Target Name: OMA1
NCBI ID: G115209
Review Report on OMA1 Target / Biomarker Content of Review Report on OMA1 Target / Biomarker
OMA1
Other Name(s): OMA1 zinc metallopeptidase homolog | ZMPOMA1 | YKR087C | Overlapping with the m-AAA protease 1 homolog | metalloprotease-related protein 1 | 2010001O09Rik | overlapping with the m-AAA protease 1 homolog | Metalloprotease-related protein 1 | peptidase | DAB1 | FLJ33782 | Metalloprotease related protein 1 | overlapping activity with M-AAA protease | MPRP-1 | OMA1 zinc metallopeptidase | zinc metallopeptidase OMA1 | LOC115209 | OMA1 homolog, zinc metallopeptidase | MPRP1 | Metalloendopeptidase OMA1, mitochondrial | OMA1_HUMAN

OMAs: Potential Drug Targets and Diseases

OMA1 (Oz conserved homolog 1) is a zinc metallopeptidase that belongs to serine protease family 18 and is an important intracellular protein. In various cancers, OMAs play key roles in tumor initiation, growth, and metastasis. In addition, OMAs are closely related to diseases such as neurological diseases, liver diseases, and immune system disorders. Therefore, OMAs have become an important class of drug targets and have good research value.

OMAs are proteins composed of a single polypeptide chain with a molecular weight of approximately 40 kDa. They play an important catalytic role in cells and participate in a variety of metabolic processes, including peptide bond hydrolysis, peptide-protein interactions, and phosphorylation. In tumorigenesis, the activation of OMAs is closely related to the growth, invasion and metastasis of tumor cells.

Currently, drug research on OMAs mainly focuses on inhibiting their activity. Many studies have proven that the activation of OMAs is closely related to the progression and invasion of various cancers. For example, patients with OMA-positive tumors have significantly lower survival rates than patients with OMA-negative tumors. In addition, OMAs are also related to the invasion and metastasis capabilities of tumors, so inhibiting the activity of OMAs is considered an effective strategy for treating tumors.

In addition to inhibiting the activity of OMAs, some studies have explored the potential of OMAs as drug targets. These studies indicate that OMAs can be used as drug targets with high stability and expression levels. For example, studies have found that OMAs are up-regulated in a variety of cancer tissues, and their expression levels are positively correlated with tumor invasion and metastasis capabilities. In addition, activation of OMAs can also induce apoptosis of tumor cells, so OMAs are also considered to be molecules with potential therapeutic effects.

In addition, OMAs are also closely related to diseases such as neurological diseases, liver diseases, and immune system disorders. For example, studies have shown that OMAs are associated with neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. In addition, OMAs are closely related to diseases such as liver disease and immune system disorders. Therefore, the research value of OMAs lies not only in their potential as drug targets but also in their association with multiple diseases, providing a new perspective for studying these diseases.

In summary, OMAs, as an important class of proteins, play a key role in tumor occurrence, growth and metastasis. Currently, research on OMAs mainly focuses on inhibiting their activity, but some studies have also explored the potential of OMAs as drug targets. With the deepening of research, OMAs will become an important class of molecules with important research value.

Protein Name: OMA1 Zinc Metallopeptidase

Functions: Metalloprotease that is part of the quality control system in the inner membrane of mitochondria (PubMed:20038677, PubMed:25605331, PubMed:32132706, PubMed:32132707). Activated in response to various mitochondrial stress, leading to the proteolytic cleavage of target proteins, such as OPA1, UQCC3 and DELE1 (PubMed:20038677, PubMed:25275009, PubMed:32132706, PubMed:32132707). Following stress conditions that induce loss of mitochondrial membrane potential, mediates cleavage of OPA1 at S1 position, leading to OPA1 inactivation and negative regulation of mitochondrial fusion (PubMed:20038677, PubMed:25275009). Also acts as a regulator of apoptosis: upon BAK and BAX aggregation, mediates cleavage of OPA1, leading to the remodeling of mitochondrial cristae and allowing the release of cytochrome c from mitochondrial cristae (PubMed:25275009). In depolarized mitochondria, may also act as a backup protease for PINK1 by mediating PINK1 cleavage and promoting its subsequent degradation by the proteasome (PubMed:30733118). May also cleave UQCC3 in response to mitochondrial depolarization (PubMed:25605331). Also acts as an activator of the integrated stress response (ISR): in response to mitochondrial stress, mediates cleavage of DELE1 to generate the processed form of DELE1 (S-DELE1), which translocates to the cytosol and activates EIF2AK1/HRI to trigger the ISR (PubMed:32132706, PubMed:32132707). Its role in mitochondrial quality control is essential for regulating lipid metabolism as well as to maintain body temperature and energy expenditure under cold-stress conditions (By similarity). Binds cardiolipin, possibly regulating its protein turnover (By similarity). Required for the stability of the respiratory supercomplexes (By similarity)

The "OMA1 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 OMA1 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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