Growth factor receptor-bound protein 10 also known as insulin receptor-binding protein Grb-IR is a
protein that in humans is encoded by the GRB10gene.[5][6][7][8]
Function
The product of this gene belongs to a small family of
adaptor proteins that are known to interact with a number of
receptor tyrosine kinases and signaling molecules. This gene encodes a growth factor receptor-binding protein that interacts with
insulin receptors and insulin-like growth-factor receptors (e.g.,
IGF1R and
IGF2R). Overexpression of some isoforms of the encoded protein inhibits tyrosine kinase activity and results in growth suppression. This gene is imprinted in a highly isoform- and tissue-specific manner. Alternatively spliced transcript variants encoding different isoforms have been identified.[5]
Animal studies
Mice whose paternally inherited Grb10 gene is inactivated are more aggressive while those whose maternally inherited allele is inactivated exhibit foetal overgrowth and are significantly bigger than wild-type litter-mates.[9]
^Morrione A, Valentinis B, Li S, Ooi JY, Margolis B, Baserga R (July 1996). "Grb10: A new substrate of the insulin-like growth factor I receptor". Cancer Res. 56 (14): 3165–7.
PMID8764099.
Midro AT, Debek K, Sawicka A, et al. (1993). "Second observation of Silver-Russel syndrome in a carrier of a reciprocal translocation with one breakpoint at site 17q25". Clin. Genet. 44 (1): 53–5.
doi:
10.1111/j.1399-0004.1993.tb03845.x.
PMID8403458.
S2CID20766311.
Morrione A, Valentinis B, Li S, et al. (1996). "Grb10: A new substrate of the insulin-like growth factor I receptor". Cancer Res. 56 (14): 3165–7.
PMID8764099.
Growth factor receptor-bound protein 10 also known as insulin receptor-binding protein Grb-IR is a
protein that in humans is encoded by the GRB10gene.[5][6][7][8]
Function
The product of this gene belongs to a small family of
adaptor proteins that are known to interact with a number of
receptor tyrosine kinases and signaling molecules. This gene encodes a growth factor receptor-binding protein that interacts with
insulin receptors and insulin-like growth-factor receptors (e.g.,
IGF1R and
IGF2R). Overexpression of some isoforms of the encoded protein inhibits tyrosine kinase activity and results in growth suppression. This gene is imprinted in a highly isoform- and tissue-specific manner. Alternatively spliced transcript variants encoding different isoforms have been identified.[5]
Animal studies
Mice whose paternally inherited Grb10 gene is inactivated are more aggressive while those whose maternally inherited allele is inactivated exhibit foetal overgrowth and are significantly bigger than wild-type litter-mates.[9]
^Morrione A, Valentinis B, Li S, Ooi JY, Margolis B, Baserga R (July 1996). "Grb10: A new substrate of the insulin-like growth factor I receptor". Cancer Res. 56 (14): 3165–7.
PMID8764099.
Midro AT, Debek K, Sawicka A, et al. (1993). "Second observation of Silver-Russel syndrome in a carrier of a reciprocal translocation with one breakpoint at site 17q25". Clin. Genet. 44 (1): 53–5.
doi:
10.1111/j.1399-0004.1993.tb03845.x.
PMID8403458.
S2CID20766311.
Morrione A, Valentinis B, Li S, et al. (1996). "Grb10: A new substrate of the insulin-like growth factor I receptor". Cancer Res. 56 (14): 3165–7.
PMID8764099.