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Validated All-in-One™ qPCR Primer for NAMPT(NM_005746.2) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
This gene encodes a protein that catalyzes the condensation of nicotinamide with 5-phosphoribosyl-1-pyrophosphate to yield nicotinamide mononucleotide, one step in the biosynthesis of nicotinamide adenine dinucleotide. The protein is an adipokine that is localized to the bloodstream and has various functions, including the promotion of vascular smooth muscle cell maturation and inhibition of neutrophil apoptosis. It also activates insulin receptor and has insulin-mimetic effects, lowering blood glucose and improving insulin sensitivity. The protein is highly expressed in visceral fat and serum levels of the protein correlate with obesity. This gene has a pseudogene on chromosome 10. [provided by RefSeq].
Gene References into function
- PBEF1 is upregulated in neutrophils by IL-1beta and functions as a novel inhibitor of apoptosis in response to a variety of inflammatory stimuli.
- isolation of visfatin; expression in plasma increases during the development of obesity;exerted insulin-mimetic effects in cultured cells; binds to and activates the insulin receptor[visfatin]
- These findings identify PBEF1 as a regulator of NAD+-dependent reactions in smooth muscle cells (SMCs), reactions that promote, among other potential processes, the acquisition of a mature SMC phenotype.
- Although PBEF had no chemotaxic effects, it was antiapoptotic for both amniotic epithelial cells and fibroblasts and may protect these cells against apoptosis that is induced by chronic distension, labor, or infection.
- visfatin plasma concentrations and visceral visfatin messenger RNA expression correlated with measures of obesity but not with visceral fat mass or waist-to-hip ratio
- PBEF contributes to acute lung injury susceptibility
- visfatin may play a role in the pathogenesis of type 2 diabetes mellitus
- A true adipokine, but it is not regulated by thiazolidineidones and, thus unlikely to contribute to the insulin-sensitizing actions of these drugs.
- increased macrophage population in obese human visceral white adipose tissue might be responsible for the enhanced production of chemokines as well as resistin and visfatin
- Visfatin/pre-B-cell colony-enhancing factor appears to be preferentially produced by the visceral adipose tissue and has insulin mimetic actions
- data suggest that genetic variation in the visfatin gene may have a minor effect on visceral and subcutaneous visfatin messenger RNA expression profiles but does not play a major role in the development of obesity or type 2 diabetes mellitus
- These data show that an inflammatory stimulus in the fetal membranes inducing NF-kappaB and AP-1 would up-regulate PBEF as well as IL-8.
- findings show that, in human obesity, plasma visfatin is reduced, whereas visfatin mRNA is differentially regulated in adipose tissue
- Circulating visfatin concentrations are increased by hyperglycaemia. This effect is suppressed by exogenous hyperinsulinaemia or somatostatin infusion.
- FK866 is bound in a tunnel at the interface of the NMPRTase dimer, and mutations in this binding site can abolish the inhibition by FK866, providing a starting point for the development of new anticancer agents.
- Pre-B cell colony-enhancing factor (PBEF) is regulated via IL-6 trans-signaling and the IL-6-related cytokine OSM. PBEF is also actively expressed during arthritis.
- results show that there are decreased concentrations of plasma visfatin in gestational diabetes mellitus subjects and this may indicate that visfatin plays a role in the pathogenesis of gestational diabetes mellitus
- visfatin is a new hypoxia-inducible gene of which expression is stimulated through the interaction of HIF-1 with HRE sites in its promoter region.
- visfatin has a local metabolic role in the recovery period following exercise.
- The results indicate that hyperglycemia causes an increase in plasma visfatin levels and, as in people with diabetes mellitus type 2 but not with impaired glucose tolerance, this increase gets more prominent as the glucose intolerance worsens.
- circulating visfatin is increased with progressive beta-cell deterioration.
- A significant association was found between two SNPs of visfatin (rs9770242 and rs1319501), in perfect linkage disequilibrium, and fasting insulin levels (P = 0.002).
- visfatin is highly expressed in lean, more insulin-sensitive subjects and is attenuated in subjects with high intramyocellular lipids, low insulin sensitivity, and high levels of inflammatory markers
- potential link with pathogenesis of glucose resistance and type 2 diabetes
- In patients with inflammatory bowel disease, plasma levels of visfatin are elevated and its mRNA expression is significantly increased in colonic tissue of Crohn's and ulcerative colitis patients
- Circulating levels of the cytokine visfatin/PBEF-1 are influenced by renal function, but are not associated with fat mass or surrogate markers of insulin resistance in patients with chronic kidney disease.
