Human IFNG peptide

Name: Human IFNG peptide
SKU: DAG326
Rating: 5 (1 reviews)

Recombinant Human IFNG peptide

COA

SDS

Datasheet

Summary

Product Overview

RecombinantHuman Interferon-gamma is a single, non-glycosylated, polypeptide chaincontaining 144 amino acids and having a molecular mass of 16,879 Dalton. Thesequence of the first five N-terminal amino acids was determined and wasfound to be Met-Gln-Asp-P

Nature

Recombinant

Tag/Conjugate

Unconjugated

Alternative Names

IFG; IFI

Format

Purified, Lyophilized; Reconstitute using sterile deionizedwater to a concentration of 100μg/ml.Further dilutions can be made in other aqueou buffers.

Concentration

1 mg/ml (prior to lyophilization) (OD280nm, E0.1% =0.64)

Buffer

Lyophilized from 10mM Sodium phosphate buffer, pH 7.4 + 0.1

Preservative

None

Storage

2-8°C short term, -20°C long term

Introduction

Produced by lymphocytes activated by specific antigens or mitogens. IFN-gamma, in addition to having antiviral activity, has important immunoregulatory functions. It is a potent activator of macrophages, it has antiproliferative effects on transformed cells and it can potentiate the antiviral and antitumor effects of the type I interferons.

Entrez Gene ID

3458

Antigen Description

Interferon-gamma (IFN-γ) is adimerized soluble cytokine that is the only member of the type II class ofinterferons. This interferon was originally called macrophage-activatingfactor, a term now used to describe a larger family of proteins to whichIFN-γ belongs. In humans, the IFN-γ protein is encoded by the IFNG gene.

Keywords

IFG; IFI; IFNG; IFN Gamma; IFN Immune; IFN-gamma; Immune Interferon; Interferon gamma; Interferon Gamma Precursor; Macrophage Activating Factor; MAF; T Cell Interferon; Type II Interferon

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Caffeine inhibits STAT1 signaling and downregulates inflammatory pathways involved in autoimmunity

CLINICAL IMMUNOLOGY

Authors: Iris, Merve; Tsou, Pei-Suen; Sawalha, Amr H.

Abstract

Caffeine is a widely consumed pharmacologically active product. We focused on characterizing immunomodulatory effects of caffeine on peripheral blood mononuclear cells. Caffeine at high doses showed a robust downregulatory effect on cytokine activity and genes related to several autoimmune diseases including lupus and rheumatoid arthritis. Dose-dependent validation experiments showed downregulation at the mRNA levels of key inflammation-related genes including STAT1, TNF, IFNG, and PPARG. TNF and PPARG were suppressed even with the lowest caffeine dose tested, which corresponds to the serum concentration of caffeine after administration of one cup of coffee. Cytokine levels of IL-8, MIP-1 beta, IL-6, IFN-gamma, GM-CSF, TNF, IL-2, IL-4, MCP-1, and IL-10 were decreased significantly with caffeine treatment. Upstream regulator analysis suggests that caffeine inhibits STAT1 signaling, which was confirmed by showing reduced phosphorylated STAT1 after caffeine treatment. Further studies exploring disease-modulating potential of caffeine in autoimmune diseases and further exploring the mechanisms involved are warranted.

Association of IFNG gene polymorphisms with pulmonary tuberculosis but not with spinal tuberculosis in a Chinese Han population

MICROBIAL PATHOGENESIS

Authors: Li, Jiong; Zhou, Ying; Zhang, Hongqi; He, Dan; Zhang, Rongmou; Li, Yanbing; Guo, Chaofeng; Guo, Qiang; Wang, Longjie; Yang, Guanteng; Gao, Qile

Abstract

Spinal tuberculosis (STB) is an extrapulmonary form of tuberculosis (TB) caused by Mycobacterium tuberculosis (Mtb), which accounts for around 2% of all TB cases and can lead to spine degeneration. It is widely accepted that host genetic factors participate in the pathogenesis of active TB, but the factors controlling which TB form will manifest after Mtb infection remain unknown. We hypothesized that a genetic difference may exist between the development of STB and pulmonary tuberculosis (PTB). Here, three single nucleotide polymorphisms (SNPs) in the IFNG gene (rs2069718), IRGM gene (rs10065172), and MBL2 gene (rs11003125) were genotyped among 183 PTB patients, 177 STB patients, and 360 healthy controls from the Chinese Han population. We found that rs2069718 genotypes were significantly associated with PTB (TT, p = 0.007; CT, p = 0.008) but not STB, and the TT genotype (p = 0.046) of rs2069718 were less common in PTB than in STB. In contrast, neither PTB nor STB were found to be associated with rs10065172 and rs11003125. Overall, we found a difference in the rs2069718 genetic distribution between the STB and PTB patients in a Chinese Han population. The rs2069718 TT genotype was associated with a protective role in PTB but not STB development during active Mtb infection. (C) 2017 Published by Elsevier Ltd.