Integrin beta-8 is a
protein that in humans is encoded by the ITGB8gene.[5]
Function
This gene is a member of the
integrin beta chain family and encodes a single-pass type I membrane protein with a VWFA domain and four cysteine-rich repeats. This protein noncovalently binds to an alpha subunit to form a
heterodimeric integrin complex. In general, integrin complexes mediate cell-cell and cell-
extracellular matrix interactions and this complex plays a role in human airway epithelial proliferation. Alternatively spliced variants which encode different protein isoforms have been described; however, not all the variants have been fully characterized.[5] Additionally, it has been shown to interact with RhoGDI1 to alter the activation of Rho GTPases to promote Glioblastoma cell invasiveness. Uncoupling the αvβ8-RhoGDI1 interaction has been seen to block GBM cell invasion by hyperactivating Rho GTPases.[6]
Clinical significance
High expression levels of ITGB8 are associated with high
angiogenic and poorly
invasiveglioblastoma tumors. Conversely low expression of ITGB8 correlates with highly invasive but low angiogenic tumors.[7]
Cambier S, Mu DZ, O'Connell D, et al. (2001). "A role for the integrin alphavbeta8 in the negative regulation of epithelial cell growth". Cancer Res. 60 (24): 7084–93.
PMID11156415.
Integrin beta-8 is a
protein that in humans is encoded by the ITGB8gene.[5]
Function
This gene is a member of the
integrin beta chain family and encodes a single-pass type I membrane protein with a VWFA domain and four cysteine-rich repeats. This protein noncovalently binds to an alpha subunit to form a
heterodimeric integrin complex. In general, integrin complexes mediate cell-cell and cell-
extracellular matrix interactions and this complex plays a role in human airway epithelial proliferation. Alternatively spliced variants which encode different protein isoforms have been described; however, not all the variants have been fully characterized.[5] Additionally, it has been shown to interact with RhoGDI1 to alter the activation of Rho GTPases to promote Glioblastoma cell invasiveness. Uncoupling the αvβ8-RhoGDI1 interaction has been seen to block GBM cell invasion by hyperactivating Rho GTPases.[6]
Clinical significance
High expression levels of ITGB8 are associated with high
angiogenic and poorly
invasiveglioblastoma tumors. Conversely low expression of ITGB8 correlates with highly invasive but low angiogenic tumors.[7]
Cambier S, Mu DZ, O'Connell D, et al. (2001). "A role for the integrin alphavbeta8 in the negative regulation of epithelial cell growth". Cancer Res. 60 (24): 7084–93.
PMID11156415.