SMAD3 antibody (pSer208)

Catalog No. ABIN3032625

The Rabbit Polyclonal anti-SMAD3 antibody (ABIN3032625) specifically detects SMAD3 in ELISA, IF and DB. The antibody is reactive with Human samples.

Quick Overview for SMAD3 antibody (pSer208) (ABIN3032625)

Target: SMAD3 (SMAD, Mothers Against DPP Homolog 3 (SMAD3))

Reactivity: Human

Host: Rabbit

Clonality: Polyclonal

Conjugate: This SMAD3 antibody is un-conjugated

Application: ELISA, Immunofluorescence (IF), Dot Blot (DB)

Product Details anti-SMAD3 Antibody

Binding Specificity: pSer208

Cross-Reactivity (Details): Expected species reactivity: Mouse, Rat, Pig, Chicken

Purification: Antigen affinity purified

Immunogen: This phospho-SMAD3 antibody was produced from rabbits immunized with a KLH conjugated synthetic phosphopeptide corresponding to amino acid residues surrounding pS208 of human SMAD3.

Isotype: Ig Fraction

Application Details

Application Notes: Titration of the phospho-SMAD3 antibody may be required due to differences in protocols and secondary/substrate sensitivity.\. Immunofluorescence: 1:10-1:100,Dot blot: 1:500

Restrictions: For Research Use only

Handling

Format: Liquid

Buffer: In 1X PBS, pH 7.4, with 0.09 % sodium azide

Preservative: Sodium azide

Precaution of Use: This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.

Storage: -20 °C

Storage Comment: Aliquot the phospho-SMAD3 antibody and store frozen at -20°C or colder. Avoid repeated freeze-thaw cycles.

Target Details for SMAD3

Target: SMAD3 (SMAD, Mothers Against DPP Homolog 3 (SMAD3))

Alternative Name: Smad3

Background: SMAD3, a receptor regulated SMAD (R-SMAD) is a transcriptional modulator activated by TGF-beta (transforming growth factor) and activin type 1 receptor kinase. SMAD3 is estimated to account for at least 80 % of all TGF-beta-mediated response. Activated type I receptor phosphorylates receptor-activated SMADS (RSMADS) at their c-terminal two extreme serines in the SSXS motif. The phosphorylated R-SMAD translocate into nucleus, where they regulate transcription of target genes. SMAD3 signal transduction appears to be important in the rgulation of muscle-specific genes. Loss of SMAD3 is a feature of pediatric T-cell lymphoblastic leukemia, while upregulation of SMAD3 may be responsible for TGFB hyperresponsiveness observed in scleroderma.

UniProt: P84022

Pathways: Cell Division Cycle, Chromatin Binding, Cell-Cell Junction Organization, Positive Regulation of Endopeptidase Activity, Autophagy