Modomics - A Database of RNA Modifications

Full name:	YTH N6-methyladenosine RNA binding protein 2
Synonym:	HGRG8,NY-REN-2,CAHL
GI:	None
Orf:	None
COG:	None
UniProt:	Q9Y5A9
Structures:	\| 4rdn \|
Complex:	None

Comments:

None

Protein sequence:

MSASSLLEQRPKGQGNKVQNGSVHQKDGLNDDDFEPYLSPQARPNNAYTAMSDSYLPSYYSPSIGFSYSLGEAAWSTGGDTAMPYLTSYGQLSNGEPHFL
PDAMFGQPGALGSTPFLGQHGFNFFPSGIDFSAWGNNSSQGQSTQSSGYSSNYAYAPSSLGGAMIDGQSAFANETLNKAPGMNTIDQGMAALKLGSTEVA
SNVPKVVGSAVGSGSITSNIVASNSLPPATIAPPKPASWADIASKPAKQQPKLKTKNGIAGSSLPPPPIKHNMDIGTWDNKGPVAKAPSQALVQNIGQPT
QGSPQPVGQQANNSPPVAQASVGQQTQPLPPPPPQPAQLSVQQQAAQPTRWVAPRNRGSGFGHNGVDGNGVGQSQAGSGSTPSEPHPVLEKLRSINNYNP
KDFDWNLKHGRVFIIKSYSEDDIHRSIKYNIWCSTEHGNKRLDAAYRSMNGKGPVYLLFSVNGSGHFCGVAEMKSAVDYNTCAGVWSQDKWKGRFDVRWI
FVKDVPNSQLRHIRLENNENKPVTNSRDTQEVPLEKAKQVLKIIASYKHTTSIFDDFSHYEKRQEEEESVKKERQGRGK

Diseases connected to this enzyme:

Description	Reaction	Disease Name
YTHDF2 is the direct target of miR-493-3p and it is frequently upregulated in both PCa tissues and cell lines. Instead, miR-493-3p is downregulated. The overexpression of YTHDF2 and inhibition of miR-493-3p reduce m6A levels and increase the proliferation and migration of cancer cells	A:m6A	Prostate cancer
YTHDF2 binds to m6A-containing mRNAs and regulates their localization and stability. YTHDF2 upregulation increases the proliferative abilities of pancreatic cells by enhancing Akt/GSK3b/CyclinD1 pathway and on the opposite side it represses the invasion and migration abilities (EMT) by supressing the YAP pathway	A:m6A	Pancreatic cancer
YTHDF2 binds to m6A-containing mRNAs and regulates their localization and stability. YTHDF2 upregulation increases the proliferative abilities of pancreatic cells by enhancing Akt/GSK3b/CyclinD1 pathway and on the opposite side it represses the invasion and migration abilities (EMT) by supressing the YAP pathway	A:m6A	Pancreatic cancer
YTHDF2 is upregulated in lung cancer tissues and it recognizes m6A sites on the 3′UTR of 6-phosphogluconate dehydrogenase(6PGD) and facilitates its translation, which advances the pentose phosphate pathway (PPP) flux , which is crucial for tumor growth.	A:m6A	Non-small cell lung cancer
Mutations found in m6A regulatory genes are associated with lower OS and EFS rates in patients with AML ( Acute myeloid Leukemia) and presence of p53 mutations.	A:m6A	Leukemia
YTHDF2 is overexpressed in AML	A:m6A	Leukemia
YTHDF2 specifically expands human HSC numbers without skewing lineage fate. Essential role of YTHDF2 in regulating HSC self-renewal BY coupling the posttranscriptional m6A modification to the degradation of mRNAs encoding key transcription factors for self renewal (Tal1)	A:m6A	Leukemia
Increased m6A methylation level is associated to a decreased HCC cells proliferation. miR145 targets YTHDF2 3'UTR region and reduces its expression. The reduced expression of YTHDF2 is associated to an increased m6A level in the cells. In HCC cells there is a downregulation of miR145, an increased expression of YTHDF2 which recognize mRNA m6A sites and mediates mRNA degradation (decrease of m6A levels)	A:m6A	Hepatocellular carcinoma
m6A methylation level decreases the expression of tumor suppressor genes like SOCS2. The upregulation of METTL3 in HCC mediates this event through an m6A-YTHDF2-dependent mechanism and increases cancer cells proliferation, migration and metastasis formation	A:m6A	Hepatocellular carcinoma
HCC exhibited a characteristic gain of m6A modification in tandem with an increase of mRNA expression, owing to YTHDF2 reduction. YTHDF2 deficiency leads to mRNA stabilization of IL-11 and Serpin E2, the key mediators in support of hypoxia-induced cancer cell survival and vascular reconstruction. YTHDF2 is inhibited by HIF- 2α	A:m6A	Hepatocellular carcinoma
YTHDF2 was specifically down-regulated by hypoxia in HCC cells, and that YTHDF2 may function as a tumor suppressor in HCC by negatively modulating the EGFR mRNA stability via its binding the m6A site in the EGFR 3’UTR of mRNA, which in turn impairs the MEK/ERK pathway and consequently impedes the cell proliferation and growth	A:m6A	Hepatocellular carcinoma
YTHDF2 overexpression in GC cells. Knockdown of YTHDF2 in MGC-803 cells inhibits cell proliferation and promotes apoptosis.	A:m6A	Gastric cancer