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- Table of Contents
5 Citations 3 Q&As
16 Citations 5 Q&As
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4 Citations 5 Q&As
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Facts about Nitric oxide synthase, brain.
Probably has nitrosylase action and mediates cysteine S-nitrosylation of cytoplasmic target proteins such SRR. .
Human | |
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Gene Name: | NOS1 |
Uniprot: | P29475 |
Entrez: | 4842 |
Belongs to: |
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NOS family |
bNOS; brain; Constitutive NOS; EC 1.14.13.39; IHPS1; Neuronal NOS; nitric oxide synthase 1 (neuronal); nNOS; N-NOS; nNOSNOS type I; NOS; NOS1; Peptidyl-cysteine S-nitrosylase NOS1
Mass (kDA):
160.97 kDA
Human | |
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Location: | 12q24.22 |
Sequence: | 12; NC_000012.12 (117208142..117361802, complement) |
Isoform 1 is ubiquitously expressed: detected in skeletal muscle and brain, also in testis, lung and kidney, and at low levels in heart, adrenal gland and retina. Not detected in the platelets. Isoform 3 is expressed only in testis. Isoform 4 is detected in testis, skeletal muscle, lung, and kidney, at low levels in the brain, but not in the heart and adrenal gland.
Cell membrane, sarcolemma; Peripheral membrane protein. Cell projection, dendritic spine. In skeletal muscle, it is localized beneath the sarcolemma of fast-twitch muscle fiber by associating with the dystrophin glycoprotein complex. In neurons, enriched in dendritic spines (By similarity).
Scientists from all over the world can submit their results for species, applications and other samples, using Boster Bio: Best Uses of the NOS1 Marker. Researchers can not only get product credits but also get special samples. This information is applicable globally to all scientists. This article will provide a guideline on how scientists can make the most of this marker to help in research.
PP2A is a post-translational alteration that regulates the expression levels of several cardiac genes. In the cardiac tissues, PP2A overexpression may alter their expression in many ways. Western Blotting and analysis of genechips revealed changes in the expression of cardiac genes related to protein phosphorylation, cell metabolism, and other factors. Several cardiac stressors, including lipopolysaccharide-induced sepsis and global ischemia, were studied in PP2A-TG mice.
The PP2A-TG compound increases Ca2+ sensitivity in myocytes that are failing in humans. However, in the failing heart, PP2A didn't alter the increase in base Ca2+ sensitivity. This could be due the diminished basal phosphorylation (PKA-dependent) of the cTnI. In failing hearts, a reduction of PP2AC protein expression is linked to increased basal Ca2+ sensitivity. In failing hearts, decreased expression of PP2AC catalytic subunit and B56a might help compensate for the increase in base Ca2+ sensitivities.
Despite the greater understanding of PP2A however, little is known about its function and distribution interactions in the mammalian heart. PP2ATG is present in human hearts but in a lesser degree than in rats, mice and human. In addition, these recent research findings demonstrate the complexity of PP2A subunit expression in mammalian hearts. These regulatory subunits might confer signaling specificity through their variable expression.
Additionally, PP2A TG may increase the heart's rate of beating. The heart with ischemia is able to produce a greater force of contraction than the WT animals. The same mechanism could be responsible for the increased heart rate in the laboratory. This theory is not supported by any evidence since PP2A dephosphorylates PDE3 which blocks the adrenoceptors.
In the ischemic rat model it is PP2A-TG that helps prevent sepsis and ischemia by reducing the levels of collagen and elastin in arteries and heart. On the other side, has a lower systolic derivative, as well as a lower ejection fraction within the left ventricular chamber.
This study suggests that PP2A holoenzyme activity is controlled by a highly-organized regulatory network. To fully understand the regulation of PP2A homoenzyme in living cells, and to determine if these alterations are adaptive/detrimental, further studies will be required on PP2A the upstream regulatory molecules for TG. The findings will also help determine whether PP2A-TG provides heart protection against sepsis and ischemia.
Exogenously applying PP2AC can have functional effects that depend on the levels of expression of subunits as well as enzyme. Additionally, a reduction in PP2AC expression could cause negative effects on myofilament contraction. Incredibly, PP2AC expression in adult heart of rats was lower than that in embryonic rat heart. The results also suggest that the levels of enzymes and proteins in adult rat hearts could be lowered, and the function of PP2AC in adult heart of rat is not sufficient to protect the heart from ischemia and sepsis.
In the event of a stress that is pathological, PLN specific phosphatase is inducible into cardiomyocytes. This maintains SR calcium homeostasis. In an ailing heart, PP2Ce may also be induced. This could be a chronically impaired response similar to b–adrenergic desensitization.
PMID: 7528745 by Hall A.V., et al. Structural organization of the human neuronal nitric oxide synthase gene (NOS1).
PMID: 7515942 by Fujisawa H., et al. Expression of two types of nitric oxide synthase mRNA in human neuroblastoma cell lines.
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