cGKII Antibody | 63-330

cGKII Antibody | 63-330 | Gentaur UK, US & Europe Distribution

Host: Rabbit

Reactivity: Human

Homology: N/A

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.

Research Area: Signal Transduction

Tested Application: WB, IHC-P

Application: For WB starting dilution is: 1:1000
For IHC-P starting dilution is: 1:50~100

Specificiy: N/A

Positive Control 1: N/A

Positive Control 2: N/A

Positive Control 3: N/A

Positive Control 4: N/A

Positive Control 5: N/A

Positive Control 6: N/A

Molecular Weight: 87 kDa

Validation: N/A

Isoform: N/A

Purification: This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis

Clonality: Polyclonal

Clone: N/A

Isotype: Rabbit Ig

Conjugate: Unconjugated

Physical State: Liquid

Buffer: Supplied in PBS with 0.09% (W/V) sodium azide.

Concentration: batch dependent

Storage Condition: 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.

Alternate Name: cGMP-dependent protein kinase 2, cGK 2, cGK2, cGMP-dependent protein kinase II, cGKII, PRKG2, PRKGR2

User Note: Optimal dilutions for each application to be determined by the researcher.

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 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.