Modomics - A Database of RNA Modifications

ID Card:

Full name: N6-adenosine-methyltransferase non-catalytic subunit
Synonym: KIAA1627
GI: 24308265
COG: COG4725
UniProt: Q9HCE5
Structures: | 5IL1 | 5IL2 | 5K7M | 5K7U | 5K7W | 5L6D | 5L6E | 5TEY | 6TTP | 6TTT | 6TTV | 6TTW | 6TTX | 6TU1 | 6Y4G | 7ACD | 7NHG | 7NHH | 7NHI | 7NHJ | 7NHV | 7NI7 | 7NI8 | 7NI9 | 7NIA | 7NID | 7O08 | 7O09 | 7O0L | 7O0M | 7O0P | 7O0Q | 7O0R | 7O27 | 7O28 | 7O29 | 7O2E | 7O2F | 7O2H | 7O2I | 7O2X | 7OED | 7OEE | 7OEF | 7OEG | 7OEH | 7OEI | 7OEJ | 7OEK | 7OEL | 7OEM | 7OQL | 7OQO | 7OQP |
Alpha Fold Predicted Structure: AF-Q9HCE5-F1
Complex: METTL3-METTL14
Enzyme type: methyltransferase
Position of modification - modification: m:many - m6A


PDB Structures:


5IL1

Structure Description:

Title:
Classification:
Technique:

Abstract of the PDB Structure's related Publication:

Chemical modifications of RNA have essential roles in a vast range of cellular processes. N(6)-methyladenosine (m(6)A) is an abundant internal modification in messenger RNA and long non-coding RNA that can be dynamically added and removed by RNA methyltransferases (MTases) and demethylases, respectively. An MTase complex comprising methyltransferase-like 3 (METTL3) and methyltransferase-like 14 (METTL14) efficiently catalyses methyl group transfer. In contrast to the well-studied DNA MTase, the exact roles of these two RNA MTases in the complex remain to be elucidated. Here we report the crystal structures of the METTL3-METTL14 heterodimer with MTase domains in the ligand-free, S-adenosyl methionine (AdoMet)-bound and S-adenosyl homocysteine (AdoHcy)-bound states, with resolutions of 1.9, 1.71 and 1.61 Å, respectively. Both METTL3 and METTL14 adopt a class I MTase fold and they interact with each other via an extensive hydrogen bonding network, generating a positively charged groove. Notably, AdoMet was observed in only the METTL3 pocket and not in METTL14. Combined with biochemical analysis, these results suggest that in the m(6)A MTase complex, METTL3 primarily functions as the catalytic core, while METTL14 serves as an RNA-binding platform, reminiscent of the target recognition domain of DNA N(6)-adenine MTase. This structural information provides an important framework for the functional investigation of m(6)A.

Download RCSB-PDB Structures:

Pdb Files   5IL0.pdb   5IL1.pdb   5IL2.pdb   5K7M.pdb   5K7U.pdb   5K7W.pdb   5L6D.pdb   5L6E.pdb   5TEY.pdb   6TTP.pdb   6TTT.pdb   6TTV.pdb   6TTW.pdb   6TTX.pdb   6TU1.pdb   6Y4G.pdb   7ACD.pdb   7NHG.pdb   7NHH.pdb   7NHI.pdb   7NHJ.pdb   7NHV.pdb   7NI7.pdb   7NI8.pdb   7NI9.pdb   7NIA.pdb   7NID.pdb   7O08.pdb   7O09.pdb   7O0L.pdb   7O0M.pdb   7O0P.pdb   7O0Q.pdb   7O0R.pdb   7O27.pdb   7O28.pdb   7O29.pdb   7O2E.pdb   7O2F.pdb   7O2H.pdb   7O2I.pdb   7O2X.pdb   7OED.pdb   7OEE.pdb   7OEF.pdb   7OEG.pdb   7OEH.pdb   7OEI.pdb   7OEJ.pdb   7OEK.pdb   7OEL.pdb   7OEM.pdb   7OQL.pdb   7OQO.pdb   7OQP.pdb  
Pdbx/mmCIF Files   5IL0.cif   5IL1.cif   5IL2.cif   5K7M.cif   5K7U.cif   5K7W.cif   5L6D.cif   5L6E.cif   5TEY.cif   6TTP.cif   6TTT.cif   6TTV.cif   6TTW.cif   6TTX.cif   6TU1.cif   6Y4G.cif   7ACD.cif   7NHG.cif   7NHH.cif   7NHI.cif   7NHJ.cif   7NHV.cif   7NI7.cif   7NI8.cif   7NI9.cif   7NIA.cif   7NID.cif   7O08.cif   7O09.cif   7O0L.cif   7O0M.cif   7O0P.cif   7O0Q.cif   7O0R.cif   7O27.cif   7O28.cif   7O29.cif   7O2E.cif   7O2F.cif   7O2H.cif   7O2I.cif   7O2X.cif   7OED.cif   7OEE.cif   7OEF.cif   7OEG.cif   7OEH.cif   7OEI.cif   7OEJ.cif   7OEK.cif   7OEL.cif   7OEM.cif   7OQL.cif   7OQO.cif   7OQP.cif  


Protein sequence:

MDSRLQEIRERQKLRRQLLAQQLGAESADSIGAVLNSKDEQREIAETRETCRASYDTSAPNAKRKYLDEGETDEDKMEEYKDELEMQQDEENLPYEEEIYKDSSTFLKGTQSLNPHNDYCQHFVDTGHRPQNFIRDVGLADRFEEYPKLRELIRLKDELIAKSNTPPMYLQADIEAFDIRELTPKFDVILLEPPLEEYYRETGITANEKCWTWDDIMKLEIDEIAAPRSFIFLWCGSGEGLDLGRVCLRKWGYRRCEDICWIKTNKNNPGKTKTLDPKAVFQRTKEHCLMGIKGTVKRSTDGDFIHANVDIDLIITEEPEIGNIEKPVEIFHIIEHFCLGRRRLHLFGRDSTIRPGWLTVGPTLTNSNYNAETYASYFSAPNSYLTGCTEEIERLRPKSPPPKSKSDRGGGAPRGGGRGGTSAGRGRERNRSNFRGERGGFRGGRGGAHRGGFPPR

Comments:

METTL14 is a methyltransferase which forms a stable heterodimer with METTL3. The complex mediates m6A deposition on nuclear RNA.




