SMAD4 (C-Term) Rabbit Monoclonal Antibody (Clone RM277)

SMAD4, also known as deleted in pancreatic carcinoma locus 4 (DPC4), is a tumor suppressor and a signal transduction protein that functions as a central mediator of the TGF-β and bone morphogenic protein (BMP) signaling pathways.^1,2 It is comprised of an N-terminal MH1 domain that binds DNA, a linker region containing a C-terminal SMAD activation domain essential to SMAD4 transcriptional activity, and a C-terminal MH2 domain that interacts with the MH1 domain of other SMAD proteins to facilitate homo- and heterodimerization.² SMAD4 is ubiquitously expressed and localized to both the nucleus and cytosol.¹ Upon TGF-β or BMP receptor activation, SMAD4 forms complexes with phosphorylated SMAD2 and SMAD3 or SMAD1, SMAD5, and SMAD8, respectively, which are translocated to the nucleus to induce cell cycle arrest and apoptosis.² Homozygous deletion of, or intragenic inactivation mutations in, SMAD4 have been found in pancreatic and colorectal cancers. Heterozygous mutations in SMAD4 have been found in approximately 20% of patients with juvenile polyposis syndrome and are positively correlated with manifestation of hereditary hemorrhagic telangiectasia.³ Cayman’s SMAD4 (C-Term) Rabbit Monoclonal Antibody can be used for immunohistochemistry (IHC) and Western blot (WB) applications.

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1. McCarthy, A.J., and Chetty, R. Smad4/DPC4. J. Clin. Pathol. 71(8), 661-664 (2018).

2. Zhao, M., Mishra, L., and Deng, C.-X. The role of TGF-β/SMAD4 signaling in cancer. Int. J. Biol. Sci. 14(2), 111-123 (2018).

3. Andrabi, S., Bekheirnia, M.R., Robbins-Furman, P., et al. SMAD4 mutation segregating in a family with juvenile polyposis, aortopathy, and mitral valve dysfunction. Am. J. Med. Genet. A. 155A(5), 1165-1169 (2011).