Human Nesfatin-1 ELISA Kit

Name: Human Nesfatin-1 ELISA Kit
SKU: DEIA4737
Rating: 5 (1 reviews)

Regulatory status: For research use only, not for use in diagnostic procedures.

COA

SDS

Datasheet

Summary

Sample

Serum, plasma (EDTA, citrate, heparin)

Species Reactivity

Human

Detection Method

sELISA

Intended Use

The Human Nesfatin-1 ELISA is a sandwich enzyme immunoassay for the quantitative measurement of human nesfatin-1.

Contents of Kit

Biotin Labelled Antibody, lyophilized, 2 vials
Streptavidin-HRP Conjugate, ready to use, 13 ml
Master Standard, lyophilized, 2 vials
Dilution Buffer, ready to use, 50 ml
Wash Solution Conc. (10×), concentrated, 100 ml
Substrate Solution, ready to use, 13 ml
Stop Solution, ready to use, 13 ml
Product Data Sheet+Certificate of Analysis,1 pc

Storage

Store the complete kit at 2-8°C. Under these conditions, the kit is stable until the expiration date (see label on the box).

Performance Characteristics

It is intended for research use only
The total assay time is less than 4 hours
The kit measures human nesfatin-1 in serum, plasma (EDTA, citrate, heparin)
Assay format is 96 wells
Standard is recombinant (E.coli) protein based
Components of the kit are provided ready to use, concentrated or lyophilized

Detection Range

0.125-4 ng/ml

Detection Limit

0.021 ng/ml

Sensitivity

Limit of Detection (LOD), defined as concentration of analyte giving absorbance higher than mean absorbance of blank plus three standard deviations of the absorbance of blank: A_blank + 3×SD_blank, is calculated from the real Nesfatin-1 values in wells and is 0.021 ng/ml.
Dilution Buffer is pipetted into blank wells.

General Description

Nesfatin-1 was first described in 2006 as a neurohormone derived from the protein NEFA/nucleobindin2 (NUCB2). It is a polypeptide consisting of 82 amino acids, with a high level of homology between human, mouse and rat. Nesfatin-1 has been localized in the brain--particularly in the nuclei of the hypothalamus, adipose tissue and the gastrointestinal tract.It is also found in serum and cerebrospinal fluid. Nesfatin-1 was identified as a satiety molecule affecting fat metabolism. Intracerebroventricular administration of nesfatin-1 induces a decrease in food intake and body weight and an increase in sympathetic nerve activity and mean arterial pressure. The effect of Nesfatin-1 is leptin-independent and is likely mediated by the melanocortin system. Several studies are currently focused on the possibility of using Nesfatin-1 in the treatment of obesity, even in individuals with leptin resistance. Serum Nesfatin-1 could also serve as a clinical marker in the diagnosis of many diseases.
The important role of nesfatin-1 in the metabolism of glucose and insulin has been reported in several studies. Different concentrations were observed in patients with diabetes mellitus type I and II. In individuals with DM type II postprandial concentration of nesfatin-1 was significantly lower than levels in individuals with DM type I and healthy subjects. Different levels of Nesfatin1 were measured in patients with anorexia nervosa and panic disorders in comparison to a healthy control group.
Data obtained in experiments with rat models indicate that nesfatin-1 acts as a peripheral modulator of the cardiac function.
Much higher levels of serum Nesfatin-1 (up to 160×) were detected in patients with newlydiagnosed epilepsy. During the treatment with anti-epileptics concentration of Nesfatin-1 decreased, but it was still about 10 times higher than the level of the hormone in healthy individuals. This suggests that it might be possible to use the Nesfatin-1 as a marker for diagnosis and monitoring of epilepsy.

