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Anti-Phospho-SMAD3 (Ser423)(S12-365R)

Anti-Phospho-SMAD3 (Ser423)(S12-365R)

  • $369.00


Description :Rabbit Polyclonal Antibody

Species :

Tag :

Expression System:

Sequence :

Specificity :Recognizes the human SMAD3 protein phosphorylated at Serine425 and Serine425

Cited Applications :ELISA, IHC, WB
Ideal working dilutions for each application should be empirically determined by the investigator

Cross Reactivity :Human, Xenopus laevis, Xenopus tropicalis, zebrafish, rat, mouse, swine, bovine and chicken.

Host Isotype / Clone# :Rabbit, IgG

Immunogen :The antibody was produced against synthesized synthesized peptide corresponding to amino acids 417-425 of human SMAD3 protein.

Purification :Immunoaffinity chromatography

Stability :1yr at –20oC from date of shipment

Sample Data :Anti-Phospho-SMAD3 (Ser423) was used at 2.5 µg/ml to detect signal in a variety of tissues including multi-human, multi-brain and multi-cancer slides. This image shows strong nuclear staining in the majority of epidermal keratinocytes at 40X. Tissue was formalin-fixed and paraffin embedded. The image shows localization of the antibody as the precipitated red signal, with a hematoxylin purple nuclear counterstain.

Sample Data :Western Blot of Rabbit anti-SMAD3 pS423 pS425 antibody- HEK293 lysate.

Scientific Background :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.

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Research Areas :AKT/PKB Pathway, Angiogenesis, Cancer, Cell Cycle, Cellular Stress, ERK/MAPK Pathway, Inflammation, JAK/STAT Pathway, JNK/SAPK Pathway, NfkB Pathway, WNT Signaling