Native Human Fibronectin Protein

Name: Native Human Fibronectin Protein
SKU: DAGC349
Rating: 5 (1 reviews)

Native Human Fibronectin Protein from Human plasma

COA

SDS

Datasheet

Summary

Target

Human Fibronectin

Nature

Native

Tag/Conjugate

Unconjugated

Bio-activity

Corning 24-well plates were coated with fibronectin in PBS (0.3 mL/well) at 37°C overnight. After blocking by BSA, TIG-3 cells (5 × 10^4 cells/1 mL DMEM/well) were added and incubated at 37°C for 90 minutes. Attached cells were counted electronically with a Coulter counter. Under these conditions, the use of a concentration of 6 μg fibronectin per milliliter resulted in the attachment of greater than 70% of the cells.

Alternative Names

fibronectin 1; FN1; FN; fibronectin

Purity

Fibronectin was purified by the method of Ruoslahti et al. using a gelatin affinity column. The purified protein
was sterile filtered (0.2 μm).

Format

Liquid

Buffer

PBS

Preservative

None

Storage

Upon initial thawing, apportion into working aliquots and store at –20°C or below. Avoid repeated
freeze/thaw cycles.

Keywords

fibronectin 1; FN1; FN; fibronectin

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Hepatitis C genotype 4: A report on resistance-associated substitutions in NS3, NS5A, and NS5B genes

REVIEWS IN MEDICAL VIROLOGY

Authors: Fadl, Nahla; Salem, Tamer Z.

Abstract

Author Contribution FN performed the literature review and wrote the manuscript; STZ coauthored, edited, and reviewed the manuscript. Treatment response in Hepatitis C virus (HCV) has generated varied effects in patients. Recently, nonresponsive and relapse patients related to host and genotype variabilities have been reported in clinical trials. However, these trials included minimal sample sizes of patients with genotype 4, the most prevalent genotype in Egypt and the Middle East, compared with genotypes 1 and 2. The genetic variabilities that have been detected within the HCV genes, especially the ones associated with genotype 4, and are linked to treatment response, will be the focus of this review with emphasis on direct acting antiviral agents. In addition, the major studies and clinical trials performed globally and their inclusivity of genotype 4 are reported. This review also delineates future study areas and missing data that need further investigation when it comes to genotype 4.

Silencing PEG3 inhibits renal fibrosis in a rat model of diabetic nephropathy by suppressing the NF-kappa B pathway

MOLECULAR AND CELLULAR ENDOCRINOLOGY

Authors: Guan, Tianjun; Fang, Fan; Su, Xiaoxuan; Lin, Kaiqiang; Gao, Qing

Abstract

As paternally expressed gene 3 (PEG3), which can activate NF-kappa B pathway, plays an important role in the development of renal fibrosis in diabetic nephropathy (DN), the present study aimed to investigate the interaction of PEG3 and the NF-kappa B pathway on renal fibrosis in a DN model. Following the induction of the rat model of DN, a series of experiments were used to measure serum creatinine (Scr), blood urea nitrogen (BUN), urine protein for 24 h (UP24 h), proliferation of renal fibroblasts, positive expression of PEG3, Collagen I and Collagen II protein, the activity of NF-kappa B, collagen fiber expression and the FSP1(+) cell ratio (fibroblast marker, reflecting renal fibrosis). Silencing of PEG3 or inhibition of the NF-kappa B pathway decreased the levels of Scr, BUN, and UP24 h, down-regulated Collagen I protein and up-regulated Collagen II protein. These treatments also downregulated the expression of PEG3, NF-kappa B, Vimentin, alpha-SMA, FN, caspase-3 and FSP1 and the extents of I kappa B alpha, inhibitor of kappa B (I kappa B) kinase beta (IKK beta), and NF-kappa B p65 phosphorylation while that of E-cadherin was up-regulated, and the ratio of FSP1(+) cells was decreased. Taken together, these results showed that silencing of PEG3 inhibited the NF-kappa B pathway, thereby alleviating renal fibrosis in DN, thus presenting PEG3 as a potential therapeutic target in renal fibrosis in DN.