Rabbit Polyclonal Antibody
Catalog No. S12-365BR
Catalog No. | Pack Size | Price (USD) | |
---|---|---|---|
S12-365BR-100 | 100 ug | $675 | |
S12-365BR-BULK | BULK | Contact Us |
Overview:
SMAD3 is a direct mediator of transcriptional activation by the TGFβ receptor. The activity of SMAD3 is regulated by the TGFβ receptors, and SMAD3 is phosphorylated and associated with the ligand-bound receptor complex. TGFβ stimulation leads to phosphorylation and activation of SMAD3, which form a complex with SMAD4 that accumulate in the nucleus and regulate transcription of target genes such as CDK inhibitor (1). SMAD3 containing a C-terminal truncation acts as a dominant-negative inhibitor of the normal TGFβ response. SMAD3 is a major physiologic substrate of the G1 cyclin-dependent kinases CDK4 and CDK2 (2).
References:
1. Inman, G. J. et al: Nucleocytoplasmic shuttling of Smads 2, 3, and 4 permits sensing of TGF-beta receptor activity. Molec. Cell 10: 283-294, 2002.
2. Matsuura, I. et al: Cyclin-dependent kinases regulate the antiproliferative function of Smads. Nature 430: 226-231, 2004.
Specificity:
Recognizes the human SMAD3 protein phosphorylated at Threonine 179
Cross Reactivity:
Human
Host Isotype / Clone#:
Rabbit, IgG
Immunogen:
The antibody was produced against synthesized peptide corresponding to an internal region of human SMAD3 protein surrounding Thr179.
Purification:
Immunoaffinity chromatography
Stability:
1yr at –20oC from date of shipment
Sample Data:
NMuMG mouse mammary epithelial cells were probed for the activation of Smad3 by detecting phosphorylation of threonine 179 using Anti-Phospho-SMAD3 (Thr179) antibody. The cells were either untreated or treated with TGF-beta. The antibody detects only Smad3 in stimulated cells.
Jiang Yanjun et al., Phosphatase PRL-3 Is a Direct Regulatory Target of TGFβ in Colon Cancer Metastasis Cancer Research January 2011 10.1158/0008-5472.CAN-10-1487
Li Zuguo et al., Response Gene to Complement 32 Is Essential for Fibroblast Activation in Renal Fibrosis Journal of Biological Chemistry December 2011 10.1074/jbc.M111.259184
AKT/PKB Pathway, Angiogenesis, Cancer, Cell Cycle, Cellular Stress, ERK/MAPK Pathway, Inflammation, JAK/STAT Pathway, JNK/SAPK Pathway, NfkB Pathway, WNT Signaling
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