Gene interactions and pathways from curated databases and text-mining

◀ Back to BCL10

BCL10 — IGF1

Text-mined interactions from Literome

Leverrier et al., Cell Death Differ 1999 : Role of PI3-kinase in Bcl-X induction and apoptosis inhibition mediated by IL-3 or IGF-1 in Baf-3 cells
Fornoni et al., Am J Pathol 2001 : We investigated whether Bcl-xL and Fas/Fas-ligand were regulated by CsA in cultured podocytes and whether CsA induced apoptosis was prevented by HGF or IGF-I ... HGF, but not IGF-I , prevented apoptosis and restored Bcl-xL levels
Yamamura et al., Am J Physiol Heart Circ Physiol 2001 (Myocardial Reperfusion Injury) : IGF-I differentially regulates Bcl-xL and Bax and confers myocardial protection in the rat heart ... These results suggest that IGF-1 differentially regulates Bcl-xL and Bax in heart mitochondria, which may be causally related to myocardial protection against ischemia-reperfusion injury
Nakao et al., J Thorac Cardiovasc Surg 2001 (Disease Models, Animal...) : Immunohistochemical studies revealed that insulin-like growth factor 1 increased expression of the antiapoptotic Bcl-xL protein and inhibited expression of the proapoptotic Bax protein in motor neuron cells 24 and 48 hours after the operation
Hilmi et al., J Invest Dermatol 2008 (Melanoma) : Accordingly, IGF1 increases the mRNA levels and protein expression of antiapoptotic members of the BCL2 family -- BCL2 and BCL-X ( L ) -- and that of the inhibitor of apoptosis protein, survivin ... Accordingly, IGF1 increases the mRNA levels and protein expression of antiapoptotic members of the BCL2 family -- BCL2 and BCL-X ( L ) -- and that of the inhibitor of apoptosis protein, survivin
Singh et al., Growth Factors 2008 (Breast Neoplasms) : Furthermore, IGF-II differentially regulated the intracellular translocation of Bcl-2 and Bcl-X ( L ), a critical process in breast cancer progression to hormone-independence
Singleton et al., J Biol Chem 1996 : Finally, increased neuronal IGF-IR expression enhances the negative death regulator Bcl-xL
Suzuki et al., FEBS Lett 1998 : It was also found that R-Ras and IGF-1 cooperatively induced Bcl-xL expression and inhibited caspase-3 activation