response of This Target Gene [7]
Responsed Disease Non-small-cell lung carcinoma ICD-11: 2C25.Y
Target Regulation Up regulation
Pathway Response Hippo signaling pathway hsa04390
Cell Process Metabolic
In-vitro Model A-549 Lung adenocarcinoma Homo sapiens CVCL_0023
Calu-6 Lung adenocarcinoma Homo sapiens CVCL_0236
NCI-H1299 Lung large cell carcinoma Homo sapiens CVCL_0060
NCI-H520 Lung squamous cell carcinoma Homo sapiens CVCL_1566
In-vivo Model Mice were injected with 5 × 106 lung cancer cells with stably expression of relevant plasmids and randomly divided into two groups (five mice per group) after the diameter of the xenografted tumors had reached approximately 5 mm in diameter. Xenografted mice were then administrated with PBS or DDP (3 mg/kg per day) for three times a week, and tumor volume were measured every second day.
Response Summary METTL3, YTHDF3, YTHDF1, and eIF3b directly promoted YAP translation through an interaction with the translation initiation machinery. METTL3 knockdown inhibits tumor growth and enhances sensitivity to DDP in vivo.m6A mRNA methylation initiated by METTL3 directly promotes YAP translation and increases YAP activity by regulating the MALAT1-hsa-miR-1914-3p-YAP axis to induce Non-small cell lung cancer drug resistance and metastasis.
Xenobiotics Compound(s) Regulating the m6A Methylation Regulator
Compound Name Cholecalciferol Investigative
Synonyms
Vitamin D3; cholecalciferol; 67-97-0; Calciol; Colecalciferol; Oleovitamin D3; Ricketon; Arachitol; Trivitan; Deparal; Delsterol; Vigorsan; Ebivit; Activated 7-dehydrocholesterol; vitamin d-3; Colecalcipherol; Quintox; Colecalciferolum; Cholecalciferolum; (+)-Vitamin D3; D3-Vicotrat; D3-Vigantol; Vi-de-3-hydrosol; NEO Dohyfral D3; Vitinc Dan-Dee-3; 1406-16-2; Cholecalciferol, D3; Vi-De3; Provitina; Duphafral D3 1000; FeraCol; Delta-D; CC; CHEBI:28940; MFCD00078131; (1S,3Z)-3-[(2E)-2-[(1R,3aS,7aR)-7a-methyl-1-[(2R)-6-methylheptan-2-yl]-2,3,3a,5,6,7-hexahydro-1H-inden-4-ylidene]ethylidene]-4-methylidenecyclohexan-1-ol; NSC 375571; 9,10-Secocholesta-5,7,10(19)-trien-3-beta-ol; 7-Dehydrocholesterol activated; Micro-dee; 7-Dehydrocholesterol, Activated; VidDe-3-hydrosol; Vitamin D3 solution; NSC-375571; Colecalciferol (INN); Colecalciferol [INN]; NCGC00159331-02; Rampage; (3beta,5Z,7E)-9,10-secocholesta-5,7,10(19)-trien-3-ol; (5Z,7E)-(3S)-9,10-seco-5,7,10(19)-cholestatrien-3-ol; (5Z,7E)-(3S)-9,10-secocholesta-5,7,10(19)-trien-3-ol; DSSTox_CID_6294; DSSTox_RID_78090; DSSTox_GSID_26294; Vitamin D3 (Cholecalciferol); UNII-1C6V77QF41; 9,10-Seco(5Z,7E)-5,7,10(19)-cholestatrien-3beta-ol; Colecalciferolo; (3S,5Z,7E)-9,10-secocholesta-5,7,10(19)-trien-3-ol; Colecalciferolo [DCIT]; 9,10-Secocholesta-5(Z),7(E),10(19)-trien-3(.beta.)-ol; Vigantol Oil; (5e)-cholecalciferol; 22350-41-0; Colecalciferol D3; (1S,3Z)-3-[(2E)-2-[(1R,3aS,7aR)-1-[(1R)-1,5-dimethylhexyl]-7a-methyl-2,3,3a,5,6,7-hexahydro-1H-inden-4-ylidene]ethylidene]-4-methylene-cyclohexanol; (S,Z)-3-(2-((1R,3aS,7aR,E)-7a-methyl-1-((R)-6-methylheptan-2-yl)octahydro-4H-inden-4-ylidene)ethylidene)-4-methylenecyclohexan-1-ol; Cyclohexanol, 3-[(2E)-2-[(1R,3aS,7aR)-1-[(1R)-1,5-dimethylhexyl]octahydro-7a-methyl-4H-inden-4-ylidene]ethylidene]-4-methylene-, (1S,3Z)-; Colecalciferolum [INN-Latin]; Vitamin D 3; 