Protein Kinase, CGMP-Dependent, Type I (PRKG1) ELISA Kits

Human Protein Kinase, CGMP-Dependent, Type I (PRKG1) interaction partners

1. results suggest that the lack of cGKI possibly leads to stellate cell activation, which stimulates chemokine expression and activates inflammatory processes, which could disturb hepatic insulin sensitivity

2. our study provides the first genome-wide evidence regarding a mechanism by which traumatic life events interact with human genetic variation of PRKG1 in relation to alcohol misuse

3. Disulfide-activated PKGIalpha regulates cardiac diastolic relaxation and fine-tunes the Frank-Starling response.

4. PRKG1, known to induce apoptosis when activated, is increased in all patient derived glioblastoma spheres

5. redox-mediated guidance required PKG1 and consequently, its deficiency in vivo resulted in defective repair and enhanced neuropathic pain after nerve injury. PKG1-dependent repair functions will outweigh its signaling functions in spinal nociceptive LTP, so that inhibition of PKG1 is no option for neuropathic pain.

6. Oxidant signaling underlies PKGIalpha modulation of Ca2+ sparks and BKCa in myogenically active arterioles

7. These affinity and activation measurements show that beta-phenyl-1,N2-ethenoguanosine 3',5'-monophosphate (PET-cGMP) is most selective for PKG I, whereas 8-(4-chlorophenylthio)guanosine-3'-5'-cyclic monophosphate (8-pCPT-cGMP) is most selective for PKG II.

8. Hence, SO2 exerted its vasodilatory effects at least partly by promoting disulfide-dependent dimerization of sGC and PKG, resulting in an activated sGC/cGMP/PKG pathway in blood vessels. These findings revealed a new mode of action and mechanisms by which SO2 regulated the vascular tone.

9. these data indicate PKG as an intermediary in EGFR-mediated cell death, likely via apoptotic pathway.

10. The heterozygous c.530G>A:p.Arg177Gln PRKG1 variant was associated with early-onset thoracic aortic aneurysm and dissection in a Spanish family.

11. cAMP is a partial agonist for PKG, and we elucidate the mechanism for cAMP partial agonism through the comparative NMR analysis of the apo, cGMP-, and cAMP-bound forms of the PKG cyclic nucleotide-binding domain B.

12. Protein kinase G has a role in regulating production of H2S, which governs oxygen sensing

13. The C42-C42' disulfide bond dramatically stabilizes PRKG1.

14. The Golgi apparatus regulates PKGIalpha compartmentation and proteolysis.

15. Study of genetic heterogeneity in systemic lupus erythematosus, the top associations in European ancestry were protein kinase, cyclic GMP-dependent, type I (PRKG1) rs7897633 (P(Meta) = 2.75 x 10(-8)) and purine nucleoside phosphorylase (PNP) rs1049564 (P(Meta) = 1.24 x 10(-7)).

16. Expression levels of miR-517a-3p and its target mRNA PRKG1 were inversely correlated in NK cells before and after obstetric delivery.

17. miR-20a expression is up-regulated in response to hypoxia in both mouse and human pulmonary arterial smooth muscle cells

18. Data show that functional cGMP/protein kinase G type 1 (PKG1) is expressed in pancreatic adenocarcinoma cells.

19. These findings characterize PKG as a novel regulator of AR-mediated transcription by enhancing AR cofactor p44/WDR77's function.

20. Neutron diffraction reveals hydrogen bonds critical for cGMP-selective activation: insights for cGMP-dependent protein kinase agonist design.

Cow (Bovine) Protein Kinase, CGMP-Dependent, Type I (PRKG1) interaction partners

1. NADPH regulation of PKG1-alpha dimerization may contribute to vascular responses to hypoxia that are associated with changes in NADPH redox.

2. The data suggest that PKG-I expression is subjected to post-transcriptional regulation in VSMC through the 3'UTR of its mRNA.

