TNFRSF1A Protein, Rat (HEK293, Fc)

TNFRSF1A (TNF RI) protein has a high ability to bind with tumor necrosis factor-alpha (TNF-α). TNFRSF1A is a STAT3 target gene that regulates the NF-κB pathway. TNFRSF1A activate NF-κB, mediate apoptosis, and function as a regulator of inflammation. TNFRSF1A Protein, Rat (HEK293, Fc) is expressed by HEK293 and has a transmembrane region (M1-A211) with a Fc tag at the C-terminus^[1].

TNFRSF1A (TNF RI) protein is a single-pass type I membrane protein belonging to the tumor necrosis factor (TNF) family. TNFRSF1A is the major signaling receptor for TNF-α. TNFRSF1A protein is a multifunctional cytokine, which is synthesized by almost all cells^[1][2].
The sequence of amino acids in TNFRSF1A from different species is very different (less than 85% similarity among human, rat and mouse).
TNFRSF1A contains a protein-protein interaction domain, called death domain (DD), can recruit other DD-containing proteins and couples the death receptors to caspase activation and apoptosis. Both soluble and membrane-bound forms of the cytokine can activate TNFRSF1A. TNFRSF1A induces cellular inflammatory damage and apoptosis by participating in mTOR, JNK, IKK, caspase 3, MAPK, and NF-κB pathways^[1][3][4].

Rat

HEK293

C-hFc

P22934 (M1-A211)

25625  [NCBI]

Approximately 59 kDa

Greater than 90% as determined by reducing SDS-PAGE

<1 EU/μg, determined by LAL method.

• [1]. Wajant H, et, al. Tumor necrosis factor signaling. Cell Death Differ. 2003 Jan;10(1):45-65.  [Content Brief]

  [2]. Fu Q, et, al. miR-29a up-regulation in AR42J cells contributes to apoptosis via targeting TNFRSF1A gene. World J Gastroenterol. 2016 May 28;22(20):4881-90.  [Content Brief]

  [3]. Zhou S, et, al. Bioinformatics Analysis Identifies TNFRSF1A as a Biomarker of Liver Injury in Sepsis TNFRSF1A is a Biomarker for Septic Liver Injury. Genet Res (Camb). 2022 Oct 15;2022:1493744.  [Content Brief]

  [4]. Egusquiaguirre SP, et, al. The STAT3 Target Gene TNFRSF1A Modulates the NF-κB Pathway in Breast Cancer Cells. Neoplasia. 2018 May;20(5):489-498.  [Content Brief]