CTSG: A Protein Involved in Fetal Development and Immune System

Target Name: CTSG

NCBI ID: G1511

CTSG

CTSG: A Protein Involved in Fetal Development and Immune System

CTSG, or Cathepsin G, is a protein that is expressed in a variety of tissues throughout the body. It is a member of the cathepsin family, which is a group of proteins that are involved in the processing of extracellular matrix (ECM) components. CTSG is unique among the cathepsins in that it is primarily expressed in the placenta, and it is involved in the formation of the ECM during fetal development.

The placenta plays a critical role in fetal development and growth, and it is responsible for providing the growing fetus with the necessary nutrients and oxygen. During pregnancy, the placenta is also responsible for removing waste products and other harmful substances from the body. CTSG is involved in both of these processes, as it helps to break down and remove ECM components that are no longer needed.

In addition to its role in the placenta, CTSG is also expressed in other tissues throughout the body. It is found in the liver, kidneys, heart, and lungs, among other organs. It is also involved in the immune system, as it has been shown to play a role in the regulation of inflammation.

Despite its involvement in a wide range of physiological processes, CTSG is not well understood. little is known about the specific functions of this protein, and there are few studies that have focused on its role in these processes.

One of the main challenges in studying CTSG is its high level of expression. It is expressed in many different tissues throughout the body, which makes it difficult to isolate and study it in a controlled manner. Additionally, CTSG is a large protein, which makes it difficult to study its function and interactions with other proteins.

However, research into CTSG is ongoing. Some studies have shown that CTSG is involved in the regulation of inflammation, specifically in the regulation of immune cell function. For example, one study published in the journal Diabetes showed that CTSG levels were decreased in individuals with type 2 diabetes, and that this decrease was associated with an increase in the levels of pro-inflammatory cytokines in the body.

Another study published in the journal Oncology found that CTSG was expressed in human cancer cells, and that this expression was associated with the development of cancer. This suggests that CTSG may be a potential biomarker for cancer, and that it may be worth further study as a drug target.

In addition to its potential role in cancer, CTSG is also being studied for its potential use as a drug target. One of the main reasons for this is its involvement in the regulation of inflammation. As mentioned earlier, CTSG has been shown to play a role in the regulation of immune cell function, which makes it a potential target for drugs that are used to treat inflammatory disorders.

Another potential mechanism by which CTSG may be used as a drug target is its role in the regulation of cell death. CTSG has been shown to play a role in the regulation of cell death, which makes it a potential target for drugs that are used to prevent or treat cell death.

Overall, CTSG is a protein that is involved in a wide range of physiological processes throughout the body. While more research is needed to fully understand its role in these processes, its potential as a drug target makes it worth further study. As the research continues, it is likely that we will learn more about the functions of CTSG and its potential as a treatment for a wide range of diseases.

Protein Name: Cathepsin G

Functions: Serine protease with trypsin- and chymotrypsin-like specificity (PubMed:8194606, PubMed:29652924). Also displays antibacterial activity against Gram-negative and Gram-positive bacteria independent of its protease activity (PubMed:2116408, PubMed:2117044). Prefers Phe and Tyr residues in the P1 position of substrates but also cleaves efficiently after Trp and Leu (PubMed:29652924). Shows a preference for negatively charged amino acids in the P2' position and for aliphatic amino acids both upstream and downstream of the cleavage site (PubMed:29652924). Required for recruitment and activation of platelets which is mediated by the F2RL3/PAR4 platelet receptor (PubMed:3390156, PubMed:10702240). Binds reversibly to and stimulates B cells and CD4(+) and CD8(+) T cells (PubMed:7842483, PubMed:9000539). Also binds reversibly to natural killer (NK) cells and enhances NK cell cytotoxicity through its protease activity (PubMed:9000539, PubMed:9536127). Cleaves complement C3 (PubMed:1861080). Cleaves vimentin (By similarity). Cleaves thrombin receptor F2R/PAR1 and acts as either an agonist or an inhibitor, depending on the F2R cleavage site (PubMed:10702240, PubMed:7744748). Cleavage of F2R at '41-Arg-|-Ser-42' results in receptor activation while cleavage at '55-Phe-|-Trp-56' results in inhibition of receptor activation (PubMed:7744748). Cleaves the synovial mucin-type protein PRG4/lubricin (PubMed:32144329). Cleaves and activates IL36G which promotes expression of chemokines CXCL1 and CXLC8 in keratinocytes (PubMed:30804664). Cleaves IL33 into mature forms which have greater activity than the unprocessed form (PubMed:22307629). Cleaves coagulation factor F8 to produce a partially activated form (PubMed:18217133). Also cleaves and activates coagulation factor F10 (PubMed:8920993). Cleaves leukocyte cell surface protein SPN/CD43 to releases its extracellular domain and trigger its intramembrane proteolysis by gamma-secretase, releasing the CD43 cytoplasmic tail chain (CD43-ct) which translocates to the nucleus (PubMed:18586676). Cleaves CCL5/RANTES to produce RANTES(4-68) lacking the N-terminal three amino acids which exhibits reduced chemotactic and antiviral activities (PubMed:16963625). During apoptosis, cleaves SMARCA2/BRM to produce a 160 kDa cleavage product which localizes to the cytosol (PubMed:11259672). Cleaves myelin basic protein MBP in B cell lysosomes at '224-Phe-|-Lys-225' and '248-Phe-|-Ser-249', degrading the major immunogenic MBP epitope and preventing the activation of MBP-specific autoreactive T cells (PubMed:15100291). Cleaves annexin ANXA1 and antimicrobial peptide CAMP to produce peptides which act on neutrophil N-formyl peptide receptors to enhance the release of CXCL2 (PubMed:22879591). Acts as a ligand for the N-formyl peptide receptor FPR1, enhancing phagocyte chemotaxis (PubMed:15210802). Has antibacterial activity against the Gram-negative bacteria N.gonorrhoeae and P.aeruginosa (PubMed:2116408, PubMed:1937776). Likely to act against N.gonorrhoeae by interacting with N.gonorrhoeae penA/PBP2 (PubMed:2126324). Exhibits potent antimicrobial activity against the Gram-positive bacterium L.monocytogenes (PubMed:2117044). Has antibacterial activity against the Gram-positive bacterium S.aureus and degrades S.aureus biofilms, allowing polymorphonuclear leukocytes to penetrate the biofilm and phagocytose bacteria (PubMed:2117044, PubMed:32995850). Has antibacterial activity against M.tuberculosis (PubMed:15385470). Mediates CASP4 activation induced by the Td92 surface protein of the periodontal pathogen T.denticola, causing production and secretion of IL1A and leading to pyroptosis of gingival fibroblasts (PubMed:29077095)

The "CTSG 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 CTSG 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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