- Visfatin is down-regulated by overfeeding
- Nampt is a longevity protein that can add stress-resistant life to human smooth muscle cells by optimizing SIRT1-mediated p53 degradation
- Serum visfatin concentration is significantly associated with parameters of iron metabolism, especially in subjects with altered glucose tolerance.
- An increase in fasting visfatin, the levels of which correlate with both fasting and post-glucose-load insulin concentrations, accompanies worsening glucose tolerance in the third trimester of pregnancy.
- Women with PCOS exhibit higher plasma visfatin levels than control subjects of similar body mass index.
- the regulation of glucose uptake, proliferation, and type I collagen production by visfatin in human osteoblasts involves IR phosphorylation, the same signal-transduction pathway used by insulin
- This review summarizes current knowledge of the various functions of PBEF/visfatin towards involvement in the pathophysiology of several diseases.
- Taken together, these results demonstrate that visfatin promotes angiogenesis via activation of mitogen-activated protein kinase ERK-dependent pathway.
- PBEF/NAMPT/visfatin level is an indicator of beneficial lipid profile in non-diabetic Caucasian subjects
- Plasma visfatin levels are increased in overweight and obese subjects with metabolic syndrome.
- Visfatin has a role in insulin resistance and markers of hyperandrogenism in lean PCOS patients
- During fasting, increased Nampt provides protection against cell death and requires an intact mitochondrial NAD(+) salvage pathway as well as the mitochondrial NAD(+)-dependent deacetylases SIRT3 and SIRT4.
- Circulating visfatin may be related with some proinflammatory condition even in a nondiabetic state
- Rosuvastatin induced a significant decrease in plasma visfatin levels in patients with primary hyperlipidemia.
- Visfatin, TNF-alpha, and IL-6 mRNA expressions are increased in peripheral mononuclear-monocytic cells from women with type 2 diabetes.
- Circulating levels of visfatin and adiponectin are associated with endothelial dysfunction in all stages of chronic kidney disease, independently of inflammation and insulin resistance.
- Severely obese women have higher than normal blood levels of visfatin.
- As a good surrogate marker, plasma visfatin level can predict the visceral adipose tissue area in obese children.
- Results show that visfatin levels may decrease with age and be related to the HDL metabolism in obese adolescents.
- PBEF is shown to exert three distinct activities of central importance to cellular energetics and innate immunity.[REVIEW]
- The -1535 promoter variant of the visfatin gene is associated with serum triglyceride and HDL-cholesterol levels in Japanese subjects.
- Chronic stretching of the amniotic epithelial cells increases PBEF expression, which protects them from apoptosis.
- C-reactive protein, migration inhibitor factor (MIF), leptin, and visfatin levels decreased after weight loss.
- These results may reveal a novel role of PBEF in the pathogenesis of acute lung injury; it interacts with ND1, IFITM3, and ferritin light chain involved in oxidative stress and inflammation.
- change of plasma visfatin concentration by intensive glycemic control may be a compensatory mechanism to ameliorate insulin deficiency due to pancreatic beta-cell dysfunction in type 2 diabetes
- analysis of the structure and function of visfatin and its relation to diabetes mellitus and other dysfunctions [review]
- Circulating visfatin are significantly increased in HLA DR2 positive narcoleptic patients compared to controls.
- PBEF1/NAmPRTase/Visfatin is a potential malignant astrocytoma/glioblastoma serum marker with prognostic value.
- PBEF1/NAmPRTase/Visfatin may have a role in progression of malignant astrocytoma/glioblastoma
- Results show that women with gestational diabetes mellitus have significantly decreased visfatin concentrations in the third trimester.
- Although the weak energetic coupling of ATP hydrolysis appears to be a nonoptimized enzymatic function, closer analysis of this remarkable protein reveals an enzyme designed to capture NAM with high efficiency at the expense of ATP hydrolysis.
- The visfatin (PBEF1) G-948T gene polymorphism is associated with increased high-density lipoprotein cholesterol in obese subjects.
- cartilage-specific gene expression in human chondrocytes is regulated by SirT1 and nicotinamide phosphoribosyltransferase
- Nicotinamide phosphoribosyltransferase may play a critical role as an inflammatory cytokine in the development of pulmonary inflammation and dysregulation of pulmonary vascular endothelial and alveolar epithelial cell barriers.
- Plasma levels of PBEF/Nampt/visfatin are decreased in patients with liver cirrhosis.
- Visfatin levevns in human cerebrospinal fluid decrease with rising body fat, supporting the assumption that visfatin transport is impaired in obesity and that central nervous visfatin insufficiency is linked to pathogenetic mechanisms of obesity.
- These data further suggest an integral role for visfatin-FGF-2 signaling axis in modulating endothelial angiogenesis.
