PRDM16 Antibody is affinity chromatography purified via peptide column.
Immunogen
PRDM16 antibody was raised against a 17 amino acid synthetic peptide from near the carboxy terminus of human PRDM16. The immunogen is located within amino acids 1120 - 1170 of PRDM16.
PRDM16
Reaktivität: Human
Wirt: Kaninchen
Polyclonal
FITC
Applikationshinweise
PRDM16 antibody can be used for detection of PRDM16 by Western blot at 1 μ,g/mL. Antibody can also be used for immunohistochemistry starting at 2 μ,g/mL. For immunofluorescence start at 20 μ,g/mL.
Antibody validated: Western Blot in human samples, Immunohistochemistry in human and mouse samples and Immunofluorescence in human and mouse samples. All other applications and species not yet tested.
Beschränkungen
Nur für Forschungszwecke einsetzbar
Format
Liquid
Konzentration
1 mg/mL
Buffer
PRDM16 Antibody is supplied in PBS containing 0.02 % sodium azide.
Konservierungsmittel
Sodium azide
Vorsichtsmaßnahmen
This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Lagerung
-20 °C,4 °C
Informationen zur Lagerung
PRDM16 antibody can be stored at 4°C for three months and -20°C, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.
PRDM16 Antibody: PRDM16 is a zinc finger transcription factor and contains an N-terminal PR domain. The reciprocal translocation t(1,3)(p36,q21) occurs in a subset of myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML). This gene is located near the 1p36.3 breakpoint and has been shown to be specifically expressed in the t(1:3)(p36, q21)-positive MDS/AML. The translocation results in the overexpression of a truncated version of this protein that lacks the PR domain, which may play an important role in the pathogenesis of MDS and AML. Recent studies have shown that PRDM16 normally acts as a Smad3 binding protein that may be important for the development of orofacial structures through modulation of the TGF-beta signaling pathway. Other experiments have indicated that PRDM16 controls a bidirectional cell fate switch between skeletal myoblasts and brown fat cells.