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AB80375

Recombinant human cGKI protein (His tag N-Terminus)

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(1 Publication)

Recombinant human cGKI protein (His tag N-Terminus) is a Human Full Length protein, expressed in Baculovirus infected Sf9 cells, with >70%, suitable for SDS-PAGE, FuncS.

View Alternative Names

PRKG1B, PRKGR1A, PRKGR1B, PRKG1, cGMP-dependent protein kinase 1, cGK 1, cGK1, cGMP-dependent protein kinase I, cGKI

2 Images
Functional Studies - Recombinant human cGKI protein (His tag N-Terminus) (AB80375)
  • FuncS

Unknown

Functional Studies - Recombinant human cGKI protein (His tag N-Terminus) (AB80375)

Image showing specific activity of ab80375.

SDS-PAGE - Recombinant human cGKI protein (His tag N-Terminus) (AB80375)
  • SDS-PAGE

Unknown

SDS-PAGE - Recombinant human cGKI protein (His tag N-Terminus) (AB80375)

0% SDS-PAGE showing ab80375 at approximately 78kDa (3μg).

Key facts

Purity

>70% SDS-PAGE

Expression system

Baculovirus infected Sf9 cells

Tags

His tag N-Terminus

Applications

SDS-PAGE, FuncS

applications

Biologically active

Yes

Biological activity

Specific Activity: 0.85 pmoles/min/μg. Enzyme reaction is conducted in a buffer containing 50 mM HEPES (pH7.5), 10 mM MgCl2, 1 mM EGTA, 200 μM ATP, 0.01% Brij-35, and 2 μM substrate (SER/THR 14) at room temperature for 1 hour.

Accession

Q13976

Animal free

No

Carrier free

No

Species

Human

Storage buffer

pH: 8 Constituents: 20% Glycerol (glycerin, glycerine), 0.58% Sodium chloride, 0.395% Tris HCl, 0.05% Sorbitan monolaurate, ethoxylated, 0.0462% (R*,R*)-1,4-Dimercaptobutan-2,3-diol

storage-buffer

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Complementary Products

Primary Antibodies

AB110124

Anti-cGKI antibody

Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - Anti-cGKI antibody (AB110124)

  • 0
  • 0
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Reactivity data

{ "title": "Reactivity Data", "filters": { "stats": ["", "Reactivity", "Dilution Info", "Notes"] }, "values": { "SDS-PAGE": { "reactivity":"TESTED_AND_REACTS", "dilution-info":"", "notes":"<p></p>" }, "FuncS": { "reactivity":"TESTED_AND_REACTS", "dilution-info":"", "notes":"<p></p>" } } }
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Sequence info

[{"sequence":"","proteinLength":"Full Length","predictedMolecularWeight":null,"actualMolecularWeight":null,"aminoAcidEnd":0,"aminoAcidStart":0,"nature":"Recombinant","expressionSystem":null,"accessionNumber":"Q13976","tags":[{"tag":"His","terminus":"N-Terminus"}]}]
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Properties and storage information

Shipped at conditions
Dry Ice
Appropriate short-term storage conditions
-80°C
Appropriate long-term storage conditions
-80°C
Aliquoting information
Upon delivery aliquot
Storage information
Avoid freeze / thaw cycle
True
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Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

CGKI also known as cyclic GMP-dependent protein kinase I or PKG I mechanically functions as an important player in the signaling pathways that depend on cyclic GMP (cGMP). cGKI is a serine/threonine protein kinase with a molecular mass of approximately 76 kilodaltons. It gets expressed in various tissues including vascular smooth muscle cells brain and platelets. The protein shows highest expression levels in tissues involved in smooth muscle regulation and neurological functions.
Biological function summary

The involvement of cGKI extends beyond basic signaling impacting diverse physiological processes. cGKI plays an important role in smooth muscle relaxation platelet function and nerve signaling. By phosphorylating various downstream targets cGKI affects muscle tone and neurotransmitter release. In the smooth muscle cGKI does not act independently but as part of a larger complex that modulates the cellular response to nitric oxide and natriuretic peptides.

Pathways

CGKI participates as an active component in the nitric oxide-cGMP signaling pathway. This pathway is significant in controlling vascular tone and neurotransmission. cGKI interacts with the proteins soluble guanylate cyclase and myosin light-chain phosphatase which together modulate blood vessel relaxation and contraction. Additionally cGKI plays a role in the cyclic nucleotide signaling pathways maintaining cardiovascular and neuronal health.

CGKI shows a connection to cardiovascular diseases and hypertension. Alterations in cGKI expression or function can lead to improper regulation of vascular tone contributing to elevated blood pressure. In the context of cardiovascular disorders cGKI interacts with proteins like PDE5A which also modulate cGMP levels in tissues. Understanding cGKI’s role in these diseases helps inform potential therapeutic targets for pharmacological intervention.
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Specifications

Form

Liquid

Additional notes

Affinity purified.

