AB3849
Anti-Smad2 Antibody, phospho-specific (Ser465/467)
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Synonym(s):
MAD, Mad, Mad protein homolog 2, Mad-related protein 2, Mothers against DPP homolog 2, SMAD, SMAD 2, SMAD family member 2, Sma- and Mad-related protein 2, mother against DPP homolog 2, mothers against DPP homolog 2, mothers against DPP homolog 2 (Drosophila), mothers against decapentaplegic homolog 2, mothers against decapentaplegic homolog 2 (Drosophila)
UNSPSC Code:
12352203
eCl@ss:
32160702
Recommended Products
biological source
rabbit
antibody form
affinity purified immunoglobulin
clone
polyclonal
purified by
affinity chromatography
using Protein A
species reactivity
zebrafish (100% sequence similarity), mouse, human, rat, Xenopus (100% sequence similarity), chicken (100% sequence similarity)
manufacturer/tradename
Chemicon®
technique(s)
immunocytochemistry: suitable
immunofluorescence: suitable
immunohistochemistry: suitable (paraffin)
western blot: suitable
NCBI accession no.
UniProt accession no.
General description
SMAD2 or Mothers against decapentaplegic homolog 2 is a polypeptide that, as its name describes, is a homolog of the Drosophila gene: "Mothers against decepentaplegic". It belongs to the SMAD family of proteins, which belong to the TGF-β superfamily of modulators. Like many other TGF-β family members SMAD2 is involved in cell signaling. SMAD2 modulates signals of activin and TGF-β′s. It interacts with SMAD anchor for receptor activation (SARA). The binding of ligands causes the phosphorylation of the SMAD2 protein and the dissociation from SARA and the association with SMAD4. It is subsequently transferred to the nucleus where it forms complexes with other proteins and acts as a transcription factor. SMAD2 is a receptor regulated SMAD (R-SMAD) and is activated by bone morphogenetic protein type 1 receptor kinase.
Specificity
By western blot, the antibody recognizes a band migrating at approximately 58 kDa corresponding to Smad2 only when dually phosphorylated at Ser465 and Ser467. The antibody may also detect phosphorylated Smad3 (Ser423 and Ser425). This antibody does not c
Immunogen
Epitope: Phospho-Ser465/467
KLH-conjugated, synthetic phospho-peptide corresponding to residues surrounding Ser465/467 of human Smad2.
Application
Research Category
Epigenetics & Nuclear Function
Epigenetics & Nuclear Function
Research Sub Category
Transcription Factors
Transcription Factors
Use Anti-Smad2 Antibody, phospho-specific (Ser465/467) (Rabbit Polyclonal Antibody) validated in ICC, IF, IHC(P), WB to detect Smad2 also known as MAD-mothers against decapentaplegic-homolog 2.
Western Blotting:
1:1,000 dilution of a previous lot was used. For best results, incubate membrane with diluted antibody in 5% w/v nonfat dry milk, 1X TBS, 0.1% Tween-20 at 4°C overnight with gentle agitation.
Immunohistochemistry (Paraffin):
1:2000 dilution of a previous lot was used.
Immunocytochemistry (IF):
1:500 dilution of a previous lot was used.
Optimal working dilutions must be determined by the end user.
1:1,000 dilution of a previous lot was used. For best results, incubate membrane with diluted antibody in 5% w/v nonfat dry milk, 1X TBS, 0.1% Tween-20 at 4°C overnight with gentle agitation.
Immunohistochemistry (Paraffin):
1:2000 dilution of a previous lot was used.
Immunocytochemistry (IF):
1:500 dilution of a previous lot was used.
Optimal working dilutions must be determined by the end user.
Target description
~58 kDa
Physical form
Purified rabbit polyclonal in buffer containing 10 mM sodium HEPES, pH 7.5, 150 mM NaCl, 100 μg/mL BSA, with 50% glycerol.
Storage and Stability
Stable for 1 year at -20ºC from date of receipt.
Analysis Note
Control
POSITIVE CONTROL: TGF-β treated HepG2 cells.
POSITIVE CONTROL: TGF-β treated HepG2 cells.
Other Notes
Concentration:Please refer to the Certificate of Analysis for the lot-specific concentration.
Legal Information
CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial
Regulatory Information
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Certificates of Analysis (COA)
Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.
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Glen A Bjerke et al.
PloS one, 9(3), e92800-e92800 (2014-03-22)
Recent work with mouse models of prostate cancer (CaP) has shown that inactivation of TGFβ signaling in prostate epithelium can cooperate with deletion of the Pten tumor suppressor to drive locally aggressive cancer and metastatic disease. Here, we show that
Caitlin E O'Brien et al.
Molecular neurodegeneration, 10, 69-69 (2015-12-23)
Beclin 1 is a key regulator of multiple trafficking pathways, including autophagy and receptor recycling in yeast and microglia. Decreased beclin 1 levels in the CNS result in neurodegeneration, an effect attributed to impaired autophagy. However, neurons also rely heavily
Ciric To et al.
The Journal of biological chemistry, 283(17), 11700-11713 (2008-02-20)
The anti-tumor synthetic triterpenoid 2-cyano-3,12-dioxooleana-1,9-dien-28-oic acid (CDDO)-imidazolide (CDDO-Im) ectopically activates the transforming growth factor beta (TGFbeta)-Smad pathway and extends the duration of signaling by an undefined mechanism. Here we show that CDDO-Imdependent persistence of Smad2 phosphorylation is independent of Smad2
Kristian P Doyle et al.
Journal of neuroinflammation, 7, 62-62 (2010-10-13)
TGFβ is both neuroprotective and a key immune system modulator and is likely to be an important target for future stroke therapy. The precise function of increased TGF-β1 after stroke is unknown and its pleiotropic nature means that it may
Anou Londesborough et al.
Development (Cambridge, England), 135(13), 2331-2338 (2008-06-10)
Inactivation of the tumor suppressor kinase Lkb1 in mice leads to vascular defects and midgestational lethality at embryonic day 9-11 (E9-E11). Here, we have used conditional targeting to investigate the defects underlying the Lkb1(-/-) phenotype. Endothelium-restricted deletion of Lkb1 led
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