Reaction Substrate SubstrateType Position (Anti)Codon Modified (Anti)Codon Amino Acid Change Transcript Name Transcript Region Cellular Localization References
A:m6A mRNA (m) many 24316715   

Alpha Fold Predicted Structure:






Clear Selection and Reset Camera

Protein sequence:

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

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-Q9HCE5-F1.pdb  
Alpha Fold Pdbx/mmCIF Files   AF-Q9HCE5-F1.cif  
DSSP Secondary Structures   Q9HCE5.dssp  





Diseases connected to this enzyme:

Description Reaction Disease Name
METTL3 and METTL14 protein levels are decreased in whole islets from T2D patients. the Insulin/IGF1 -AKT-PDX1 pathway is significantly affected by hypomethylation in T2D A:m6A
Type 2 Diabetes
Increased P2RX6 mRNA m6A methylation level (induced by METTL14) enhances P2RX6 pre-mRNA splicing, decreases ATP-P2RX6-Ca2+ −p-ERK1/2-MMP9 axis and protects against RCCs migration and invasion. A:m6A
Renal cell carcinoma
Reduced levels of METTL3/METTL14 may lead to pathogenesis and progression of E/R-positive acute lymphoblastic leukemia and increase relapse rates. A:m6A
Leukemia
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
METTL14 is highly expressed in normal hematopoietic stem/progenitor cells (HSPCs) and acute myeloid leukemia (AML) cells carrying t(11q23), t(15;17), or t(8;21), and is down-regulated during myeloid differentiation. Mechanistically, METTL14 exerts its oncogenic role by regulating its mRNA targets (e.g., MYB and MYC) through m6A modification, which in turn leads to enhanced self-renewal/proliferation of LSCs/LICs and blockage of myeloid differentiation A:m6A
Leukemia
m6A methylation of pri-miR126 enhances its recogntion by DGCR8 and its subsequent processing to mature miRNA. miR126 plays an important role in tumor metastasis by acting as a tumor suppressor. The downregulation of METTL14 in HCC cells leads to the decreased processing of pri-miR126 thus reducing its tumor-suppressor activity A:m6A
Hepatocellular carcinoma
Decreased methylation promotes GSCs growth and self-renewal. METTL14 induced methylation protects against GSCs growth and self-renewal A:m6A
Glioblastoma
Decreased m6A methylation level, by METTL14 downregulation or FTO upregulation, promotes the activation of oncogenic signaling pathways, such as Wnt and PI3K‐Akt and supports GC cell proliferation, migration and invasion. A:m6A
Gastric cancer
~70% of tumor samples from endometrial cancer patients exhibited decreased m6A levels due to either decreased expression of METTL3 or loss of function mutation in METTL14 (R298P). This generates a reduction in m6A mRNA methylation levels and an enhancement in proliferation and tumorigenicity. Reductions in m6A methylation lead to decreased expression of the negative AKT regulator PHLPP2 and increased expression of the positive AKT regulator mTORC2. Increased AKT activation is one of the main mediators of increased proliferation in cells. A:m6A
Endometrial cancer
METTL14 is downregulated in CRC tissues and cell lines. It reduces m6A levels in total RNAs and promotes CRC cell growth and metastasis, METTL14 decreases miR-375 expression levels by modulating DGCR8 binding to primary miR-375 (primiR-375) in a m6A-dependent manner. A:m6A
Colorectal cancer
m6A levels are decreased in immortalized and oncogenically transformed human mammary epithelial cells. The levels of METTL3 are descresed and ALKBH5 are increased. Overexpression of METTL3 and METTL14 and knockdown of ALKBH5 results in increased proliferation and migaration of immortalized cells. m6A levels may be downregulated in immortalized cells. Hypoxia increased m6A levels throgh mechanisms that are independent of METTL3, METTL14 and ALKBH5 expression levels. Increases of m6A levels in hypoxia are regulated by HIF. A:m6A
Breast cancer
m6A inhibits breast cancer (BC) cell viability, the ability of MDA-MB-231 cells to form colonies and suppressed cell migratory abilities resulting in an overall effect of inhibition of BC growth and metastasis. Reduced expression of m6A is associated with poor prognostic in patient. Functionally, reducing m6A expression by overexpressing METTL14 and/or knockdown of ALKBH5 could inhibit breast cell viability, colony formation and cell migration. A:m6A
Breast cancer
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
m6A modification and METTL14 are lowly expressed in bladder cancer. METTL14 and m6A modification participate in the RNA stability of Notch1 mRNA. Notch1 m6A modification inhibits its RNA stability. Notch1 plays an essential role in bladder tumorigenesis and bladder tumor initiating cells self-renewal A:m6A
Bladder cancer

Publications:

Title Authors Journal Details PubMed Id DOI
A METTL3-METTL14 complex mediates mammalian nuclear RNA N-adenosine methylation. Liu J, Yue Y, Han D, Wang X, Fu Y, Zhang L, Jia G, Yu M, Lu Z, Deng X, Dai Q, Chen W, He C... Nat Chem Biol [details] 24316715 -

Links:

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