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Our findings indicate an important role of CD9 for lentiviral vector and exosome biogenesis and point out a remarkable function of this tetraspanin in membrane fusion, viral infectivity, and exosome-mediated horizontal information transfer.
assays. Results from the present study demonstrated that CD9 was highly expressed in the highly metastatic Hepatocellular carcinoma (HCC)cells and promoted HCC cell migration. This protein may be a novel target for regulating the invasive phenotype in HCC.
The species-specific traits in CD9 and CD81 distribution during sperm maturation were compared between mice and humans. A mutual position of CD9/CD81 is shown in human spermatozoa in the acrosomal cap, however in mice, CD9 and CD81 occupy a distinct area.
CD9 expression predicts some clinical characteristics and indicates an unfavorable prognosis in acute lymphoblastic leukemia patients.
CD9-CD81 blockage reduces exosome-mediated HIV-1 entry.
CD9 stabilizes gp130 by blocking its ubiquitin-dependent lysosomal degradation to promote the IL6-gp130-bone marrow X-linked non-receptor tyrosine kinase-STAT3 signaling for maintaining GSC selfrenewal and tumorigenic capacity.
CD9 was highly expressed on extravillous trophoblast (EVT) at the boundary region of EVT invasion and intravascular EVT. CD9 expression on Swan71 cells was reduced under hypoxic conditions, while its expression was increased by co-culture with HUVEC. CD9 could attenuate EVT invasion under the influence of an oxygen environment and maternal endothelial cells, proposing CD9 as a potential regulator of human placentation.
As for 18Lin(-), CD34(-) HSCs are characterized by low expression of the tetraspanin CD9, which promotes homing, and high expression of the peptidase CD26, which inhibits homing.
The findings suggest that, in contrast with previous models, the ligand-binding site of integrin alphaVbeta3, binds to the constant region (helices A and B) of the EC2 domain of CD9, CD81, and CD151 antigens.
Data suggest that CD9 should be further evaluated as a target for glioblastoma treatment.
Collectively, using tetraspanin CD9 in tandem with E-cadherin as a biomarker in renal cell carcinoma will help to not only distinguish between types, but also predict the metastatic potential of RCC.
Data indicate that CD9 is implicated in BCC invasiveness and metastases by cellular mechanisms that involve specific CD9+ plasma membrane protrusions of BCCs.
Results indicate that CD9 downregulation promoted pancreatic cancer cell proliferation and migration through at least in part, enhancing the cell surface expression of EGFR.
CD9 plays a role in the dysmegakaryopoiesis that occurs in primary myelofibrosis.
High CD9 is associated with B acute lymphoblastic leukemia.
Mice lacking RXRalpha in myeloid cells exhibit reduced levels of CCL6 and CCL9, impaired recruitment of leukocytes to sites of inflammation, and lower susceptibility to sepsis.
CCL6 gene activation and production induced by SCF in the presence or absence of rather specific inhibitors for certain pathways demonstrated that the MEK/MAPK pathway but not the PI-3K pathway was crucial for the SCF-induced CCL6 gene activation.
This gene encodes a member of the transmembrane 4 superfamily, also known as the tetraspanin family. Tetraspanins are cell surface glycoproteins with four transmembrane domains that form multimeric complexes with other cell surface proteins. The encoded protein functions in many cellular processes including differentiation, adhesion, and signal transduction, and expression of this gene plays a critical role in the suppression of cancer cell motility and metastasis.