Modomics - A Database of RNA Modifications

ID Card:

Full name: Pre-mRNA-splicing regulator WTAP
Synonym: KIAA0105,MGC3925,Mum2
GI: 47117889
UniProt: Q15007
Structures: | 7VF5 | 7VF2 | 7YG4 | 7YFJ |
Alpha Fold Predicted Structure: AF-Q15007-F1


PDB Structures:


7VF5

Structure Description:

Title:
Classification:
Technique:

Abstract of the PDB Structure's related Publication:

N 6 -methyladenosine (m 6 A) is the most abundant ribonucleotide modification among eukaryotic messenger RNAs. The m 6 A "writer" consists of the catalytic subunit m 6 A-METTL complex (MAC) and the regulatory subunit m 6 A-METTL-associated complex (MACOM), the latter being essential for enzymatic activity. Here, we report the cryo-electron microscopy (cryo-EM) structures of MACOM at a 3.0-Å resolution, uncovering that WTAP and VIRMA form the core structure of MACOM and that ZC3H13 stretches the conformation by binding VIRMA. Furthermore, the 4.4-Å resolution cryo-EM map of the MACOM-MAC complex, combined with crosslinking mass spectrometry and GST pull-down analysis, elucidates a plausible model of the m 6 A writer complex, in which MACOM binds to MAC mainly through WTAP and METTL3 interactions. In combination with in vitro RNA substrate binding and m 6 A methyltransferase activity assays, our results illustrate the molecular basis of how MACOM assembles and interacts with MAC to form an active m 6 A writer complex.

Download RCSB-PDB Structures:

Pdb Files   7VF2.pdb   7VF5.pdb   7YFJ.pdb   7YG4.pdb  
Pdbx/mmCIF Files   7VF2.cif   7VF5.cif   7YFJ.cif   7YG4.cif  


Protein sequence:

MTNEEPLPKKVRLSETDFKVMARDELILRWKQYEAYVQALEGKYTDLNSNDVTGLRESEEKLKQQQQESARRENILVMRLATKEQEMQECTTQIQYLKQVQQPSVAQLRSTMVDPAINLFFLKMKGELEQTKDKLEQAQNELSAWKFTPDSQTGKKLMAKCRMLIQENQELGRQLSQGRIAQLEAELALQKKYSEELKSSQDELNDFIIQLDEEVEGMQSTILVLQQQLKETRQQLAQYQQQQSQASAPSTSRTTASEPVEQSEATSKDCSRLTNGPSNGSSSRQRTSGSGFHREGNTTEDDFPSSPGNGNKSSNSSEERTGRGGSGYVNQLSAGYESVDSPTGSENSLTHQSNDTDSSHDPQEEKAVSGKGNRTVGSRHVQNGLDSSVNVQGSVL

Comments:





Alpha Fold Predicted Structure:






Clear Selection and Reset Camera

Protein sequence:

M T N E E P L P K K V R L S E T D F K V M A R D E L I L R W K Q Y E A Y V Q A L E G K Y T D L N S N D V T G L R E S E E K L K Q Q Q Q E S A R R E N I L V M R L A T K E Q E M Q E C T T Q I Q Y L K Q V Q Q P S V A Q L R S T M V D P A I N L F F L K M K G E L E Q T K D K L E Q A Q N E L S A W K F T P D S Q T G K K L M A K C R M L I Q E N Q E L G R Q L S Q G R I A Q L E A E L A L Q K K Y S E E L K S S Q D E L N D F I I Q L D E E V E G M Q S T I L V L Q Q Q L K E T R Q Q L A Q Y Q Q Q Q S Q A S A P S T S R T T A S E P V E Q S E A T S K D C S R L T N G P S N G S S S R Q R T S G S G F H R E G N T T E D D F P S S P G N G N K S S N S S E E R T G R G G S G Y V N Q L S A G Y E S V D S P T G S E N S L T H Q S N D T D S S H D P Q E E K A V S G K G N R T V G S R H V Q N G L D S S V N V Q G S V L

Secondary Structure Alphabet

  • G: 3-turn helix (310helix)
  • H: α-helix
  • I: 𝝅-helix (5 - turn helix)
  • T: Hydrogen Bonded Turn
  • B: β-sheet
  • S: Bend
  • C: Coil (residues not present in any of the above conformations)
  • N: Not assigned

Download PDB Structures & DSSP Secondary Structures:

Alpha Fold Pdb Files   AF-Q15007-F1.pdb  
Alpha Fold Pdbx/mmCIF Files   AF-Q15007-F1.cif  
DSSP Secondary Structures   Q15007.dssp  





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)

Publications:

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