Dieses Kaninchen Polyklonal-Antikörper erkennt spezifisch SMAD3 in IF und DB. Er zeigt eine Reaktivität gegenüber Human und wurde in 1 Publikation erwähnt.
This antibody is purified through a protein A column, followed by peptide affinity purification.
Immunogen
This SMAD3 Antibody is generated from rabbits immunized with a KLH conjugated synthetic phosphopeptide corresponding to amino acid residues surrounding S208 of human SMAD3.
KO Validated
SMAD3
Reaktivität: Human
WB, IHC, IF, IP
Wirt: Kaninchen
Monoclonal
unconjugated
Applikationshinweise
IF: 1:200. IF: 1:10~50. DB: 1:500
Beschränkungen
Nur für Forschungszwecke einsetzbar
Format
Liquid
Buffer
Purified polyclonal antibody supplied in PBS with 0.09 % (W/V) sodium azide.
Konservierungsmittel
Sodium azide
Vorsichtsmaßnahmen
This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Handhabung
Avoid freeze-thaw cycles.
Lagerung
4 °C,-20 °C
Informationen zur Lagerung
Maintain refrigerated at 2-8 °C for up to 6 months. For long term storage store at -20 °C in small aliquots.
Haltbarkeit
6 months
Cohen-Solal, Merrigan, Chan, Goydos, Chen, Foran, Liu, Lasfar, Reiss: "Constitutive Smad linker phosphorylation in melanoma: a mechanism of resistance to transforming growth factor-?-mediated growth inhibition." in: Pigment cell & melanoma research, Vol. 24, Issue 3, pp. 512-24, (2011) (PubMed).
Target
SMAD3
(SMAD, Mothers Against DPP Homolog 3 (SMAD3))
Andere Bezeichnung
SMAD3
Hintergrund
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.