7-Dehydrocholestrol, activated; Irradiated 7-dehydrocholesterol; CCRIS 5813; CCRIS 6286; HSDB 820; 7-Dehydrocholesterol, irradiated; Vitamin D3 emulsifiable; EINECS 200-673-2; EINECS 215-797-2; EPA Pesticide Chemical Code 202901; Vitamin D3; Cholecalciferol; 1C6V77QF41; Devaron; Videkhol; NSC375571; Granuvit D3; DP-R206; CAS-67-97-0; Prestwick_63; Cholecalciferol D3; Cyclohexanol, 3-((2E)-2-((1R,3aS,7aR)-1-((1R)-1,5-dimethylhexyl)octahydro-7a-methyl-4H-inden-4-ylidene)ethylidene)-4-methylene-, (1S,3Z)-; Cholecalciferol [USP:BAN:JAN:ISO]; ()-Vitamin D3; 9,10-Seco(5Z,7E)-5,7,10(19)-cholestatrien-3-ol; Delta-D (TN); 9,10-Secocholesta-5,7,10(19)-trien-3-ol, (3beta,5Z,7E)-; Prestwick3_000429; bmse000507; UPCMLD-DP152; SCHEMBL3126; Vitamin d (cholecalciferol); CHEMBL1042; BSPBio_000418; Cholecalciferol; 67-97-0; Cholecalciferol (JP17/USP); BPBio1_000460; MEGxm0_000458; DTXSID6026294; UPCMLD-DP152:001; ACon1_001997; Vitamin d3 (as cholecalciferol); HMS2096E20; Vitamin d assay system suitability; Cholecalciferol, >=98% (HPLC); 9,10-Secocholestra-5,7,10(19)-trien-3-ol, (3beta,5Z,7E)-; Cholecalciferol, analytical standard; ZINC4474460; Tox21_111578; Tox21_202546; BDBM50030475; LMST03020001; s4063; AKOS015950641; AC-8884; CCG-268466; CS-1179; DB00169; SMP1_000068; AK R215 COMPONENT COLECALCIFEROL; AK-R215 COMPONENT COLECALCIFEROL; NCGC00091072-01; NCGC00159331-04; NCGC00260095-01; BS-42465; HY-15398; K119; Vitamin D3 10 microg/mL in Acetonitrile; 9,10-secocholesta-5,7,10-trien-3-ol; Cholecalciferol (D3), analytical standard; C05443; D00188; 9,10-Secocholesta-5,7,10(19)-trien-3-ol; Cholecalciferol, meets USP testing specifications; 078V131; 9,10-Secocholesta-5,7,10(19)-trien-3?-ol; Q139347; (5E,7E)-9,10-Secocholesta-5,7,10-trien-3-ol; Q-201931; 3-beta,Z,7E-9,10-Secocholestr-5,7,10(19)-trien-3-ol; Vitamin D3 solution, 100 mug/mL in ethanol, 97% (CP); (3beta,Z,7E)-9,10-Secocholesta-5,7,10(19)-trien-3-ol; 9,10-Secocholesta-5,7,10(19)-trien-3-ol, (3b,5Z,7E)-; Cholecalciferol, European Pharmacopoeia (EP) Reference Standard; Colecalciferol, British Pharmacopoeia (BP) Reference Standard; Cholecalciferol, United States Pharmacopeia (USP) Reference Standard; Cholecalciferol for system suitability, European Pharmacopoeia (EP) Reference Standard; Vitamin D3 solution, 1 mg/mL in ethanol, ampule of 1 mL, certified reference material; (1S,3Z)-3-[(2E)-2-[7a-Methyl-1-(6-methylheptan-2-yl)-2,3,3a,5,6,7-hexahydro-1H-inden-4-ylidene]ethylidene]-4-methylidenecyclohexan-1-ol; Cholecalciferol (Vitamin D3), Pharmaceutical Secondary Standard; Certified Reference Material
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Description
vitamin D3 protects vascular endothelial cells from HCMV-induced apoptosis by reducing the elevated translation of MCU induced by HCMV through METTL3- and YTHDF3-dependent mechanisms via VDR/AMPK/METTL3 pathway.
[18]
References
Ref 1 YTHDF3 Induces the Translation of m(6)A-Enriched Gene Transcripts to Promote Breast Cancer Brain Metastasis. Cancer Cell. 2020 Dec 14;38(6):857-871.e7. doi: 10.1016/j.ccell.2020.10.004. Epub 2020 Oct 29.
Ref 2 The m(6)A reading protein YTHDF3 potentiates tumorigenicity of cancer stem-like cells in ocular melanoma through facilitating CTNNB1 translation. Oncogene. 2022 Feb;41(9):1281-1297. doi: 10.1038/s41388-021-02146-0. Epub 2022 Feb 3.
