Product Name: cGKII Antibody
Species Reactivity: Human
Tested Applications: IHC-P, WB
Applications: For WB starting dilution is: 1:1000For IHC-P starting dilution is: 1:50~100
User Note: Optimal dilutions for each application to be determined by the researcher.
Predicted Molecular Weight: 87 kDa
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.
Host Species: Rabbit
Purification: This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis
Physical State: Liquid
CAS NO.: 70356-09-1
Product: Avobenzone
Buffer: Supplied in PBS with 0.09% (W/V) sodium azide.
Concentration: 1.2 mg/ml
Storage Conditions: 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.
Clonality: Polyclonal
Conjugate: Unconjugated
Alternate Names: cGMP-dependent protein kinase 2, cGK 2, cGK2, cGMP-dependent protein kinase II, cGKII, PRKG2, PRKGR2
Accession NO.: Q13237
Protein Ino: 6226833
Official Symbol: PRKG2
Geneid: 5593
Background: 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 travelers 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.
PubMed ID:http://aac.asm.org/content/35/12/2562.abstract
