AlphaFold predicted structure
ARPC1B · O15143

Mean pLDDT
92.4/ 100
Very high
372 residues
Confidence breakdown
- Very high(≥ 90)86%
- Confident(70–90)6%
- Low(50–70)6%
- Very low(< 50)3%
AlphaFold (Jumper et al., 2021) · CC BY 4.0
actin related protein 2/3 complex subunit 1B
Annotations refreshed 10 hours ago.
Diagnostic Grade (Green)
Bleeding and platelet disorders
BIALLELIC, autosomal or pseudoautosomalCOVID-19 research
BIALLELIC, autosomal or pseudoautosomalInherited bleeding disorders
BIALLELIC, autosomal or pseudoautosomalPrimary immunodeficiency or monogenic inflammatory bowel disease
BIALLELIC, autosomal or pseudoautosomalCytopenia - NOT Fanconi anaemia
BIALLELIC, autosomal or pseudoautosomalplatelet abnormalities with eosinophilia and immune-mediated inflammatory disease
combined immunodeficiency
Combined T and B cell immunodeficiency
autoimmune disorder of central nervous system
cutaneous leishmaniasis
neurodegenerative disease
immunodeficiency disease
placental retention
schizophrenia
hereditary disease
Score is the Open Targets composite evidence score (0-1). Higher = stronger gene-disease association.
Actin-related protein 2/3 complex subunit 1B
Component of the Arp2/3 complex, a multiprotein complex that mediates actin polymerization upon stimulation by nucleation-promoting factor (NPF) (PubMed:11741539, PubMed:9230079). The Arp2/3 complex mediates the formation of branched actin networks in the cytoplasm, providing the force for cell motility (PubMed:11741539, PubMed:9230079). In addition to its role in the cytoplasmic cytoskeleton, the Arp2/3 complex also promotes actin polymerization in the nucleus, thereby regulating gene transcription and repair of damaged DNA (PubMed:29925947). The Arp2/3 complex promotes homologous recombination (HR) repair in response to DNA damage by promoting nuclear actin polymerization, leading to drive motility of double-strand breaks (DSBs) (PubMed:29925947)
ARPC1B · O15143

Mean pLDDT
92.4/ 100
Very high
372 residues
Confidence breakdown
AlphaFold (Jumper et al., 2021) · CC BY 4.0