SMAD5 Protein, Mouse (sf9, His-GST)

SMAD5 (dwarfin C, JV5-1, MAD5) is a receptor activated Smad (R-Smad) belonging to the dwarfin/SMAD family. SMAD5 protein is activated by TGF-β receptor type I and binds to SMAD4 to form a trimer active form. SMAD5 is involved in BMP signaling pathway, regulates osteogenesis and is related to embryonic development. SMAD5 can up-regulate Runx2 expression and target osteocalcin and alkaline phosphatase (ALP) to function^[1]. SMAD5 Protein, Mouse (sf9, His-GST) has 464 amino acids expressed by sf9 insect cells with N-terminal His- and GST-tag.

SMAD5 is a receptor activated Smad (R-Smad), also known as dwarfin C, JV5-1 and MAD5, which belong to the dwarfin/SMAD family. The SMAD5 protein consists of an N-terminal domain responsible for DNA binding, a C-terminal domain primarily used for protein-protein interactions, and a junction region containing moths necessary for ubiquitination degradation. SMAD5 is activated by an activated type I TGF-β receptor, and phosphorylated SMAD5 binds to SMAD4 (common SMAD) to form heterotrimer complexes that enter the nucleus as transcription factors. At the same time, SMAD4 is also bound by inhibitory SMAD (SMAD6 and SMAD7), making R-Smad compete for receptors or interact with Smad4, and target degradation and negative regulation of TGF-β signaling. SMAD5 mainly responds to BMP signaling pathways. During embryonic development, SMAD5 is widely expressed in mice from gastrum formation. During this period, the loss of SMAD5 leads to mutations in the embryo, or defects in the yolk sac outside the embryo, and death in the second trimester. Furthermore, the BMP/SMAD5 pathway can regulate osteogenesis by up-regulating transcription of the transcription factor Runx2, or by targeting multiple cis-acting promoter elements in osteogenic specific genes, including osteocalcin and alkaline phosphatase (ALP). Alps bind to Smad interacting protein 1 (SIP1) and inhibit Smad5-induced SIP1 activation. A significant expansion of primitive multipotent progenitor cells showing normal terminal maturation was reported in embryonic stem cells from Smad5-deficient mice, suggesting that conditional activation or deactivation of Smad5-specific signaling pathways may contribute to hematopoietic and osteogenic tissue engineering^[1].

Smad5 is found to mediate TGF-β/BMP/MIS signaling in Smad5 knockout mice^[2].

Mouse

Sf9 insect cells

N-His;N-GST

P97454 (T2-S465)

17129  [NCBI]

75-88 kDa

Greater than 90% as determined by reducing SDS-PAGE

<1 EU/μg, determined by LAL method.

• [1]. Liu B, et al. Smad5: signaling roles in hematopoiesis and osteogenesis. Int J Biochem Cell Biol. 2004 May;36(5):766-70.  [Content Brief]

  [2]. Umans L, et al. Generation of a floxed allele of Smad5 for cre-mediated conditional knockout in the mouse. Genesis. 2003 Sep;37(1):5-11.  [Content Brief]