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The CD82 is a functional surface marker of long-term repopulating hematopoietic stem cells (LT-HSCs) that maintains quiescence through interaction with DARC (show DARC Proteins)-expressing macrophages in the bone marrow stem cell niche.
The perturbation of CD82-ganglioside-CD44 (show CD44 Proteins) signaling attenuates pathological angiogenesis.
Loss of Kai1 expression is associated with neoplasm metastasis.
The synergistic effects of CD82 and GM3 (show GRM6 Proteins) or GM2 (show CYB5D2 Proteins)/GM3 (show GRM6 Proteins) ganglioside on EGFR (show EGFR Proteins) expression and phosphorylation and cMet activation are responsible for CD82 inhibition of EGF (show EGF Proteins)- and HGF (show HGF Proteins)-dependent cell motility and migration of Hepa1-6 cells.
CD81 (show CD81 Proteins) promotes the microvillus formation and/or extension while tetraspanin CD82 inhibits these events. In addition, CD81 (show CD81 Proteins) enhances the outward bending of the plasma membrane while CD82 inhibits it.
the CD82 tetraspanin is specifically recruited to pathogen-containing phagosomes prior to fusion with lysosomes.
KAI1 has a role in promotion of cell proliferation and mammary gland hyperplasia by the gp78 ubiquitin ligase
Hypoxia-dependent induction of KAI1 was directly mediated by hypoxia-inducible factor-1alpha binding on the promoter, which subsequently caused increased recruitment of RNA polymerase II for transcriptional activation.
An antibody to this protein that can specifically detect murine Kai1/CD82, should be useful in addressing the mechanism of action of Kai1 in metastatic suppression.
gp78 (show AMFR Proteins) promotes sarcoma metastasis by targeting KAI1 for degradation
The positive expression rates of KAI1 and nm23 (show NME1 Proteins) were significantly lower in laryngeal squamous cell carcinoma than normal laryngeal mucosa.
these data propose a mechanism where CD82 membrane organization regulates sustained PKCalpha (show PKCa Proteins) signaling that results in an aggressive leukemia phenotype. These observations suggest that the CD82 scaffold may be a potential therapeutic target for attenuating aberrant signal transduction in acute myeloid leukemia (show BCL11A Proteins) (AML (show RUNX1 Proteins)).
CD82 is a component of the promiscuous TIMP-1 (show TIMP1 Proteins) interacting protein complex on cell surface of human pancreatic adenocarcinoma cells. CD82 directly binds to TIMP-1 (show TIMP1 Proteins) N-terminal region through its large extracellular loop and co-localizes with TIMP-1 (show TIMP1 Proteins).
the results suggest that CD82 suppresses epithelial-to-mesenchymal transition in prostate cancer cells adhered to the fibronectin (show FN1 Proteins) matrix by repressing adhesion signaling through lateral interactions with the associated alpha3beta1 and alpha5beta1 integrins, leading to reduced cell migration and invasive capacities.
Overexpression of LAMC2 (show LAMC2 Proteins) and knockdown of CD82 markedly promoted GC cell invasion and activated EGFR (show EGFR Proteins)/ERK1/2-MMP7 (show MMP7 Proteins) signaling via upregulation of the expression of phosphorylated (p)-EGFR (show EGFR Proteins), p-ERK1/2 and MMP7 (show MMP7 Proteins).
Authors showed that miR (show MLXIP Proteins)-K6-5p directly targeted the coding sequence of CD82 molecule (CD82), a metastasis suppressor.
a sub-population of DeltaNp63 and CD82-positive cells, whose disruption significantly perturbs the development of prostate metastatic tumor growth.
These findings uncovered a hitherto unappreciated function of CD82 in severing the linkage between U2AF2 (show U2AF59 Proteins)-mediated CD44 (show CD44 Proteins) alternative splicing and cancer aggressiveness, with potential prognostic and therapeutic implications in melanoma
a mechanism where the membrane organization of CD82, through specific posttranslational modifications, regulates N-cadherin (show CDH2 Proteins) clustering and membrane density, which impacts the in vivo trafficking of AML (show RUNX1 Proteins) cells.
Methylation of CpG islands within the KAI1 promoter region was observed in the low KAI1-expressing prostate cancer cells.
This metastasis suppressor gene product is a membrane glycoprotein that is a member of the transmembrane 4 superfamily. Expression of this gene has been shown to be downregulated in tumor progression of human cancers and can be activated by p53 through a consensus binding sequence in the promoter. Its expression and that of p53 are strongly correlated, and the loss of expression of these two proteins is associated with poor survival for prostate cancer patients. Two alternatively spliced transcript variants encoding distinct isoforms have been found for this gene.
, inducible membrane protein R2
, kangai 1 (suppression of tumorigenicity 6, prostate)
, metastasis suppressor Kangai-1 homolog
, CD82 antigen
, kangai 1 (suppression of tumorigenicity 6, prostate; CD82 antigen (R2 leukocyte antigen, antigen detected by monoclonal and antibody IA4))
, metastasis suppressor Kangai-1
, CD82 antigen (R2 leukocyte antigen antigen detected by monoclonal and antibody IA4))
, CD82 antigen (R2 leukocyte antigen, antigen detected by monoclonal and antibody IA4))
, Kangai 1 (suppression of tumerigenicity 6 prostate) CD82 antigen
, Kangai 1 (suppression of tumorigenicity 6, prostate; CD82 antigen (R2 leukocyte antigen, antigen detected by monoclonal and antibody IA4))
, kangai 1 (suppression of tumorigenicity 6), prostate