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Key Documents

04-953

Sigma-Aldrich

Anti-phospho-Smad2 (Ser465/467) Antibody, clone A5S, rabbit monoclonal

culture supernatant, clone A5S, Upstate®

Synonym(s):

Anti-Anti-CHTD8, Anti-Anti-JV18, Anti-Anti-JV18-1, Anti-Anti-LDS6, Anti-Anti-MADH2, Anti-Anti-MADR2, Anti-Anti-hMAD-2, Anti-Anti-hSMAD2

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About This Item

UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41

biological source

rabbit

Quality Level

antibody form

culture supernatant

antibody product type

primary antibodies

clone

A5S, monoclonal

species reactivity

human, zebrafish, mouse, canine

manufacturer/tradename

Upstate®

technique(s)

western blot: suitable

isotype

IgG

NCBI accession no.

UniProt accession no.

shipped in

dry ice

target post-translational modification

phosphorylation (pSer465/pSer467)

Gene Information

human ... SMAD2(4087)

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 TGFb superfamily of modulators. Like many other TGFb family members SMAD2 is involved in cell signalling. SMAD2 modulates signals of activin and TGFb′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

Predicted to cross-react with X. laevis based on sequence homology.
Recognizes phosphorylated Smad2. No Cross-reactivity with Smad3.

Immunogen

KLH-conjugated, synthetic peptide corresponding to amino acids [pS]M[pS] surrounding sites Ser465/467 of human Smad2

Application

Detect phospho-Smad2 (Ser465/467) with Anti-phospho-Smad2 (Ser465/467) Antibody, clone A5S (Rabbit Monoclonal Antibody), that has been shown to work in WB.

Quality

Routinely evaluated by immunoblot analysis.

Target description

55-60 kDa

Linkage

Replaces: 05-953

Analysis Note

Control
HL60 cell lysate, HepG2 cells treated with TGFa, or HepG2 cells treated with TGFβ

Other Notes

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

Legal Information

UPSTATE is a registered trademark of Merck KGaA, Darmstadt, Germany

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Storage Class

10 - Combustible liquids

wgk_germany

WGK 1


Certificates of Analysis (COA)

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Shunsuke Sawada et al.
Molecular medicine reports, 13(3), 2023-2031 (2016-01-20)
Cytokines and their intercellular signals regulate the multipotency of mesenchymal stem cells (MSCs). The present study established the MSC lines SG‑2, ‑3, and ‑5 from the bone marrow of green fluorescent protein (GFP)‑transgenic mice. These cell lines clearly expressed mouse
Cathepsin K expression and activity in canine osteosarcoma.
J M Schmit,H C Pondenis,A M Barger,L B Borst,L D Garrett,J M Wypij,Z L Neumann,T M Fan
Journal of Veterinary Internal Medicine null
Oddrun Elise Olsen et al.
PloS one, 12(11), e0187349-e0187349 (2017-11-22)
Purified recombinant proteins for use in biomedical research are invaluable to investigate protein function. However, purity varies in protein batches made in mammalian expression systems, such as CHO-cells or HEK293-cells. This study points to caution while investigating effects of proteins
Linjia Jiang et al.
The Journal of experimental medicine, 215(5), 1337-1347 (2018-04-20)
Cell cycle quiescence is critical for hematopoietic stem cell (HSC) maintenance. TGF-β signaling in bone marrow niche has been identified in regulating HSC quiescence; however, the intrinsic regulatory mechanisms remain unclear. This study reports that Shp-1 knockout HSCs have attenuated
Aida M Bertoli-Avella et al.
Journal of the American College of Cardiology, 65(13), 1324-1336 (2015-04-04)
Aneurysms affecting the aorta are a common condition associated with high mortality as a result of aortic dissection or rupture. Investigations of the pathogenic mechanisms involved in syndromic types of thoracic aortic aneurysms, such as Marfan and Loeys-Dietz syndromes, have

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