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抗Human NNT 抗体:
抗Mouse (Murine) NNT 抗体:
抗Rat (Rattus) NNT 抗体:
Cow (Bovine) Polyclonal NNT Primary Antibody for WB - ABIN2782785
Mehrle, Rosenfelder, Schupp, del Val, Arlt, Hahne, Bechtel, Simpson, Hofmann, Hide, Glatting, Huber, Pepperkok, Poustka, Wiemann: The LIFEdb database in 2006. in Nucleic acids research 2005
Human Monoclonal NNT Primary Antibody for IF, ELISA - ABIN565110
Picklo: Ethanol intoxication increases hepatic N-lysyl protein acetylation. in Biochemical and biophysical research communications 2008
evidence for expression in the gut, the pharyngeal-intestinal valve and certain neurons
nnt-1 is important in the defense against mitochondrial oxidative stress
Overexpression of nicotinamide nucleotide transhydrogenase (NNT) was associated with shorter overall and disease free survival in gastric cancer. Knockdown of NNT caused significantly NADPH reduction, induced high levels of Reactive Oxygen Species and significant cell apoptosis under oxidative stress conditions such as glucose deprival and anoikis.
Findings suggest that NNT is essential to homeostasis of NADH and NADPH pools, anomalies of which affect HIF-1alpha- and HDAC1-dependent pathways, and hence retrograde response of mitochondria.
Study describes the fi rst structural model of the human NNT. The 3D model identifies functional and structural H-NNT key motifs and gain essential insight into the structural and functional effect of deleterious amino acid substitutions causing glucocorticoid de fi ciency and LVNC cardiomyopathy, as well as rare homozygote amino acid variations.
NNT should be sequenced in all primary adrenal insufficiencies for which the most frequent etiologies have been ruled out. As NNT is involved in oxidative stress, careful follow-up is needed to evaluate mineralocorticoid biosynthesis extent, and gonadal, heart and thyroid function.
identified a 6.67 Mb homozygous region harboring the NNT gene in a Dutch patient presenting with familial glucocorticoid deficiency (FGD); a novel homozygous mutation (NM_012343.3: c.1259dupG) in NNT was revealed; reviewed the literature for all the reported NNT mutations and their clinical presentation
This report of a novel NNT mutation, p.G200S, expands the phenotype of NNT mutations to include mineralocorticoid deficiency. It provides the first evidence that NNT mutations can cause oxidative stress and mitochondrial defects.
Data suggest mutations in nicotinamide nucleotide transhydrogenase (NNT) as contributory to left ventricular noncompaction (LVNC).
NNT mRNA expression is significantly higher in visceral fat of obese patients and correlates with body weight, BMI, % body fat, visceral and sc fat area, waist and hip circumference, and fasting plasma insulin.
Results suggest that NNT may have a role in ROS detoxification in human adrenal glands.
In the failing heart a partial loss of Nnt activity adversely impacts NADPH-dependent enzymes and the capacity to maintain membrane potential, thus contributing to a decline in bioenergetic capacity, redox regulation and antioxidant defense.
the expression of the transhydrogenase gene in subsections of the human brain showed a distribution that apparently varied as a function of neuronal density
NNT mediates the effects of glucose on islet NADPH and mitochondrial glutathione redox state by reducing its reverse mode of operation, which consumes NADPH, from non-stimulating to stimulating glucose concentrations.
NNT plays a critical role in counteracting mitochondrial redox imbalance, pyruvate dehydrogenase inhibition and advancement of Non-alcoholic Fatty Liver Disease in mice fed a high fat diet.
Loss of NNT increases vascular ROS production and exacerbates atherosclerotic plaque development.
adrenal redox homeostasis mediated not only by under expression of NNT but also by its overexpression
this study demonstrates that the respiratory state and/or substrates that sustain energy metabolism markedly influence the relative contribution of NNT (i.e. varies between nearly 0 and 100%) to NADPH-dependent mitochondrial peroxide metabolism.
Pathologic workload reverses Nnt to deplete NADPH and antioxidative capacity. Reverse Nnt induces mitochondrial oxidative stress and necrosis.
In mitochondria, genetic or pharmacological disruptions in the PDHC-NNT redox circuit negate counterbalance changes in energy expenditure
Data conclude that Herpud1 regulates insulin secretion via control of Nnt expression.
our data suggest that NNT functions as a high-capacity source of mitochondrial NADPH and that its functional loss due to the Nnt mutation results in mitochondrial redox abnormalities
the role of NNT in regulating central carbon metabolism via redox balance, calling for other mechanisms that coordinate substrate preference to maintain a functional TCA cycle.
Our results demonstrate a novel role for NNT as a regulator of macrophage-mediated inflammatory responses
A normal Nnt allele can help with better cardiac function in MnSOD-deficient mice during fetal development.
The presence of a truncated Nnt did not affect insulin secretion or glucose tolerance on the C57BL/6 background.
Nnt was identified as a novel candidate gene for contribution to glucose intolerance through reduced beta cell activity.
Mutations/deletion uncouple pancreatic beta cell mitochondrial metabolism leading to less ATP production, enhanced KATP channel activity, and consequently impaired insulin secretion.
Nnt deficiency results in defective insulin secretion and inappropriate glucose homeostasis in male C57BL/6J mice.
NNT must play an important role in beta cell function and its effect on the high insulin secretory capacity of the DBA/2 mouse may predispose beta cells of these mice to failure.
decreased glucose tolerance in Nnt knockout mice observed in our experiments does not require UCP2.
This gene encodes an integral protein of the inner mitochondrial membrane. The enzyme couples hydride transfer between NAD(H) and NADP(+) to proton translocation across the inner mitochondrial membrane. Under most physiological conditions, the enzyme uses energy from the mitochondrial proton gradient to produce high concentrations of NADPH. The resulting NADPH is used for biosynthesis and in free radical detoxification. Two alternatively spliced variants, encoding the same protein, have been found for this gene.
Nicotinamide Nucleotide Transhydrogenase family member (nnt-1)
, nicotinamide nucleotide transhydrogenase
, NAD(P) transhydrogenase, mitochondrial
, pyridine nucleotide transhydrogenase
, Nicotinamide nucleotide transhydrogenase (NAD(P)+ transhydrogenase)