Standard Curve

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Documents

pdf COA

pdf SDS

pdf Datasheet

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Customer Reviews

References

Prognostic Impact of Modulators of G proteins in Circulating Tumor Cells from Patients with Metastatic Colorectal Cancer

SCIENTIFIC REPORTS

Authors: Barbazan, Jorge; Dunkel, Ying; Li, Hongying; Nitsche, Ulrich; Janssen, Klaus-Peter; Messer, Karen; Ghosh, Pradipta

Abstract

The consequence of a loss of balance between G-protein activation and deactivation in cancers has been interrogated by studying infrequently occurring mutants of trimeric G-protein alpha-subunits and GPCRs. Prior studies on members of a newly identified family of non-receptor guanine nucleotide exchange factors (GEFs), GIV/Girdin, Daple, NUCB1 and NUCB2 have revealed that GPCR-independent hyperactivation of trimeric G proteins can fuel metastatic progression in a variety of cancers. Here we report that elevated expression of each GEF in circulating tumor cells (CTCs) isolated from the peripheral circulation of patients with metastatic colorectal cancer is associated with a shorter progression-free survival (PFS). The GEFs were stronger prognostic markers than two other markers of cancer progression, S100A4 and MACC1, and clustering of all GEFs together improved the prognostic accuracy of the individual family members; PFS was significantly lower in the high-GEFs versus the low-GEFs groups [H.R = 5, 20 (95% CI; 2,15-12,57)]. Because nucleotide exchange is the rate-limiting step in cyclical activation of G-proteins, the poor prognosis conferred by these GEFs in CTCs implies that hyperactivation of G-protein signaling by these GEFs is an important event during metastatic progression, and may be more frequently encountered than mutations in G-proteins and/or GPCRs.

Comparison of the therapeutic effects of sildenafil citrate, heparin and neuropeptides in a rat model of acetic acid-induced gastric ulcer

LIFE SCIENCES

Authors: Kalayci, Mehmet; Kocdor, Mehmet Ali; Kuloglu, Tuncay; Sahin, Ibrahim; Sarac, Mehmet; Aksoy, Aziz; Yardim, Meltem; Dalkilic, Semih; Gursu, Onur; Aydin, Suna; Akkoc, Ramazan Fazil; Ugras, Meltem; Artas, Gokhan; Ozercan, Ibrahim Hanifi; Ugur, Kader; Aydin, Suleyman

Abstract

Aims: The purpose of our investigative work has been to determine whether there can be therapeutic roles in the administration of sildenafil citrate, heparin and several neuropeptides on an animal model where gastric ulcers were induced with acetic acid, and to compare their efficacy. Materials and methods: The animals were divided into 13 groups, with 4 animals in each. Gastric ulcers was induced in the animals of 12 groups with one untreated group being left as the control (Group I - control; given normal saline (NS)). The other groups were: Group II (ulcer + NS); Group III (5 mg/kg sildenafil citrate, low dose); Group IV (10 mg/kg sildenafil citrate, high dose); Group V (0.6 mg/kg heparin, low dose); Group VI (6 mg/kg heparin, high dose); Group VII (20 nmol/kg des-acyl ghrelin); Group VIII (40 nmol/kg des-acyl ghrelin); Group IX (4 nmol/kg acyl ghrelin); Group X (8 nmol/kg acly ghrelin); Group XI (20 pmol/kg Nesfatin-1); Group XII (15 nmol/kg Obestatin) and Group XIII (5 nmol/kg Neuropeptide Y). Gastric neuropeptide expression was measured using an immunohistochemical method, and the amount in circulation was detected using ELISA. To compare with no treatment, the controls and other treatment groups, we recorded loss of the surface epithelium of the stomach, erosion, bleeding and inflammatory cell infiltration in the upper halves of the gastric glands. Key findings: The muscularis and the layers beneath it were, however, apparently normal. The gastric mucosa healed with little or no inflammation when sildenafil citrate, low dose heparin, ghrelin, NUCB2/Nesfatin-1, obestatin, Neuropeptide Y were administered. Significance: Overall the data indicate that low dose heparin, and especially sildenafil citrate and neuropeptides, can be used clinically as an alternative approach in the treatment of the gastric ulcer.