4.6.1.2: guanylate cyclase
This is an abbreviated version!
For detailed information about guanylate cyclase, go to the full flat file.
Word Map on EC 4.6.1.2
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4.6.1.2
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cgmp
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artery
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guanosine
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nitroprusside
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monophosphate
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phosphodiesterase
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methylene
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vasodilation
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endothelium
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cgmp-dependent
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l-name
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l-arginine
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pkg
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tone
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endothelium-dependent
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blocker
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aorta
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acetylcholine
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vasorelaxation
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endothelium-derived
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ng-nitro-l-arginine
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snap
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phenylephrine
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8-br-cgmp
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ng-monomethyl-l-arginine
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endothelium-denuded
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nnos
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nomega-nitro-l-arginine
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apamin
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no-dependent
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zaprinast
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tetraethylammonium
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8-bromo-cgmp
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glibenclamide
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sin-1
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s-nitroso-n-acetylpenicillamine
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no-mediated
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sildenafil
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no-induced
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precontracted
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nitroglycerin
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diagnostics
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trinitrate
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molecular biology
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analysis
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iberiotoxin
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cavernosum
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7-nitroindazole
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no-donors
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pharmacology
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medicine
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phototransduction
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charybdotoxin
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endothelium-intact
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drug development
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nitrergic
- 4.6.1.2
- cgmp
- artery
- guanosine
- nitroprusside
- monophosphate
- phosphodiesterase
-
methylene
-
vasodilation
- endothelium
-
cgmp-dependent
-
l-name
- l-arginine
- pkg
-
tone
-
endothelium-dependent
-
blocker
- aorta
- acetylcholine
-
vasorelaxation
-
endothelium-derived
- ng-nitro-l-arginine
- snap
- phenylephrine
- 8-br-cgmp
- ng-monomethyl-l-arginine
-
endothelium-denuded
- nnos
- nomega-nitro-l-arginine
-
apamin
-
no-dependent
- zaprinast
- tetraethylammonium
- 8-bromo-cgmp
- glibenclamide
- sin-1
- s-nitroso-n-acetylpenicillamine
-
no-mediated
- sildenafil
-
no-induced
-
precontracted
- nitroglycerin
- diagnostics
- trinitrate
- molecular biology
- analysis
-
iberiotoxin
- cavernosum
