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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-expressing macrophages in the bone marrow stem cell niche.
The perturbation of CD82-ganglioside-CD44 signaling attenuates pathological angiogenesis.
Loss of Kai1 expression is associated with neoplasm metastasis.
The synergistic effects of CD82 and GM3 or GM2/GM3 ganglioside on EGFR expression and phosphorylation and cMet activation are responsible for CD82 inhibition of EGF- and HGF-dependent cell motility and migration of Hepa1-6 cells.
CD81 promotes the microvillus formation and/or extension while tetraspanin CD82 inhibits these events. In addition, CD81 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 promotes sarcoma metastasis by targeting KAI1 for degradation
The transgenic adenocarcinoma of mouse prostate model encompasses androgen depletion independent sublines with increased tumorigenicity and invasiveness. All showed downregulation in tumor suppressor, E-cadherin, and metastatis suppressor, KAI-1.
Low CD82 expression is associated with Biochemical Failure in Prostate cancer.
The inhibition of miR-338-5p suppressed growth and metastasis of A375 cells. CD82 mRNA was identified as a direct target mRNA of miR-338-5p.
The positive expression rates of KAI1 and nm23 were significantly lower in laryngeal squamous cell carcinoma than normal laryngeal mucosa.
these data propose a mechanism where CD82 membrane organization regulates sustained PKCalpha 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 (AML).
CD82 is a component of the promiscuous TIMP-1 interacting protein complex on cell surface of human pancreatic adenocarcinoma cells. CD82 directly binds to TIMP-1 N-terminal region through its large extracellular loop and co-localizes with TIMP-1.
the results suggest that CD82 suppresses epithelial-to-mesenchymal transition in prostate cancer cells adhered to the fibronectin 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 and knockdown of CD82 markedly promoted GC cell invasion and activated EGFR/ERK1/2-MMP7 signaling via upregulation of the expression of phosphorylated (p)-EGFR, p-ERK1/2 and MMP7.
Authors showed that miR-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-mediated CD44 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 clustering and membrane density, which impacts the in vivo trafficking of AML cells.
Methylation of CpG islands within the KAI1 promoter region was observed in the low KAI1-expressing prostate cancer cells.
CD82 function may be important for muscle stem cell function in muscular disorders.
The overexpression of KAI1/CD82 inhibited the proliferation and invasion of OSCC-15 cells.
Our present work therefore suggests that CD82 on EC is a potential target for anti-angiogenic therapy in VEGFR2-dependent tumor angiogenesis.
that a loss of KAI1/CD82 and an increase in PDGFR expression in gliomas relate to a progressive tumor growth
KAI1 underexpression is associated with gastric cancer.
KAI1-induced decreases in VEGFC expression are mediated via Src/STAT3 signaling pathways in pancreatic cancer cells.
The simultaneous overexpression of p12CDK2-AP1 and CD82 significantly suppressed the in vivo tumor growth.
Lack of expression of the KAI1 might indicate a more aggressive form of breast cancer.
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