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General info

Function

Serine/threonine protein kinase that acts as a key mediator of the nitric oxide (NO)/cGMP signaling pathway. GMP binding activates PRKG1, which phosphorylates serines and threonines on many cellular proteins. Numerous protein targets for PRKG1 phosphorylation are implicated in modulating cellular calcium, but the contribution of each of these targets may vary substantially among cell types. Proteins that are phosphorylated by PRKG1 regulate platelet activation and adhesion, smooth muscle contraction, cardiac function, gene expression, feedback of the NO-signaling pathway, and other processes involved in several aspects of the CNS like axon guidance, hippocampal and cerebellar learning, circadian rhythm and nociception. Smooth muscle relaxation is mediated through lowering of intracellular free calcium, by desensitization of contractile proteins to calcium, and by decrease in the contractile state of smooth muscle or in platelet activation. Regulates intracellular calcium levels via several pathways : phosphorylates IRAG1 and inhibits IP3-induced Ca(2+) release from intracellular stores, phosphorylation of KCNMA1 (BKCa) channels decreases intracellular Ca(2+) levels, which leads to increased opening of this channel. PRKG1 phosphorylates the canonical transient receptor potential channel (TRPC) family which inactivates the associated inward calcium current. Another mode of action of NO/cGMP/PKGI signaling involves PKGI-mediated inactivation of the Ras homolog gene family member A (RhoA). Phosphorylation of RHOA by PRKG1 blocks the action of this protein in myriad processes : regulation of RHOA translocation; decreasing contraction; controlling vesicle trafficking, reduction of myosin light chain phosphorylation resulting in vasorelaxation. Activation of PRKG1 by NO signaling alters also gene expression in a number of tissues. In smooth muscle cells, increased cGMP and PRKG1 activity influence expression of smooth muscle-specific contractile proteins, levels of proteins in the NO/cGMP signaling pathway, down-regulation of the matrix proteins osteopontin and thrombospondin-1 to limit smooth muscle cell migration and phenotype. Regulates vasodilator-stimulated phosphoprotein (VASP) functions in platelets and smooth muscle.

Sequence similarities

Belongs to the protein kinase superfamily. AGC Ser/Thr protein kinase family. cGMP subfamily.

Post-translational modifications

Autophosphorylation increases kinase activity.. 65 kDa monomer is produced by proteolytic cleavage.

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Product protocols

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Target data

Serine/threonine protein kinase that acts as a key mediator of the nitric oxide (NO)/cGMP signaling pathway. GMP binding activates PRKG1, which phosphorylates serines and threonines on many cellular proteins. Numerous protein targets for PRKG1 phosphorylation are implicated in modulating cellular calcium, but the contribution of each of these targets may vary substantially among cell types. Proteins that are phosphorylated by PRKG1 regulate platelet activation and adhesion, smooth muscle contraction, cardiac function, gene expression, feedback of the NO-signaling pathway, and other processes involved in several aspects of the CNS like axon guidance, hippocampal and cerebellar learning, circadian rhythm and nociception. Smooth muscle relaxation is mediated through lowering of intracellular free calcium, by desensitization of contractile proteins to calcium, and by decrease in the contractile state of smooth muscle or in platelet activation. Regulates intracellular calcium levels via several pathways : phosphorylates IRAG1 and inhibits IP3-induced Ca(2+) release from intracellular stores, phosphorylation of KCNMA1 (BKCa) channels decreases intracellular Ca(2+) levels, which leads to increased opening of this channel. PRKG1 phosphorylates the canonical transient receptor potential channel (TRPC) family which inactivates the associated inward calcium current. Another mode of action of NO/cGMP/PKGI signaling involves PKGI-mediated inactivation of the Ras homolog gene family member A (RhoA). Phosphorylation of RHOA by PRKG1 blocks the action of this protein in myriad processes : regulation of RHOA translocation; decreasing contraction; controlling vesicle trafficking, reduction of myosin light chain phosphorylation resulting in vasorelaxation. Activation of PRKG1 by NO signaling alters also gene expression in a number of tissues. In smooth muscle cells, increased cGMP and PRKG1 activity influence expression of smooth muscle-specific contractile proteins, levels of proteins in the NO/cGMP signaling pathway, down-regulation of the matrix proteins osteopontin and thrombospondin-1 to limit smooth muscle cell migration and phenotype. Regulates vasodilator-stimulated phosphoprotein (VASP) functions in platelets and smooth muscle.
See full target information PRKG1
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Publications (1)

Recent publications for all applications. Explore the full list and refine your search

British journal of pharmacology 177:1434-1452 PubMed31658364

2020

Icariside II, a phosphodiesterase 5 inhibitor, attenuates cerebral ischaemia/reperfusion injury by inhibiting glycogen synthase kinase-3β-mediated activation of autophagy.

Applications

Unspecified application

Species

Unspecified reactive species

Jianmei Gao,Long Long,Fan Xu,Linying Feng,Yuangui Liu,Jingshan Shi,Qihai Gong
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