- 7-nitroindazole
-
no-donors
- pharmacology
- medicine
-
phototransduction
-
charybdotoxin
-
endothelium-intact
- drug development
-
nitrergic
Reaction
Synonyms
alpha1 sGC, alpha1 soluble guanylyl cyclase, alpha1beta1 guanylyl cyclase, alpha1beta1 sGC, ANF-RGC, ANPRA, ANPRB, atrial natriuretic factor receptor guanylate cyclase, Atrial natriuretic peptide A-type receptor, Atrial natriuretic peptide B-type receptor, atrial natriuretic peptide receptor 2, BERhGC, BR1-GC, brassinosteroid receptor 1, CaRhGC, CNP-sensitive guanyly cyclase, CNP-sensitive guanylyl cyclase, CsGC-YO1, GC-A, GC-A receptor, GC-B, GC-C, GC-D, GC-G, GC1, GC2, GCA, GCC, gcy-18, gcy-23, GCY-35, gcy-8, GTP-pyrophosphate liase cyclizing, GTP-pyrophosphate lyase, guanyl cyclase, guanyl cyclase B, Guanylate cyclase, guanylate cyclase 1, guanylate cyclase 2, Guanylate cyclase 2D, retinal, Guanylate cyclase 2E, Guanylate cyclase 2F, retinal, guanylate cyclase A, guanylate cyclase B, guanylate cyclase C, Guanylate cyclase, olfactory, guanylyl cyclase, guanylyl cyclase A, guanylyl cyclase B, guanylyl cyclase C, guanylyl cyclase C receptor, guanylyl cyclase-A, guanylyl cyclase-A receptor, guanylyl cyclase-C, guanylyl cyclase-D, guanylyl cyclase-G, Gyc-88E, Gyc-89Da, Gyc-89Db, Gyca-99B, Gycb-100B, H-NOX, hSTAR, Intestinal guanylate cyclase, KSGC, L1 H-NOX, L2 H-NOX, membrane bound guanylate cyclase, membrane bound guanylyl cyclase, membrane guanylate cyclase, membrane guanylyl cyclase receptor, membrane-bound GC, membrane-bound guanylate cyclase, membrane-bound guanylyl cyclase, mGc, More, natriuretic peptide-activated guanylate cyclase, nitric oxid sensitive guanylyl cyclase, nitric oxide sensitive guanylyl cyclase, nitric oxide sensitive-guanylyl cyclase, nitric oxide-sensitive guanylate cyclase, nitric-oxide-sensitive guanylyl cyclase, NO receptor, NO receptor soluble guanylyl cyclase, NO sensitive guanylyl cyclase, NO- and haem-independent sGC, NO- and haem-independent soluble guanylate cyclase, NO-GC, NO-GC1, NO-GC2, NO-independent, heme-dependent soluble guanylate cyclase, NO-sensitive GC, NO-sensitive guanylyl cyclase, NO-sGC, NOGC1, NOsGC, NP-GC, NPR A, NPR-A, NPR-B, NPR1, NPR2, ONE-GC, ONE-GC membrane guanylate cyclase, Pac2, Pac3, particulate GC, particulate guanylate cyclase, particulate guanylyl cyclase, PepR1-GC, peptide hormone receptor guanylyl cyclase-C, PGC, photoreceptor guanylyl cyclase, phytosulfokine receptor, PSK receptor, PSKR1, ratGC, receptor guanylyl cyclase, receptor-type guanylyl cyclase, RET-GC1, retGC, RetGC1, RetGC2, retinal guanylate cyclase, retinal guanylyl cyclase, retinal membrane guanylyl cyclase, rGC, rhodopsin-guanylyl cyclase, Rod outer segment membrane guanylate cyclase, rod outer segment membrane guanylate cyclase type 1, ROS-GC, ROS-GC1, ROS-GC2, sGC, sGC alpha2 inhibitory isoform, sGC alpha2 isoform, sGCalpha1, sGCalpha2beta1, sGCbeta1, sGCbeta3, soluble GC, soluble guanylate cyclase, soluble guanylate cyclase alpha1, soluble guanylate cyclase alpha2, soluble guanylyl cyclase, SONO, STA, STA receptor, Tar4 protein
ECTree
4.6.1.2 guanylate cyclaseAdvanced search results
results (
results (Engineering
Engineering on EC 4.6.1.2 - guanylate cyclase
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PROTEIN VARIANTS 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
C122A
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site-directed mutagenesis of the aldosterone modification site, the mutant is insensitive to inhibition by aldosterone or H2O2
I145Y
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substitution in the full-length beta-subunit of the sGC heterodimer, does not produce an oxygen-binding enzyme, but impedes the association of NO and destabilizes the NO-heme complex. The tyrosine in the distal heme pocket impedes both the binding and dissociation of the CO ligand. Mutation does not affect stimulatory effect of manganese ion on the activity of the enzyme, thus function of the catalytic domain is not directly affected
Y140L
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yields a protein that no longer binds O2, but still binds NO. Introduction of a tyrosine residue anywhere in the distal pocket that is able to reach an iron-bound O2 is key in stabilization of the FeII-O2 complex, rescuing the mutant
E497K/C566D
D100N/D102G
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the mutant shows altered binding of guanylyl cyclase activating protein 1 compared to the wild-type enzyme
D530A
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mutation in alpha subunit. Protein levels of the catalytically inactive, non-nucleotide binding mutant a1/b1 are not affected by activator drugs
