Human Tumor Necrosis Factor alpha (aa 158)

Name: Human Tumor Necrosis Factor alpha (aa 158)
SKU: DAG330
Rating: 5 (1 reviews)

Human Tumor Necrosis Factor alpha (aa 158), recombinant protein from E. coli

COA

SDS

Datasheet

Summary

Product Overview

Recombinant Human Tumor Necrosis Factor alpha is a single, non-glycosylated, polypeptide chain containing 158 amino acids (157 a.a. of the mature human TNF-alpha and an N-terminal methionine) and having a molecular weight of 17.5 kDa.

Nature

Recombinant

Tag/Conjugate

Unconjugated

Purity

> 95% pure (RP-HPLC and SDS-PAGE). Purified by chromatographic techniques. Product is sterile filtered.

Format

Purified, LyophilizedReconstitute using sterile deionized water to a concentration ≥ 100 μg/mL. Further dilutions can be made in other aqueou buffers.

Concentration

1 mg/ml (OD280nm, E0.1% = 1.234) (prior to lyophilization).

Preservative

None

Storage

2-8°C short term, -20°C long term

Introduction

This gene encodes a multifunctional proinflammatory cytokine that belongs to the tumor necrosis factor (TNF) superfamily. This cytokine is mainly secreted by macrophages. It can bind to, and thus functions through its receptors TNFRSF1A/TNFR1 and TNFRSF1B/TNFBR. This cytokine is involved in the regulation of a wide spectrum of biological processes including cell proliferation, differentiation, apoptosis, lipid metabolism, and coagulation. This cytokine has been implicated in a variety of diseases, including autoimmune diseases, insulin resistance, and cancer. Knockout studies in mice also suggested the neuroprotective function of this cytokine.

Antigen Description

Keywords

TNF; tumor necrosis factor; DIF; TNFA; TNFSF2; TNF-alpha; tumor necrosis factor (TNF superfamily, member 2); superfamily, member 2; Tumor necrosis factor; Cachectin; TNF-alpha; Tumor necrosis factor ligand superfamily member 2; TNF-a; Tumor necrosis facto

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Documents

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References

Hypoxia in utero increases the risk of pulmonary hypertension in rat offspring and is associated with vasopressin type-2 receptor upregulation

MOLECULAR MEDICINE REPORTS

Authors: Ding, Hao; Luo, Yuchuan; Hu, Ke; Huang, Huaying; Liu, Pei; Xiong, Mengqing; Zhu, Li; Yi, Jing; Xu, Ying

Abstract

Pulmonary hypertension (PH) in newborns and adults is a disease that can lead to right heart failure and result in a shorter lifespan. PH was induced by maintaining pregnant rats in a hypoxic chamber for 4 h twice a day, from days 7-21 of pregnancy. Hypoxia was confirmed by a decrease in the partial pressure of oxygen (PaO2) and the oxygen saturation (SaO(2)) of arterial blood in the aorta. The body weight of newborns from hypoxic rats was similar to 20% decreased compared with the control newborns of normoxic rats. The vascular wall thickness/vascular diameter values of hypoxia treated pubs were increased compared with that of control newborns 7 days after birth; however, it decreased to similar levels than in the control group after 3 months, and then further decreased to significantly lower levels than in the control group at 6 months after birth. At birth, the lung tissues of newborns from hypoxic rats exhibited an increase in the levels of mRNA and proteins associated with PH such as HIF-1 alpha, HIF-2 alpha, V2R, TGF-beta, TNF-alpha, Ang-2 and alpha-SMA. At 3 and 6 months after birth, the levels of both V2R mRNA and protein in offspring from hypoxic rats were at least 2-fold higher, whereas the expression of all other factors decreased compared with the control offspring. By contrast, HIF-2 alpha and Ang-2 expression levels were significantly increased in the 6-month-old control offspring from normoxic rats. V2R overexpression in pups induced by hypoxia in maternal rats was sustained until their adulthood. V2R may be a marker for detecting PH.

The sustained release of dexamethasone from TiO2 nanotubes reinforced by chitosan to enhance osteoblast function and anti-inflammation activity

MATERIALS SCIENCE & ENGINEERING C-MATERIALS FOR BIOLOGICAL APPLICATIONS

Authors: Shen, Ke; Tang, Qiang; Fang, Xingtang; Zhang, Chunlei; Zhu, Zhaojing; Hou, Yanhua; Lai, Min

Abstract

Controlling macrophage response to biomaterials is critical for the reduction of inflammation after implantation. Here we designed a sustained release system from TiO2 nanotubes (TNTs) to improve osteogenesis on titanium implants with anti-inflammatory properties. TNTs (around 70 nm diameter) were first fabricated on titanium surfaces by anodization, directly filled with the anti-inflammatory drug, dexamethasone (DEX) and then covered by chitosan (CHI) multilayer films. Primary osteoblast and macrophage (RAW 264.7) cells were cultured on untreated and treated titanium surfaces in vitro. Osteoblasts grown on CHI-coated Dex-filled TNTs surfaces displayed higher alkaline phosphatase (ALP) and mineralization, which was consistent with qRT-PCR analysis of osteoblastic genes including collagen type I (Col I), osteocalcin (OCN), osteopontin (OPN) and runt related transcription factor 2 (Runx2). In contrast, protein levels of nitric oxide (NO) and proinflammatory cytokines (TNF-alpha and IL-1 beta) from macrophages on Dex-filled TNTs, CHI-coated TNTs and CHI-coated Dex-filled TNTs were significantly lower, especially on CHI-coated Dex-filled TNTs surfaces compared to levels on titanium and TNTs. These results indicate that CHI-coated Dex-filled TNTs enhanced osteoblast differentiation and decreased the inflammatory response of macrophages. The approach presented here provides new insight into the modification of TNTs for the development of titanium-based implants.