3. Report roles for redox mechanisms controlling protein kinase G in pulmonary and coronary artery responses to hypoxia.

4. Crystal structure of cGMP-dependent protein kinase reveals novel site of interchain communication

5. purified cGMP kinase signaling complex contained alpha-actin, calponin H1, and phospholamban

6. studies suggest that cross-activation of PKA in response to iNOS expression by inflammatory mediators downregulates cGMP-dependent protein kinase expression in bovine aortic vascular smooth muscle cells

7. Demonstrate a novel PKG-dependent pathway by which the Rac1/Pak1 pathway is activated.

8. cGMP-dependent protein kinase expression is regulated by soluble guanylyl cyclase in vascular smooth muscle cells

9. cGMP-dependent protein kinase Ibeta binds to TFII-I and IRAG through a common interaction motif

10. cGMP binding destabilizes the N-terminus of cGMP-dependent protein kinase I alpha isozyme at the hinge region, centered around residue 77, while the C-terminus is protected from degradation.

Mouse (Murine) Protein Kinase, CGMP-Dependent, Type I (PRKG1) interaction partners

1. the NF-kappaB/miR-155-5p/PKG1 axis may be crucial in the pathogenesis of inflammatory vascular diseases, such as atherosclerotic intimal hyperplasia and preeclamptic hypertension.

2. Prkg1 cascade role in platelet activation and thrombosis.

3. These data thus demonstrate the existence of two differently distributed cGKI isoforms in the dorsal root ganglion, and may provide insight into the cellular and molecular mechanisms of pain.

4. This study demonstrates that H- ras deletion protects against AngII-induced cardiac remodeling, possibly via a mechanism in which PKG-Ibeta overexpression could play a partial role, and points to H-Ras and/or downstream proteins as potential therapeutic targets in cardiovascular disease.

5. that PKG-I expressed in nociceptors is not only a key determinant of dorsal root ganglion hyperexcitability and spinal synaptic plasticity but also an important modulator of cortical neuronal activity in pathological pain states

6. Despite robust evidence for PKG Ialpha oxidation during NOS uncoupling in cell models, it is unlikely that PKG Ialpha oxidation occurs to a significant extent in vivo during diet-induced obesity and so is unlikely to mediate the associated cardiovascular dysfunction.

7. analysis of the role of binding interface with protein kinase G-Ialpha leucine zipper in vascular function

8. Brown adipose tissue, via Nox4-derived hydrogen peroxide, induces cyclic GMP-dependent protein kinase G type-1alpha activation, resulting in reduced vascular contractility.

9. disulfide formation at Cys(43) does not directly activate PKGIalpha, and the C43S-mutant PKGIalpha has a higher Ka for cGMP. Results highlight that mutant enzymes should be carefully biochemically characterized before making in vivo inferences.

10. PKG Ialpha disulfide formation triggers cardiac injury, and this initiation of maladaptive signaling can be blocked by pharmacological therapies that elevate cGMP, which binds kinase to limit its oxidation.

11. Cyclic GMP kinase deletion causes iron deficiency anemia, duodenal ulcers, and bleeding in the knockout mice.

12. Protein kinase G has a role in regulating production of H2S, which governs oxygen sensing

13. cGMP/protein kinase G signaling suppresses Itpr1 phosphorylation and promotes endoplasmic reticulum stress in photoreceptors of Cnga3-deficient mice.

14. these results demonstrate that myocardial PKG1alpha oxidation prevents a beneficial response to pathological stress, may explain variable responses to PKG1alpha pathway stimulation in heart disease

15. Data show that cGMP-dependent kinase (cGK-Ialpha) knockdown partially rescued TNF-alpha-induced decrease in 42-kDa cGMP-dependent protein kinase-anchoring protein (GKAP42) and impairment of insulin signals.

16. miR-20a expression is up-regulated in response to hypoxia in both mouse and human pulmonary arterial smooth muscle cells

17. These findings characterize PKG as a novel regulator of AR-mediated transcription by enhancing AR cofactor p44/WDR77's function.

18. A functional leucine zipper domain in PKG-1alpha is essential for maintenance of a low pulmonary vascular tone in normoxia.

19. For the initial phase of angiotenin II-induced cardiac hypertrophy, lack of cardiomyocyte cGKI activity does not worsen hypertrophic growth.

20. the key role of PKG-I in transforming growth factor beta1 induction by like weak inducer of apoptosis in kidney cells

Rabbit Protein Kinase, CGMP-Dependent, Type I (PRKG1) interaction partners

1. The novel cGMP/PKG/ROS/calmodulin/CaMKII signaling pathway may regulate cardiomyocyte excitability by opening K(ATP) channels and contribute to cardiac protection against ischemia-reperfusion injury.