DELTAN364
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alpha1 DELTAN364 deletion mutant shows a complete loss of sensitivity towards NO or 3-(5'-hydroxymethyl-2'-furyl)-1-benzylindazole and a slight decrease in basal sGC activity
E75Q/E111Q/E155Q
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the mutant shows altered binding of guanylyl cyclase activating protein 1 compared to the wild-type enzyme
G959A
missense mutation, mutant binds C-type natriuretic peptide on the surface of cells but fails to synthesize cGMP in membrane guanylate cyclase assays. Mutant protein is dephosphorylated and incompletely glycosylated
H105C
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heme-deficient mutant, 70 times higher basal sGC activity than wild-type, basal activity is not affected by NO, heme reconstituted mutant regains No activation
I734T
substitution in the kinase homology domain linked to Leber congenital amaurosis, prevents binding of both GCAP1-GFP and GCAP2-GFP
L658F
missense mutation, mutant binds C-type natriuretic peptide on the surface of cells but fails to synthesize cGMP in membrane guanylate cyclase assays. Mutant protein is dephosphorylated and incompletely glycosylated
R776W
missense mutation, mutant binds C-type natriuretic peptide on the surface of cells but fails to synthesize cGMP in membrane guanylate cyclase assays. Mutant protein is dephosphorylated and incompletely glycosylated
S473A
mutation of potential phosphorylation site, reduces vmax value by 13-55%
S473E
mutation of potential phosphorylation site, reduces vmax value by 13-55%
S473E/S497E/T500E/S502E/S506E/S510E/T513E
2fold increase of Km value compared to wild-type
S487A
mutation of potential phosphorylation site, reduces vmax value by 13-55%
S487E
mutation of potential phosphorylation site, reduces vmax value by 13-55%
S497A
mutation of potential phosphorylation site, mutation increases Km value about 4fold
S497E
mutation of potential phosphorylation site, reduces vmax value by 13-55%
S497E/T500E/S502E/S506E/S510E/T513E
mutations in potential phosphorylation sites, about 20% of the activity of phosphorylated wild-type
S502A
mutation of potential phosphorylation site, reduces vmax value by 13-55%
S502E
mutation of potential phosphorylation site, reduces vmax value by 13-55%
S506A
mutation of potential phosphorylation site, reduces vmax value by 13-55%
S506E
mutation of potential phosphorylation site, reduces vmax value by 13-55%
S510A
mutation of potential phosphorylation site, reduces vmax value by 13-55%
S510E
mutation of potential phosphorylation site, reduces vmax value by 13-55%
T500A
mutation of potential phosphorylation site, reduces vmax value by 13-55%
T500E
mutation of potential phosphorylation site, reduces vmax value by 13-55%
T513A
mutation of potential phosphorylation site, reduces vmax value by 13-55%
T513E
mutation of potential phosphorylation site, reduces vmax value by 13-55%
W708R
substitution in the kinase homology domain linked to Leber congenital amaurosis, prevents binding of both GCAP1-GFP and GCAP2-GFP
Y708C
missense mutation, mutant binds C-type natriuretic peptide on the surface of cells but fails to synthesize cGMP in membrane guanylate cyclase assays. Mutant protein is dephosphorylated and incompletely glycosylated
F142Y
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L2 H-NOX mutant, shift of the equilibrium of the FeII-NO complex at 20°C exclusively to the 6-coordinate complex
H105F
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the enzyme of heme-free alpha1-subunit/H105F beta1-subunit sGC mutant is not activated by sodium nitroprusside, but by HMR-1766, 1H-[1,2,4]oxidazolol[4,3a]quinoxalin-1-one does not potentiate the activating effect of HMR-1766 in mutant cells, while it does in wild-type cells, binding structure of H105F mutant with HMR-1766, overview
W669A
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the mutant is only slightly responsive to the ATP/ANF signal, at about 29% compared to the wild-type enzyme
W669L
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the mutant is only slightly responsive to the ATP/ANF signal, at about 29% compared to the wild-type enzyme
K237E/D306K/T308G
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isoform PAC2, engineering of photoactivated adenylyl cyclase to photoactivated guanylyl cyclase, via mutagenesis of the substrate binding-specific residues in cyclase homology domain. The mutant shows typical BLUF photoreceptor properties
K332E/D400K/T402G
