PDB StructureKAI1 was modeled based on crystal structure of the extracellular domain of tetraspanin protein member, CD81 1G8Q
KAI1 cell-surface glycoprotein and the molecular mechanisms underlying the TIP60 coactivator complexes for the metastasissuppressorgeneNGF reverts by the expression of the, KAI1: for 'kang ai' (抗癌 Chinese for anticancer) locus: 11p11.2; [§§] is a members of the Transmembrane 4 superfamily (TM4SF), are likely to be a selective downregulation strategy for many genes it is an 'activation antigen' of T cells at the level of transcription or posttranscription is down-regulated in the progression of common solid epithelial tumors that leads to the down-regulation of the KAI1 gene. KAI1 is the human homolog of the mouse leukocyte surface antigen R2. DARC is essential for the function of CD82 antigen KAI1, CD82 specifically suppresses tumor metastasis of antigen R2, CD82 (KIA), is incorporated into the viral envelope, gp78 [AMFR-autocrine motility factor receptor] associates with KAI1 (also known as CD82) involved in ER-associated (endoplasmic reticulum) degradation (ERAD), calnexin (CANX) may play a role in this process. Notch1 can trans-activate an APPtarget gene, Kai1, and vice versa. Tetraspanin-enriched microdomains is important for KAI1/CD82's motility-inhibitory activity are glycoproteins of unknown function, and is directly associated with the EGF receptor (EGFR). KAI1 was modeled based on crystal structure of the extracellular domain of tetraspanin protein member, CD81 and two other tetraspans, CD9-(MRP-1) and CD19. DARC - Duffy blood group, chemokine receptor (Homo sapiens) is essential for the function of CD82, early B cell marker CD9 a molecular partner (CD9P-1) and CD151 (Raph blood group) was found to be coupled. CD151 and CO-029 (TSPAN8 tetraspanin 8) are supposed to promote metastasis formation. KISS1 triggers dormancy in solitary, metastatic tumor cells. COOH-terminal interacting tetraspanin (KITENIN)-vang-like 1 (van gogh, Drosophila) by interacting with KAI1 participates in the regulation of the tumor formation as well as increased invasiveness and cells. Adhesion forces laterally organize cellular membranes via the presence vs absence of,inversely associatedunivariateandmultivariate, Laminin (LN)- or (FN) fibronectin, associations that usually occur in the context of "tetraspaninweb"; its mechanism of action has not yet been fully elucidated.