Anti-GBM IgG ELISA Kit

Name: Anti-GBM IgG ELISA Kit
SKU: DEIA6109
Rating: 5 (1 reviews)

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

COA

SDS

Datasheet

Summary

Sample

Serum, plasma

Species Reactivity

Human

Detection Method

Indirect-ELISA

Intended Use

Anti-GBM is an indirect solid phase enzyme immunoassay (ELISA) for the quantitative measurement of IgG class autoantibodies to glomerular basement membrane (GBM) in human serum or plasma.

Contents of Kit

No.	Components	Size	Storage Conditions
1	Divisible microplate	12 × 8	2-8°C
2	Anti-GBM calibrators (A-E)	1.5 ml × 5	2-8°C
3	Anti-GBM controls	1.5 ml × 2	2-8°C
4	Sample buffer	50 ml × 2	2-8°C
5	Enzyme conjugate solution	12 ml × 1	2-8°C
6	TMB substrate solution	12 ml × 1	2-8°C
7	Stop solution	12 ml × 1	2-8°C
8	Wash solution, concentrate (20×)	50 ml × 1	2-8°C

Storage

1. Store the kit at 2-8 °C.
2. Keep microplate wells sealed in a dry bag with desiccants.
3. The reagents are stable until expiration of the kit.
4. Do not expose test reagents to heat, sun or strong light during storage and usage.

Sensitivity

The lower detection limit for Anti-GBM has been determined at 1.0 U/ml.

General Description

The glomerular basement membrane (GBM) of the kidney is the basal lamina layer of the glomerulus. The Glomerular capillary endothelial cells, the GBM and the filtration slits between the podocytes perform the filtration function of the glomerulus, separating the blood in the capillaries from the filtrate that forms in Bowman's capsule. The GBM is a fusion of the endothelial cell and podocyte basal laminas.
Primarily, Goodpasture syndrome is an autoimmune disorder of the kidneys. Ernest Goodpasture, an American pathologist was the first in 1919 who described the coexistence of a fatal lung hemorrhage coming along with proliferative glomerulonephritis in a young man. The syndrome is now considered as an autoimmune disorder consisting of the triad of glomerulonephritis, lung hemorrhage and anti-glomerular basement antibodies formation.
The incidence of the Goodpasture syndrome is about 0.5 to 1 cases per million inhabitants per year. Patients in the third and seventh decade are mainly affected. Goodpasture syndrome is a medical emergency with a case fatality rate of 75 to 90 % due to kidney and respiratory insufficiency, if not treated. Histological, the disorder is characterized by continuous linear deposition of immunoglobulins along the glomerular basement membrane (GBM), demonstrable by direct immunofluorescence on kidney biopsies. Nowadays, the determination of circulating autoantibodies against the C-terminal end of the α-3 chain of type IV collagen is considered the diagnostic criterion.
Basement membranes form an anatomical barrier wherever epithelia meet connective tissue. Type IV collagen that is only found in GBM forms a matrix in which additional molecules (e.g. Laminin, Entactin) are integrated. Three out of six alpha-chains (polypeptides with more than 1,650 amino acids) form a triple helix and characterize the structural subunits of type IV collagen. All C-terminal ends of the alpha-chains form a globular domain that can be dissolved from the triple helix by treatment with bacterial collagenase.
The reactivity of Goodpasture specific anti-GBM autoantibodies is directed against the 29 kDa NC1 domain of the alpha-3 chain of type IV collagen of GBM. After the target antigen has been entirely characterized nowadays the triad of glomerulonephritis, lung hemorrhage and the antibodies against the alpha-3 chain of type IV collagen of GBM are the essential elements of diagnosis of Goodpasture syndrome. ELISA test systems provided with the corresponding pure antigen exhibit sensitivities and specificities of about 98 to 99%.