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isoform PAC3, engineering of photoactivated adenylyl cyclase to photoactivated guanylyl cyclase, via mutagenesis of the substrate binding-specific residues in cyclase homology domain. The mutant shows typical BLUF photoreceptor properties
C594D
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no 1-benzyl-3-(hydroxymethyl-2-furyl)indazole activation, no synergy with NO
C594Y
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reduced level of NO and 1-benzyl-3-(hydroxymethyl-2-furyl)indazole activation
D477A
E138A
the mutant is less responsive to nitric oxide in comparison to the wild type enzyme
E525K/C594D
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mutation in alpha subunit, mutant does not show a non-competitive mechanism with Mg2+GTPgammaS and Mg2+ATPgammaS that is observed with wild-type enzyme
G114A
the mutant has characteristics similar to the wild type enzyme
I111A
the mutant has a decreased basal activity and is less responsive to activators in comparison to the wild type enzyme
I41A
the mutant is strongly activated by YC-1, nitric oxide and to a lesser extent by protoporphyrin IX
M537N
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high level of 1-benzyl-3-(hydroxymethyl-2-furyl)indazole activation
R40A
the mutation results in a drastic decrease not only in basal activity but also in stimulated activity in response to protoporphyrin IX, YC-1, nitric oxide
S64A
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an alpha1/beta1 sGC mutant, shows resistance to phosphorylation by the cGMP-dependent protein kinase
S64D
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an alpha1/beta1 sGC mutant, is less activated by NO in comparison to the wild-type enzyme
K196E/D264K/T266G
additional information
E497K/C566D
mutations within the nucleotide binding site generates rhodopsin-adenylyl cyclase
E497K/C566D
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mutations within the nucleotide binding site generates rhodopsin-adenylyl cyclase
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D477A
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reduced level of NO and 1-benzyl-3-(hydroxymethyl-2-furyl)indazole activation
D477A
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mutation in beta subunit, mutant does not show a non-competitive mechanism with Mg2+GTPgammaS and Mg2+ATPgammaS that is observed with wild-type enzyme
K196E/D264K/T266G
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engineering of photoactivated adenylyl cyclase to photoactivated guanylyl cyclase, via mutagenesis of the substrate binding-specific residues in cyclase homology domain. The mutant shows typical BLUF photoreceptor properties
K196E/D264K/T266G
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engineering of photoactivated adenylyl cyclase to photoactivated guanylyl cyclase, via mutagenesis of the substrate binding-specific residues in cyclase homology domain. The mutant shows typical BLUF photoreceptor properties
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additional information
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deletion of the gene coding for the atypical sGC, gcy-35, results in loss of O2-dependent behavioral preference for 5-12% oxygen in worms, also prevents the expression of a feeding behavioral polymorphism
additional information
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double mutants for gcy genes show defects in thermotaxis, triple mutants for the gcy genes show severe defects in thermotaxis but respond normally to odorants and NaCl, abnormal phenotype of the gcy triple mutants can be rescued by expression of any one of the three GCY proteins, gcy-8, gcy-18, and gcy-23. In the AFD neurons no defects in thermotaxis behaviors in gcy single mutants
additional information
double mutants for gcy genes show defects in thermotaxis, triple mutants for the gcy genes show severe defects in thermotaxis but respond normally to odorants and NaCl, abnormal phenotype of the gcy triple mutants can be rescued by expression of any one of the three GCY proteins, gcy-8, gcy-18, and gcy-23. In the AFD neurons no defects in thermotaxis behaviors in gcy single mutants
additional information
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misexpression of a Gal4-VP16 induced gene or deletion of gene gucy2F leads to multiple defects including morphological defects and loss of forebrain neurons. Screening for gain-of-function mutants, method development for use in large-scale genetic screens in a vertebrate model organism, evaluation, overview. Increased cGMP in embryos with gucy2F overexpression