Ref 3 m(6)A reader Ythdf3 protects hematopoietic stem cell integrity under stress by promoting the translation of Foxm1 and Asxl1 transcripts. Haematologica. 2022 Aug 1;107(8):1922-1927. doi: 10.3324/haematol.2021.279300.
Ref 4 RNA-binding protein YTHDF3 suppresses interferon-dependent antiviral responses by promoting FOXO3 translation. Proc Natl Acad Sci U S A. 2019 Jan 15;116(3):976-981. doi: 10.1073/pnas.1812536116. Epub 2018 Dec 27.
Ref 5 KDM5B promotes self-renewal of hepatocellular carcinoma cells through the microRNA-448-mediated YTHDF3/ITGA6 axis. J Cell Mol Med. 2021 Apr 7;25(13):5949-62. doi: 10.1111/jcmm.16342. Online ahead of print.
Ref 6 N(6)-methyladenosine modification of ITGA6 mRNA promotes the development and progression of bladder cancer. EBioMedicine. 2019 Sep;47:195-207. doi: 10.1016/j.ebiom.2019.07.068. Epub 2019 Aug 10.
Ref 7 m(6)A mRNA methylation initiated by METTL3 directly promotes YAP translation and increases YAP activity by regulating the MALAT1-miR-1914-3p-YAP axis to induce NSCLC drug resistance and metastasis. J Hematol Oncol. 2019 Dec 9;12(1):135. doi: 10.1186/s13045-019-0830-6.
Ref 8 circ_KIAA1429 accelerates hepatocellular carcinoma advancement through the mechanism of m(6)A-YTHDF3-Zeb1. Life Sci. 2020 Sep 15;257:118082. doi: 10.1016/j.lfs.2020.118082. Epub 2020 Jul 10.
Ref 9 YTHDF3 facilitates triple-negative breast cancer progression and metastasis by stabilizing ZEB1 mRNA in an m(6)A-dependent manner. Ann Transl Med. 2022 Jan;10(2):83. doi: 10.21037/atm-21-6857.
Ref 10 N6-methyladenosine reader YTH N6-methyladenosine RNA binding protein 3 or insulin like growth factor 2 mRNA binding protein 2 knockdown protects human bronchial epithelial cells from hypoxia/reoxygenation injury by inactivating p38 MAPK, AKT, ERK1/2, and NF-KappaB pathways. Bioengineered. 2022 May;13(5):11973-11986. doi: 10.1080/21655979.2021.1999550.
Ref 11 YTHDF3 Facilitates eIF2AK2 and eIF3A Recruitment on mRNAs to Regulate Translational Processes in Oxaliplatin-Resistant Colorectal Cancer. ACS Chem Biol. 2022 Jul 15;17(7):1778-1788. doi: 10.1021/acschembio.2c00131. Epub 2022 Jun 15.
Ref 12 Long noncoding RNA GAS5 inhibits progression of colorectal cancer by interacting with and triggering YAP phosphorylation and degradation and is negatively regulated by the m(6)A reader YTHDF3. Mol Cancer. 2019 Oct 16;18(1):143. doi: 10.1186/s12943-019-1079-y.
Ref 13 A reciprocal feedback between N6-methyladenosine reader YTHDF3 and lncRNA DICER1-AS1 promotes glycolysis of pancreatic cancer through inhibiting maturation of miR-5586-5p. J Exp Clin Cancer Res. 2022 Feb 19;41(1):69. doi: 10.1186/s13046-022-02285-6.
Ref 14 m(6)A RNA modification and its writer/reader VIRMA/YTHDF3 in testicular germ cell tumors: a role in seminoma phenotype maintenance. J Transl Med. 2019 Mar 12;17(1):79. doi: 10.1186/s12967-019-1837-z.
Ref 15 Increased m6A methylation level is associated with the progression of human abdominal aortic aneurysm. Ann Transl Med. 2019 Dec;7(24):797. doi: 10.21037/atm.2019.12.65.
Ref 16 m6A regulator-mediated RNA methylation modification patterns and immune microenvironment infiltration characterization in severe asthma. J Cell Mol Med. 2021 Nov;25(21):10236-10247. doi: 10.1111/jcmm.16961. Epub 2021 Oct 14.
Ref 17 Resveratrol Attenuates High-Fat Diet Induced Hepatic Lipid Homeostasis Disorder and Decreases m(6)A RNA Methylation. Front Pharmacol. 2020 Dec 18;11:568006. doi: 10.3389/fphar.2020.568006. eCollection 2020.
Ref 18 Vitamin D3 Suppresses Human Cytomegalovirus-Induced Vascular Endothelial Apoptosis via Rectification of Paradoxical m6A Modification of Mitochondrial Calcium Uniporter mRNA, Which Is Regulated by METTL3 and YTHDF3. Front Microbiol. 2022 Mar 11;13:861734. doi: 10.3389/fmicb.2022.861734. eCollection 2022.