Phospho-Smad3 (Ser423/425) Rabbit mAb
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Application
| WB, IHC-P |
|---|---|
| Primary Accession | P84022 |
| Reactivity | Human, Mouse |
| Host | Rabbit |
| Clonality | Monoclonal Antibody |
| Isotype | IgG |
| Conjugate | Unconjugated |
| Purification | Affinity Purified |
| Calculated MW | 48081 Da |
| Gene ID | 4088 |
|---|---|
| Other Names | SMAD3 |
| Dilution | WB~~1:1000 IHC-P~~1:50~200 |
| Format | 1xPBS(pH 7.4), 150mM NaCl, 50% Glycerol, 0.02% Sodium azide and 0.05% BSA |
| Storage | Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles. |
For Research Use Only. Not For Use In Diagnostic Procedures.
| Name | SMAD3 (HGNC:6769) |
|---|---|
| Synonyms | MADH3 |
| Function | Receptor-regulated SMAD (R-SMAD) that is an intracellular signal transducer and transcriptional modulator activated by TGF-beta (transforming growth factor) and activin type 1 receptor kinases. Binds the TRE element in the promoter region of many genes that are regulated by TGF-beta and, on formation of the SMAD3/SMAD4 complex, activates transcription. Also can form a SMAD3/SMAD4/JUN/FOS complex at the AP- 1/SMAD site to regulate TGF-beta-mediated transcription. Has an inhibitory effect on wound healing probably by modulating both growth and migration of primary keratinocytes and by altering the TGF-mediated chemotaxis of monocytes. This effect on wound healing appears to be hormone-sensitive. Regulator of chondrogenesis and osteogenesis and inhibits early healing of bone fractures. Positively regulates PDPK1 kinase activity by stimulating its dissociation from the 14-3-3 protein YWHAQ which acts as a negative regulator. |
| Cellular Location | Cytoplasm. Nucleus Note=Cytoplasmic and nuclear in the absence of TGF-beta. On TGF-beta stimulation, migrates to the nucleus when complexed with SMAD4 (PubMed:15799969, PubMed:21145499). Through the action of the phosphatase PPM1A, released from the SMAD2/SMAD4 complex, and exported out of the nucleus by interaction with RANBP1 (PubMed:16751101, PubMed:19289081). Co-localizes with LEMD3 at the nucleus inner membrane (PubMed:15601644). MAPK-mediated phosphorylation appears to have no effect on nuclear import (PubMed:19218245). PDPK1 prevents its nuclear translocation in response to TGF-beta (PubMed:17327236). Localized mainly to the nucleus in the early stages of embryo development with expression becoming evident in the cytoplasm of the inner cell mass at the blastocyst stage (By similarity). {ECO:0000250|UniProtKB:Q8BUN5, ECO:0000269|PubMed:15601644, ECO:0000269|PubMed:15799969, ECO:0000269|PubMed:16751101, ECO:0000269|PubMed:17327236, ECO:0000269|PubMed:19218245, ECO:0000269|PubMed:19289081, ECO:0000269|PubMed:21145499} |
Research Areas
Application Protocols
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
Smad3 transcription factor phosphorylated and activated by TGF-beta-type receptors. A receptor-regulated Smad (R-smad). Binds directly to consensus DNA-binding elements in the promoters of target genes. In mouse required for establishemnt of the mucosal immune response and proper development of skeleton.
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