additional information
mutant sGCdeltacat with point mutation introduced in the catalytic site, loses catalytic activity, shows poor myosin localization at the back, but excellent localization of the sGC protein at the leading edge, where it enhances the probability that a new pseudopod is made in proximity to previous pseudopodia, resulting in a decrease of the degree of turning. Mutant sGCdeltaN with deletion of the N-terminal 877 amino acids, exhibits excellent cGMP formation and myosin localization in the back of the cell, but exhibits poor orientation at the leading edge
additional information
generation of an isozyme Gyc-89Da deficient mutant, reduced levels of cGMP in Gyc-89Da neurons have no effect on larval ecdysis or eclosion, but isozyme expression is necessary early in adult development to prevent eclosion, phenotype, overview
additional information
generation of an isozyme Gyc-89Da deficient mutant, reduced levels of cGMP in Gyc-89Da neurons have no effect on larval ecdysis or eclosion, but isozyme expression is necessary early in adult development to prevent eclosion, phenotype, overview
additional information
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generation of an isozyme Gyc-89Da deficient mutant, reduced levels of cGMP in Gyc-89Da neurons have no effect on larval ecdysis or eclosion, but isozyme expression is necessary early in adult development to prevent eclosion, phenotype, overview
additional information
generation of an isozyme Gyc-89Db deficient mutant, reduced levels of cGMP in Gyc-89Db neurons have no effect on larval ecdysis or eclosion, but isozyme expression is necessary early in adult development to prevent eclosion, phenotype, overview
additional information
generation of an isozyme Gyc-89Db deficient mutant, reduced levels of cGMP in Gyc-89Db neurons have no effect on larval ecdysis or eclosion, but isozyme expression is necessary early in adult development to prevent eclosion, phenotype, overview
additional information
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generation of an isozyme Gyc-89Db deficient mutant, reduced levels of cGMP in Gyc-89Db neurons have no effect on larval ecdysis or eclosion, but isozyme expression is necessary early in adult development to prevent eclosion, phenotype, overview
additional information
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identification of CT and GA polymorphisms in the 5'-flanking region and the promoter region that acts synergistically to affect the GC-A promoter, transcription activity of genotypes, overview
additional information
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the depletion of sGC by RNA interference fails to prevent Y-27632- and staurosporine-induced neurite outgrowth
additional information
deletion of a residues Tyr1016-Ser1103 fragment in RetGC1 does not block GCAP2 binding to the cyclase
additional information
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endothelial NO synthase and natriuretic peptide receptor-A knockout mice, sodium nitroprusside and atrial natriuretic peptide produce enhanced dose-dependent reductions in mean arterial blood pressure in endothelial NO synthase knockout mice. In natriuretic peptide receptor-A knockout mice, sodium nitroprusside produces a dose-dependent reduction in mean arterial blood pressure that is significantly higher than that in wild-type mice. Responsiveness to the cAMP-dependent vasodilator epoprostenol is similar in wild-type, endothelial NO synthase and natriuretic peptide receptor-A knockout animals. Atrial natriuretic peptide causes vasodilatation of the forearm resistance vasculature that is significantly higher in individuals lacking endothelium-derived NO
additional information
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GC1-/-, GC2-/- and GC1/GC2 double knock-out mice, GC1 expression level is maintained in GC2-/- retina and GC2 expression level is maintained in GC1-/- retina. Deletion of GC1 and GC2 renders rod and cone photoreceptors nonfunctional and unstable. In the rod outer segments of guanylate cyclase double knock-out mice, guanylate cyclase-activating proteins 1 and 2, and cyclic GMP phosphodiesterase are undetectable, although rhodopsin and transducin alpha-subunit are mostly unaffected. Outer segment membranes of GC1-/- and GC double knock-out cones are destabilized and devoid of cone transducin (alpha- and gamma-subunits), cone phosphodiesterase, and G protein-coupled receptor kinase 1, whereas cone pigments are present at reduced levels. Down-regulated proteins show normal RNA transcript levels, indicating that down-regulation is posttranslational
