Western Blotting (WB), Immunohistochemistry (Paraffin-embedded Sections) (IHC (p))
Aufreinigung
This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis
Immunogen
This cGKII antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 714-744 amino acids from the C-terminal region of human cGKII.
This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Lagerung
4 °C,-20 °C
Informationen zur Lagerung
Store 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.
Target
PRKG2
(Protein Kinase, CGMP-Dependent, Type II (PRKG2))
MGC82580 antikoerper, PRKG2 antikoerper, si:dkey-18e17.2 antikoerper, PRKGR2 antikoerper, cGKII antikoerper, GDPKII antikoerper, AW212535 antikoerper, CGKII antikoerper, Prkgr2 antikoerper, cGK-II antikoerper, protein kinase, cGMP-dependent, type II antikoerper, protein kinase, cGMP-dependent, type II L homeolog antikoerper, cGMP-dependent protein kinase 2 antikoerper, PRKG2 antikoerper, prkg2.L antikoerper, prkg2 antikoerper, LOC100541294 antikoerper, Prkg2 antikoerper
Hintergrund
CGKII is thought to play a key role in a diverse set of physiological pathway. cGKII may mediate intestinal secretion of water and electrolytes induced by the E. coli toxin STa and the intestinal peptide guanylin. Edentification of the pathway that mediates intestinal fluid secretion by E. coli STa has potential medical implications because STa causes traveler's diarrhea and about 50 % of infant mortality in developing countries. Transfection experiments in human cells disclose that cGKII phosphorylates SOX9 and attenuates SOX9 function by inhibiting its nuclear entry. Impaired differentiation of cultured KMI chondrocytes can be restored by silencing Sox9 by RNA interference. cGKII is postulated to be a molecular switch that couples the cessation of proliferation and the start of hypertrophic chondrocyte differentiation through attenuating SOX9 function.