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Documents

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QA & Reviews

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References

Lactobacillus pentosus strain S-PT84 improves steatohepatitis by maintaining gut permeability

JOURNAL OF ENDOCRINOLOGY

Authors: Sakai, Yuriko; Arie, Hideyuki; Ni, Yinhua; Zhuge, Fen; Xu, Liang; Chen, Guanliang; Nagata, Naoto; Suzuki, Takuya; Kaneko, Shuichi; Ota, Tsuguhito; Nagashimada, Mayumi

Abstract

Intestinal mucosal barrier dysfunction is closely related to the pathogenesis of nonalcoholic steatohepatitis (NASH). Gut immunity has been recently demonstrated to regulate gut barrier function. The Lactobacillus pentosus strain S-PT84 activates helper T cells and natural killer/natural killer T cells. In this study, we examined the effect of S-PT84 on NASH progression induced by high-cholesterol/high-fat diet (CL), focusing on the immune responses involved in gut barrier function. C57BL/6 mice were fed a normal chow or CL diet with or without 1 x 10(10) S-PT84 for 22 weeks. S-PT84 administration improved hepatic steatosis by decreasing triglyceride and free fatty acid levels by 34% and 37%, respectively. Furthermore, S-PT84 inhibited the development of hepatic inflammation and fibrosis, suppressed F4/80(+) macrophage/Kupffer cell infiltration, and reduced liver hydroxyproline content. Administration of S-PT84 alleviated hyperinsulinemia and enhanced hepatic insulin signalling. Compared with mice fed CL diet, mice fed CL+S-PT84 had 71% more CD11c(-)CD206(+) M2 macrophages, resulting in a significantly decreased M1/M2 macrophage ratio in the liver. Moreover, S-PT84 inhibited the CL diet-mediated increase in intestinal permeability. Additionally, S-PT84 reduced the recruitment of interleukin-17-producing T cells and increased the levels of intestinal tight junction proteins, including zonula occludens-1, occludin, claudin-3, and claudin-7. In conclusion, our findings suggest that S-PT84 attenuates diet-induced insulin resistance and subsequent NASH development by maintaining gut permeability. Thus, S-PT84 represents a feasible approach to prevent the development of NASH.

Three-gene risk model in papillary renal cell carcinoma: a robust likelihood-based survival analysis

AGING-US

Authors: Wang, Yutao; Yan, Kexin; Lin, Jiaxing; Wang, Jianfeng; Zheng, Zhenhua; Li, Xinxin; Hua, Zhixiong; Bu, Yuepeng; Shi, Jianxiu; Sun, Siqing; Li, Xuejie; Liu, Yang; Bi, Jianbin

Abstract

Background: Papillary renal cell carcinoma (PRCC) accounts for 15% of all renal cell carcinomas. The molecular mechanisms of renal papillary cell carcinoma remain unclear, and treatments for advanced disease are limited. Result: We built the computing model as follows: Risk score = 1.806 * TPX2 -0.355 * TXNRD2 -0.805 * SLC6A20. The 3-year AUC of overall survival was 0.917 in the training set (147 PRCC samples) and 0.760 in the test set (142 PRCC samples). Based on the robust model, M2 macrophages showed positive correlation with risk score, while M1 macrophages were the opposite. PRCC patients with low risk score showed higher tumor mutation burden. TPX2 is a risk factor, and co-expression factors were enriched in cell proliferation and cancer-related pathways. Finally, the proliferation and invasion of PRCC cell line were decreased in the TPX2 reduced group, and the differential expression was identified. TPX2 is a potential risk biomarker which involved in cell proliferation in PRCC. Conclusion: We conducted a study to develop a three gene model for predicting prognosis in patients with papillary renal cell carcinoma. Our findings may provide candidate biomarkers for prognosis that have important implications for understanding the therapeutic targets of papillary renal cell carcinoma. Method: Gene expression matrix and clinical data were obtained from TCGA (The Cancer Genome Atlas), GSE26574, GSE2048, and GSE7023. Prognostic factors were identified using "survival" and "rbsurv" packages, and a risk score was constructed using Multivariate Cox regression analysis. The co-expression networks of the factors in model were constructed using the "WGCNA" package. The co-expression genes of factors were enriched and displayed the biological process. Based on this robust risk model, immune cells infiltration proportions and tumor mutation burdens were compared between risk groups. Subsequently, using the PRCC cell line, the role of TPX2 was determined by Cell proliferation assay, 5-Ethynyl-20deoxyuridine assay and Transwell assay.