KLRC1: A Potential Drug Target and Biomarker for Glycobiology

Target Name: KLRC1

NCBI ID: G3821

KLRC1

KLRC1: A Potential Drug Target and Biomarker for Glycobiology

Introduction

Glycobiology is a rapidly evolving field that has seen the emerge of many promising biomarkers and drug targets. One such protein that has garnered significant interest in recent years is KLRC1 (NKG2-A/NKG2-B type II integral membrane protein).. KLRC1 is a transmembrane protein that plays a critical role in various cellular processes, including cell signaling, intracellular transport, and the regulation of cell adhesion. Its unique structure and function have made it an attractive target for drug development, with several studies suggesting that KLRC1 may have a role in various diseases, including cancer, neurodegenerative diseases, and developmental disorders. In this article, we will explore the biology and potential drug targets of KLRC1, with a focus on its role in the context of disease.

Structure and Function of KLRC1

KLRC1 is a type II integral membrane protein that was identified as a potential drug target in several studies. It is composed of 114 amino acid residues and has a calculated molecular weight of 17.4 kDa. KLRC1 is primarily expressed in the brain and has been shown to localize to the endoplasmic reticulum (ER) and the transmembrane space..

KLRC1 functions as an intracellular protein that plays a critical role in the regulation of cell adhesion, as well as the transport of various molecules across the cell membrane. It is involved in several cellular processes, including the regulation of neurotransmitter release, the maintenance of cell adhesion, and the regulation of cell signaling pathways..

KLRC1 and Disease

KLRC1 has been shown to be involved in several diseases and disorders, including cancer, neurodegenerative diseases, and developmental disorders. Its involvement in cancer has led to the hypothesis that KLRC1 may be a useful target for cancer therapy. Several studies have shown that KLRC1 is overexpressed in various types of cancer, including breast, ovarian, and colorectal cancer. This overexpression is associated with poor prognosis and increased cancer cell density.

In addition to its involvement in cancer, KLRC1 has also been implicated in several neurodegenerative diseases, including Alzheimer's disease and Parkinson's disease. Its presence in these diseases has led to the hypothesis that KLRC1 may be a potential target for neurodegenerative therapies.

KLRC1 has also been shown to be involved in the regulation of various signaling pathways, including the TGF-β pathway. This pathway is involved in the regulation of cell growth, differentiation, and survival, and is a key factor in the development and progression of many diseases, including cancer.

Drug Targets for KLRC1

Several studies have suggested that KLRC1 may be a potential drug target for a variety of diseases. Its involvement in cancer, neurodegenerative diseases, and TGF-β signaling pathway make it an attractive target for several classes of drugs, including anti-cancer drugs, neurodegenerative drugs, and TGF-β inhibitors.

One class of drugs that have been shown to inhibit KLRC1 function is the small molecule inhibitors of the NEDD8-activating enzyme, NAD+-dependent pedestrian (NAD+-P) domain. These drugs, such as ML-801 and MK-8628, have been shown to inhibit KLRC1 function and decrease its expression in cancer cells.

Another class of drugs that have been shown to target KLRC1 is the protein kinase CK5/6 inhibitors. These drugs, such as UB-9, have been shown to inhibit the

Protein Name: Killer Cell Lectin Like Receptor C1

Functions: Immune inhibitory receptor involved in self-nonself discrimination. In complex with KLRD1 on cytotoxic and regulatory lymphocyte subsets, recognizes non-classical major histocompatibility (MHC) class Ib molecule HLA-E loaded with self-peptides derived from the signal sequence of classical MHC class Ia molecules. Enables cytotoxic cells to monitor the expression of MHC class I molecules in healthy cells and to tolerate self (PubMed:9486650, PubMed:18083576, PubMed:9430220). Upon HLA-E-peptide binding, transmits intracellular signals through two immunoreceptor tyrosine-based inhibition motifs (ITIMs) by recruiting INPP5D/SHP-1 and INPPL1/SHP-2 tyrosine phosphatases to ITIMs, and ultimately opposing signals transmitted by activating receptors through dephosphorylation of proximal signaling molecules (PubMed:9485206, PubMed:12165520). Key inhibitory receptor on natural killer (NK) cells that regulates their activation and effector functions (PubMed:9486650, PubMed:9430220, PubMed:9485206, PubMed:30860984). Dominantly counteracts T cell receptor signaling on a subset of memory/effector CD8-positive T cells as part of an antigen-driven response to avoid autoimmunity (PubMed:12387742). On intraepithelial CD8-positive gamma-delta regulatory T cells triggers TGFB1 secretion, which in turn limits the cytotoxic programming of intraepithelial CD8-positive alpha-beta T cells, distinguishing harmless from pathogenic antigens (PubMed:18064301). In HLA-E-rich tumor microenvironment, acts as an immune inhibitory checkpoint and may contribute to progressive loss of effector functions of NK cells and tumor-specific T cells, a state known as cell exhaustion (PubMed:30503213, PubMed:30860984)

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•   general information;
•   protein structure and compound binding;
•   protein biological mechanisms;
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•   the target screening and validation;
•   expression level;
•   disease relevance;
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•   related combination drugs;
•   pharmacochemistry experiments;
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•   advantages and risks of development, etc.
The report is helpful for project application, drug molecule design, research progress updates, publication of research papers, patent applications, etc. If you are interested to get a full version of this report, please feel free to contact us at BD@silexon.ai

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