L’anticorps Lapin Polyclonal anti-SMAD3 a été validé pour WB et IHC (p). Il convient pour détecter SMAD3 dans des échantillons de Humain. Il y a 1 publication disponible.
This antibody is purified through a protein A column, followed by peptide affinity purification.
Immunogène
This SMAD3 Antibody is generated from rabbits immunized with a KLH conjugated synthetic phosphopeptide corresponding to amino acid residues surrounding S213 of human SMAD3.
KO Validated
SMAD3
Reactivité: Humain
WB, IHC, IF, IP
Hôte: Lapin
Monoclonal
unconjugated
Indications d'application
WB: 1:1000. WB: 1:1000. IHC-P: 1:50~100
Restrictions
For Research Use only
Format
Liquid
Buffer
Purified polyclonal antibody supplied in PBS with 0.09 % (W/V) sodium azide.
Agent conservateur
Sodium azide
Précaution d'utilisation
This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Stock
4 °C,-20 °C
Stockage commentaire
Maintain refrigerated at 2-8 °C for up to 6 months. For long term storage store at -20 °C in small aliquots to prevent freeze-thaw cycles.
Date de péremption
6 months
Wu, Bian, Dou, Gong, Tan, Xia, Dai: "Asiaticoside hinders the invasive growth of keloid fibroblasts through inhibition of the GDF-9/MAPK/Smad pathway." dans: Journal of biochemical and molecular toxicology, Vol. 31, Issue 8, (2017) (PubMed).
Antigène
SMAD3
(SMAD, Mothers Against DPP Homolog 3 (SMAD3))
Autre désignation
SMAD3
Sujet
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.