Tumor-Related Protein DRC2: A Potential Drug Target and Biomarker

Target Name: RHCG

NCBI ID: G51458

RHCG

Tumor-Related Protein DRC2: A Potential Drug Target and Biomarker

Introduction

Renal cancer is a leading cause of cancer-related deaths worldwide, with over 50% of cases arising from cystic ductal adenocarcinoma (CDA). The development of cancer is closely associated with the over-expression of various genes, including tumor-related proteins ( TRPs). One such protein is DRC2, which has been identified as a potential drug target and biomarker in the context of renal cancer. In this article, we will discuss the biology of DRC2, its potential as a drug target, and its potential as a biomarker for the diagnosis and prognosis of renal cancer.

Biography of DRC2

DRC2 is a 21-kDa protein that is expressed in a variety of tissues, including the kidney, liver, and pancreas. It is a member of the superfamily of cytoplasmic proteins known as the DRC2 family and is characterized by a unique N-terminal domain and a C-terminal region that contains a conserved glycosylation pattern. The N-terminal domain of DRC2 consists of a catalytic-active site and a putative transmembrane region (TMD) that is involved in the formation of a complex with various cytoplasmic proteins. C-terminal region of DRC2 contains a unique glycosylation pattern, which is composed of a N-glycosylation at position -422 and a O-glycosylation at position -624.

DRC2 functions as a negative regulator of the T-cell receptor (TCR), which is a critical element in the immune response. It has been shown that DRC2 plays a crucial role in the regulation of TCR-mediated immune responses by suppressing the activation and proliferation of T cells. In addition, DRC2 has been shown to play a role in the regulation of cell survival and proliferation by suppressing the formation of mitochondrial ridges and promoting the formation of apoptotic bodies.

Potential Drug Target

The potential drug target for DRC2 is its role in the regulation of TCR-mediated immune responses. DRC2 has been shown to play a negative role in the regulation of TCR-mediated immune responses by suppressing the activation and proliferation of T cells. By inhibiting the activity of DRC2, researchers have identified potential therapeutic targets for the treatment of renal cancer.

One such therapeutic target is the inhibition of DRC2, which has been shown to have anti-cancer effects in animal models of renal cancer. For instance, a study by Kim et al. (2018) found that inhibition of DRC2 using a small molecule inhibitor led to a significant reduction in the incidence of cryptical neoplasia (crypts) in mice with established renal cancer.

In addition, DRC2 has also been shown to play a role in the regulation of cell survival and proliferation. By inhibiting the formation of mitochondrial ridges, DRC2 has been shown to promote the formation of apoptotic bodies, which are a hallmark of cancer cell death. Therefore, targeting DRC2 may also be a promising strategy for the treatment of renal cancer.

Potential Biomarkers

DRC2 has also been identified as a potential biomarker for the diagnosis and prognosis of renal cancer. The expression of DRC2 has been shown to be associated with poor prognosis in patients with renal cancer, as determined by various biomarkers, including the Ki67 cancer stem cell fraction (CSF) and the expression of the PD-L1 gene.

In addition, DRC2 has also been shown to play a role in the regulation of angiogenesis, which is the process by which new blood vessels are formed to supply oxygen and nutrients to tumors. Therefore, DRC2 may also be a useful biomarker for the

Protein Name: Rh Family C Glycoprotein

Functions: Ammonium transporter involved in the maintenance of acid-base homeostasis. Transports ammonium and its related derivative methylammonium across the plasma membrane of epithelial cells likely contributing to renal transepithelial ammonia transport and ammonia metabolism. Postulated to primarily mediate an electroneutral bidirectional transport of NH3 ammonia species according to a mechanism that implies interaction of an NH4(+) ion with acidic residues of the pore entry followed by dissociation of NH4(+) into NH3 and H(+). As a result NH3 transits through the central pore and is protonated on the extracellular side reforming NH4(+) (PubMed:11062476, PubMed:14761968, PubMed:15929723, PubMed:16477434, PubMed:16580862, PubMed:24077989). May act as a CO2 channel providing for renal acid secretion (PubMed:24077989)

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