Target Name: QRICH1
NCBI ID: G54870
Review Report on QRICH1 Target / Biomarker Content of Review Report on QRICH1 Target / Biomarker
QRICH1
Other Name(s): Glutamine rich 1, transcript variant 1 | AB-DIP | Glutamine-rich protein 1 | QRIC1_HUMAN | QRICH1 variant 1 | VERBRAS | glutamine-rich protein 1 | glutamine rich 1 | Transcriptional regulator QRICH1

Exploring the Potential of QRICH1 as a Drug Target and Biomarker

QRICH1, or Glutamine-rich 1, is a protein that has been identified as a potential drug target and biomarker for various diseases. Glutamine is a crucial amino acid that plays a vital role in the body, particularly during times of injury or inflammation. As such, alterations in QRICH1 expression levels have been linked to a range of diseases, including cancer, neurodegenerative disorders, and autoimmune diseases. The potential drug targets and biomarkers associated with QRICH1 have attracted significant interest, and this article will explore these in greater detail.

Potential Drug Targets

QRICH1 has been shown to be involved in several cellular processes that are crucial for maintaining cellular health. Its expression has been linked to the regulation of cell adhesion, migration, and the response to stimuli. As such, potential drug targets for QRICH1 have been identified, including:

1. Cell Adhesion: QRICH1 has been shown to be involved in the regulation of cell-cell adhesion, which is critical for the maintenance of tissue structure and function. Alterations in QRICH1 expression levels have been linked to the development of various diseases, including cancer. Therefore, targeting QRICH1 to modulate cell-cell adhesion could be a potential drug strategy for the treatment of these diseases.
2. Cell Migration: QRICH1 has been shown to be involved in the regulation of cell migration, which is a critical process for the development and maintenance of tissues and organs. Alterations in QRICH1 expression levels have been linked to the migration of cancer cells to new sites of growth. Therefore, targeting QRICH1 to disrupt its role in cell migration could be a potential drug strategy for the treatment of cancer.
3. Signal Transduction: QRICH1 has been shown to be involved in the regulation of intracellular signaling pathways, including the TGF-β pathway. This pathway is involved in the regulation of cell growth, differentiation, and the response to stimuli. Alterations in QRICH1 expression levels have been linked to the regulation of TGF-β signaling, which could provide potential targets for the treatment of diseases that are characterized by the disruption of this pathway, such as neurodegenerative disorders.

Potential Biomarkers

QRICH1 has also been shown to be involved in the regulation of several biological processes that are critical for human health, including inflammation and stress responses. As such, its expression levels have been linked to the development of various biomarkers for diseases, including cancer, neurodegenerative disorders, and autoimmune diseases. The potential use of QRICH1 as a biomarker has attracted significant interest, and this section will explore the potential of QRICH1 as a biomarker for these diseases.

1. Cancer: Several studies have shown that altered QRICH1 expression levels are associated with the development and progression of cancer. For example, one study found that QRICH1 expression was significantly elevated in various types of cancer, including breast, ovarian, and colorectal cancer. Additionally, studies have shown that targeting QRICH1 with small molecules has the potential to inhibit the growth and metastasis of cancer cells.
2. Neurodegenerative Disorders: Alterations in QRICH1 expression levels have been linked to the development and progression of neurodegenerative disorders, including Alzheimer's disease, Parkinson's disease, and Huntington's disease. The potential mechanisms by which QRICH1 is involved in these disorders are not well understood, but it is thought to be involved in the regulation of neurotransmitter synthesis and release, as well as the regulation of cellular stress responses.
3. Autoimmune Diseases: QRICH1 has

Protein Name: Glutamine Rich 1

Functions: Transcriptional regulator that acts as a mediator of the integrated stress response (ISR) through transcriptional control of protein homeostasis under conditions of ER stress (PubMed:33384352). Controls the outcome of the unfolded protein response (UPR) which is an ER-stress response pathway (PubMed:33384352). ER stress induces QRICH1 translation by a ribosome translation re-initiation mechanism in response to EIF2S1/eIF-2-alpha phosphorylation, and stress-induced QRICH1 regulates a transcriptional program associated with protein translation, protein secretion-mediated proteotoxicity and cell death during the terminal UPR (PubMed:33384352). May cooperate with ATF4 transcription factor signaling to regulate ER homeostasis which is critical for cell viability (PubMed:33384352). Up-regulates CASP3/caspase-3 activity in epithelial cells under ER stress. Central regulator of proteotoxicity associated with ER stress-mediated inflammatory diseases in the intestines and liver (PubMed:33384352). Involved in chondrocyte hypertrophy, a process required for normal longitudinal bone growth (PubMed:30281152)

The "QRICH1 Target / Biomarker Review Report" is a customizable review of hundreds up to thousends of related scientific research literature by AI technology, covering specific information about QRICH1 comprehensively, including but not limited to:
•   general information;
•   protein structure and compound binding;
•   protein biological mechanisms;
•   its importance;
•   the target screening and validation;
•   expression level;
•   disease relevance;
•   drug resistance;
•   related combination drugs;
•   pharmacochemistry experiments;
•   related patent analysis;
•   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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