Sequence Browser (O94851-2)

Available Structures (Graph-View Mode)

UniProt (Ref Seq)
Displayed Structure
Experimental Tertiary/Complex (PDB:XRay/EM)
Experimental Tertiary/Complex (PDB:NMR)
Modelled Tertiary (Phyre)
If the whole structure is coloured grey in '3D Structure Viewer' panel, please click the icon - on the top left corner of the viewer.
(If nothing changes then 'Sequence ↔ Structure' mapping may be unavailable).
1
1124

Isoforms (From UniProt)

Isoform
Remark
Ref
O94851-1
O94851-2  
VSP_009859 VSP_009860 VSP_009861
O94851-6
VSP_042593 VSP_009861
O94851-3
VSP_042595
O94851-4
VSP_042594 VSP_042596 VSP_009861
O94851-5
VSP_042594
Click on Isoform of interest to be redirected to the corresponding page

3D Structure Viewer - JSMol  

To analyse the structural impact of your missense variant:

  • Select the corresponding experimental/modelled structure from the "Available Structures" Panel.
  • Right-click on the target structure and download it.
  • Go to our web server Missense3D to analyse structural impact.

    • Go to Missense3D

Protein Information (From UniProt)

Protein:
[F-actin]-monooxygenase MICAL2
Other Names:
Molecule interacting with CasL protein 2
Primary Accession:
O94851
Other Accessions:
B4DGZ0, B7Z849, D3DQW5, G3XAC8, Q5KTR3, Q5KTR4, Q7Z3A8
Gene :
MICAL2*, synonyms (KIAA0750, MICAL2PV1, MICAL2PV2)
Organism :
Human
Entry Name :
MICA2_HUMAN
Length :
1,124
Mass (Da) :
126,689
Last modified :
01-Jan-1999
Version :
v1
Isoforms :
6 
Structures :
Experimental 0 | Phyre prediction 4
Function : Show Hide

Nuclear monooxygenase that promotes depolymerization of F-actin by mediating oxidation of specific methionine residues on actin to form methionine-sulfoxide, resulting in actin filament disassembly and preventing repolymerization. In the absence of actin, it also functions as a NADPH oxidase producing H(2)O(2) (By similarity). Acts as a key regulator of the SRF signaling pathway elicited by nerve growth factor and serum: mediates oxidation and subsequent depolymerization of nuclear actin, leading to increase MKL1/MRTF-A presence in the nucleus and promote SRF:MKL1/MRTF-A-dependent gene transcription. Does not activate SRF:MKL1/MRTF-A through RhoA.