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Fig. 2 | Cell Communication and Signaling

Fig. 2

From: Integrinβ-1 in disorders and cancers: molecular mechanisms and therapeutic targets

Fig. 2

ITGB1 and physiological function, benign disease. A ITGB1-deficient VSMCs have an enhanced cell proliferation capacity, while the ability to differentiate and support blood vessels is impaired. B Upregulation of the ITGB1 expression accelerates skeletal muscle regeneration in mice. C Upregulation of the ITGB1 expression in adipose derived stem cells (ADSCs) promotes cartilage differentiation of ADSCs. D The deletion of the ITGB1 subunit in proximal tubular cells leads to their conversion from loose epithelial cells characterized by a low expression of E-calmodulin and claudin-7 and a high expression of claudiin-2 to very dense epithelial cells. This leads to picomolecular diuresis under basal conditions and impaired urine concentration after water restriction. E Inhibition of the ITGB1 expression in glial cells may lead to neurodegenerative and behavioral abnormalities in adult mice. F YTHDF2 induces instability of ITGB1 mRNA and leads to mRNA degradation in the form of m6A. After ITGB1 silencing, it inhibits the FAK/PI3K/AKT signaling pathway. Moreover, the change in the YTHDF2 activity is caused by KAT1. YTHDF2-mediated instability of ITGB1 mRNA can slow the progression of diabetes retinopathy

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