Full name: Pre-mRNA-splicing regulator WTAP
Synonym: KIAA0105,MGC3925,Mum2
GI: None
Orf: None
COG: None
UniProt: Q15007
Structures: | |
Complex: None

Comments:

None

Protein sequence:

MTNEEPLPKKVRLSETDFKVMARDELILRWKQYEAYVQALEGKYTDLNSNDVTGLRESEEKLKQQQQESARRENILVMRLATKEQEMQECTTQIQYLKQV
QQPSVAQLRSTMVDPAINLFFLKMKGELEQTKDKLEQAQNELSAWKFTPDSQTGKKLMAKCRMLIQENQELGRQLSQGRIAQLEAELALQKKYSEELKSS
QDELNDFIIQLDEEVEGMQSTILVLQQQLKETRQQLAQYQQQQSQASAPSTSRTTASEPVEQSEATSKDCSRLTNGPSNGSSSRQRTSGSGFHREGNTTE
DDFPSSPGNGNKSSNSSEERTGRGGSGYVNQLSAGYESVDSPTGSENSLTHQSNDTDSSHDPQEEKAVSGKGNRTVGSRHVQNGLDSSVNVQGSVL


Diseases connected to this enzyme:

Description Reaction Disease Name
In RCC cell lines and tissues, WTAP is significantly overexpressed. Mechanistic studies exhibited that CDK2 expression is positively associated with the expression of WTAP. Moreover, WTAP stabilizes CDK2 transcript to enhance CDK2 expression via binding to 3′-UTR of CDK2 transcript. A:m6A
Renal cell carcinoma
WTAP is significantly up-regulated in HCC and promotes liver cancer development. WTAP-guided m6A modification contributes to the progression of HCC via the HuR-ETS1-p21/p27 axis. ETS proto-oncogene 1 (ETS1) was identified as the downstream effector of WTAP. The m6A modification regulated by WTAP led to post-transcriptional suppression of ETS1, with the implication of Hu-Antigen R (HuR) as an RNA stabilizer. Then ETS1 was found to inhibit the progression of HCC and could rescue the phenotype induced by WTAP deficiency. Moreover, WTAP modulated the G2/M phase of HCC cells through a p21/p27-dependent pattern mediated by ETS1. A:m6A
Hepatocellular carcinoma
WTAP overexpression increases proliferation, migration, invasion and tumorigenicity of glioblastoma cells A:m6A
Glioblastoma
"m6A levels are reduced in breast cancer samples due to a decrease in m6A methylases expression and an increase in demethylases expression; expression levels of METTL3, METTL14, WTAP and FTO were correlated with poor survival and cancer progression; m6A higher levels suppress cancer cell viability, inhibit MDA-MB-231 colony-formation abilities and cell migratory abilities.Expression levels of writers and readers differes according to the subtype of breast cancer ( luminal A/B vs. triple negative)." A:m6A
Breast cancer
WTAP is downregulated in brain AVM lesions compared with normal cerebral vessels. DSP is stabilized via WTAP-m6A-IGF2BPs- dependent manner and participated in the regulation of angiogenesis. A:m6A
Brain arteriovenous malformations (AVMs)

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