additional information
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basal cGMP levels are lower in sGCalpha1 knockout strips but NO still significantly increases cGMP levels versus basal. In conclusion, in the absence of sGCalpha1beta1, exogenous NO is able to partially act through sGCalpha2beta1, comparison of the soluble guanylate cyclase (sGC) isoforms ?1?1 and ?2?1, and of wild-type with sGCalpha1 knockout mice in the relaxation of distal colon by exogenous NO and by NANC nerve stimulation, overview
additional information
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construction and phenotype of sGCalpha1 KO mice, expression levels of sGC subunits are altered in the mutant compared to the wild-type mice, the KO mice show reduced enzyme activation and induced muscle relaxation by CO, overview
additional information
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construction of a deletion mutant of ANF-RGC lacking the 669WTAPELL675 motif
additional information
construction of a mutant GC-ADELTALys314-Gln330 and transfection into HEK-293 cells leading to complete inhibition of binding of atrial natriuretic peptide and atrial natriuretic peptide-induced cyclic GMP formation, overview. Alternative splicing does not affect membrane localization of GC-A, overview
additional information
construction of a truncated GCC 1-430 construct, GCC ECD, containing the extracellular ligand-binding domain and a C-terminus His6-tag in in colorectal cancer cells using a viral vector, overview
additional information
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construction of a truncated GCC 1-430 construct, GCC ECD, containing the extracellular ligand-binding domain and a C-terminus His6-tag in in colorectal cancer cells using a viral vector, overview
additional information
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construction of GC-A knockout mice that show significant chronic hypervolemic hypertension, phenotype, overview
additional information
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construction of isozyme sGCalpha1-deficient mice, in contrast to wild-type mice, the neurologic and myocardial functions are reduced in cardiac arrest and cardiopulmonary resuscitation, CPR, the detrimental effects are associated with enhanced inflammation of heart and liver, and increased cell death in heart, liver, and brain, which can be prevented by overexpression of NO synthase 3, overview
additional information
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construction of mice deficient in one of the two isozymes NO-GC1 and NO-GC2 or in both, phenotypes, overview
additional information
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GC-C knckout in intestinal epithelial cells increases apoptosis following radiation-injury, supplementation with cGMP ameliorates radiation-induced apoptosis, overview
additional information
generation of a mutant mouse with a targeted disruption of the GC-G gene Gucy2g, which shows no histologic abnormalities at baseline, but after I/R injury, elevations in serum creatinine and urea are attenuated in GC-G knockout mice compared with wild-type controls, and this correlated with less tubular disruption, less tubular cell apoptosis, and less caspase-3 activation, phenotype, overview. Direct transfer of a GC-G expression plasmid to the kidneys of GC-G-deficient mice results in a dramatically higher mortality after renal I/R injury
additional information
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generation of a mutant mouse with a targeted disruption of the GC-G gene Gucy2g, which shows no histologic abnormalities at baseline, but after I/R injury, elevations in serum creatinine and urea are attenuated in GC-G knockout mice compared with wild-type controls, and this correlated with less tubular disruption, less tubular cell apoptosis, and less caspase-3 activation, phenotype, overview. Direct transfer of a GC-G expression plasmid to the kidneys of GC-G-deficient mice results in a dramatically higher mortality after renal I/R injury
additional information
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generation of sGCalpha1 subunit KO mice, that show abolished muscle relaxation after electric field stimulation more pronounced in female than in male KO mice
additional information
