TBC1D22A antibodies are immunological reagents designed to detect and analyze TBC1D22A (TBC1 domain family member 22A), a 517-amino-acid protein encoded by the TBC1D22A gene on human chromosome 22 . These antibodies facilitate research into the protein’s roles in Rab GTPase regulation, Golgi membrane dynamics, and disease mechanisms .
Protein Structure: Contains a Rab-GAP TBC domain critical for GTPase-activating activity .
Ortholog Conservation: 92% sequence identity with mouse, 59% with rat .
| Property | Detail |
|---|---|
| UniProt ID | Q8WUA7 (Human) |
| Molecular Weight | ~59 kDa (observed via SDS-PAGE) |
| Aliases | C22orf4, HSC79E021 |
ACBD3 Interaction: TBC1D22A/B binds ACBD3 (acyl-CoA binding domain protein 3) at residues 246–321, competing with PI4KB (phosphatidylinositol 4-kinase beta) for binding . This competition modulates Golgi phosphatidylinositol 4-phosphate (PI4P) levels, influencing membrane organization .
Viral Pathogenesis: Enteroviruses (e.g., poliovirus) exploit ACBD3-TBC1D22A interactions to hijack Golgi membranes for replication. Poliovirus 3A protein enhances TBC1D22A-ACBD3 binding, while Aichi virus 3A does not .
| Competitive Binding Assay (ACBD3) | Result |
|---|---|
| TBC1D22A overexpression | Reduces PI4KB-ACBD3 interaction |
| TBC1D22A N-terminal domain | Sufficient for competition |
Cancer: High TBC1D22A expression correlates with poor prognosis in ovarian serous cystadenocarcinoma .
Neurological Disorders: Chromosome 22 mutations involving TBC1D22A are linked to autism, schizophrenia, and Phelan-McDermid syndrome .
Leukemia: Chromosomal translocations involving 22q13.2 may contribute to BCR-Abl fusion proteins in Philadelphia chromosome-positive leukemias .