The gene SMAD4 (mothers against decapentaplegic homolog 4), also known as DPC4 (deleted in pancreatic carcinoma), is mapped to human chromosome 18q21.1. The protein localizes in the cytoplasm and nucleus.
Immunogen
SMAD4 (NP_005350, 56 a.a. ~ 165 a.a) partial recombinant protein with GST tag. MW of the GST tag alone is 26 KDa.
Upon TGFβ (transforming growth factor β) activation, SMAD (mothers against decapentaplegic homolog) proteins are responsible for transcription activation in the nucleus. SMAD4 is a crucial protein of TGFβ signaling. It promotes association of SMAD2/4 to DNA and helps SMAD1/2 in transcription stimulation. Mutations in SMAD4 are linked with juvenile polyposis syndrome, hereditary haemorrhagic telangiectasia and Myhre syndrome. In renal cell carcinoma, it activates forkhead box protein H1 and thereby inhibits the progression of the carcinoma. SMAD4 is considered as a tumor suppressor protein.
Physical form
Solution in phosphate buffered saline, pH 7.4
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Mutations in the SMAD4/DPC4 gene in juvenile polyposis.
Howe JR
Science, 280, 1086-1088 (1998)
SMAD4 suppresses AURKA-induced metastatic phenotypes via degradation of AURKA in a TGF?-independent manner.
Jia L
Molecular Cancer Research, 12, 1779-1795 (2014)
Dual role of the Smad4/DPC4 tumor suppressor in TGFbeta-inducible transcriptional complexes.
Liu F
Genes & Development, 11, 3157-3167 (1997)
A restricted spectrum of mutations in the SMAD4 tumor-suppressor gene underlies Myhre syndrome.
Caputo V
American Journal of Human Genetics, 90, 161-169 (2012)
3-Phosphoinositide-dependent PDK1 negatively regulates transforming growth factor-beta-induced signaling in a kinase-dependent manner through physical interaction with Smad proteins.
Seong HA
The Journal of Biological Chemistry, 282, 12272-12289 (2007)
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