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mice deficient in isozyme GC-A show marked cardiac hypertrophy and fibrosis, which can be inhibited by both genetic and pharmacological blockade of type 1 angiotensin II receptors. The mutant mice show increased expression of atrial and brain natriuretic peptides, and increased systemic blood pressure and heart weight to body weight ratios compared to the wild-type mice, overview
additional information
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mouse line lacking retGC-1, GCE null, light-induced transducin redistribution occurs faster in mice lacking ret-GC1, phenotype, overview
additional information
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nociceptive behavior of mice deficient in NO-sensitive guanylyl cyclase, GC-KO mice fail to develop pain sensitization induced by intrathecal administration of drugs releasing NO or carbon monoxide, NO-, CO-, and cGMP-induced pain behavior in GC-KO mice, overview
additional information
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GC-C knckout in intestinal epithelial cells increases apoptosis following radiation-injury, supplementation with cGMP ameliorates radiation-induced apoptosis, overview
-
additional information
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construction of a truncated GCC 1-430 construct, GCC ECD, containing the extracellular ligand-binding domain and a C-terminus His6-tag in in colorectal cancer cells using a viral vector, overview
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additional information
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GC1-/-, GC2-/- and GC1/GC2 double knock-out mice, GC1 expression level is maintained in GC2-/- retina and GC2 expression level is maintained in GC1-/- retina. Deletion of GC1 and GC2 renders rod and cone photoreceptors nonfunctional and unstable. In the rod outer segments of guanylate cyclase double knock-out mice, guanylate cyclase-activating proteins 1 and 2, and cyclic GMP phosphodiesterase are undetectable, although rhodopsin and transducin alpha-subunit are mostly unaffected. Outer segment membranes of GC1-/- and GC double knock-out cones are destabilized and devoid of cone transducin (alpha- and gamma-subunits), cone phosphodiesterase, and G protein-coupled receptor kinase 1, whereas cone pigments are present at reduced levels. Down-regulated proteins show normal RNA transcript levels, indicating that down-regulation is posttranslational
-
additional information
-
endothelial NO synthase and natriuretic peptide receptor-A knockout mice, sodium nitroprusside and atrial natriuretic peptide produce enhanced dose-dependent reductions in mean arterial blood pressure in endothelial NO synthase knockout mice. In natriuretic peptide receptor-A knockout mice, sodium nitroprusside produces a dose-dependent reduction in mean arterial blood pressure that is significantly higher than that in wild-type mice. Responsiveness to the cAMP-dependent vasodilator epoprostenol is similar in wild-type, endothelial NO synthase and natriuretic peptide receptor-A knockout animals. Atrial natriuretic peptide causes vasodilatation of the forearm resistance vasculature that is significantly higher in individuals lacking endothelium-derived NO
-
additional information
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alpha1-sGC and beta1-sGC deletion mutants, coexpression of alpha1-YNV deletion mutants with wild-type-beta1-YCV as well as beta1-YCV deletion mutants with wild-type-beta1-YNV-sGC results in functional heterodimerization of both sGC subunits in the cytosol of the cell
additional information
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GCC lacking the amino acids from the conserved 63 amino acid span, localized in an unpolarized manner at both the apical and basolateral membranes, GCC protein lacking 32 or 52 amino acids from the COOH terminus, both mutations have no effect on the apical localization of GCC
additional information
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ONE-GCdeltaext mutant, deleted extracellular domain of ONE-GC, basal guanylate cyclase activity almost identical to that of wild-type, deletion of the extracellular domain has no effect on the tertiary structure of the protein, cannot be stimulated by uroguanylin. Tm bound mutant and soluble cat mutant, both have intrinsic catalytic activity, mutations have not effect on their tertiary structures
additional information
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construction of heme domain mutant comprising residues beta1(1-194) or beta2(1-217)
additional information
recombinant miniGC-C, comprising the exracellular enzyme domain, binds the heat-stable enterotoxin STp-(5-17) with high affinity, ligand binding and structure analysis, overview
