HIVEP3: A Protein Implicated in Blood Pressure, Inflammation and Fibrosis

Target Name: HIVEP3

NCBI ID: G59269

HIVEP3

HIVEP3: A Protein Implicated in Blood Pressure, Inflammation and Fibrosis

HIVEP3 (ZAS3) is a protein that is expressed in various tissues of the body, including the brain, heart, and kidneys. It is a member of the ZAS family of proteins, which are known for their role in cell signaling. HIVEP3 has been shown to play a role in a variety of physiological processes, including blood pressure, inflammation, and fibrosis. As a result, HIVEP3 has potential as a drug target or biomarker.

The ZAS family of proteins was identified in the 1990s as a source of putative transcription factors. These proteins are characterized by a C-type zinc finger motif, which is a structural element that is commonly found in gene promoters. ZAS proteins are thought to play a role in regulating gene expression by binding to specific DNA sequences and activating or repressing gene transcription.

HIVEP3 is a 21-kDa protein that is expressed in the brain, heart, and kidneys. It is a member of the ZAS family of proteins and is thought to play a role in regulating gene expression in these tissues. HIVEP3 has been shown to interact with several other proteins, including the transcription factor NF-kappa-B.

One of the most interesting functions of HIVEP3 is its role in blood pressure regulation. High levels of HIVEP3 have been shown to increase blood pressure, while low levels have been shown to decrease blood pressure. This suggests that HIVEP3 may play a role in the regulation of blood pressure and may be a potential drug target for hypertension.

In addition to its role in blood pressure regulation, HIVEP3 has also been shown to play a role in inflammation and fibrosis. High levels of HIVEP3 have been shown to increase inflammation in response to an infection or injury, while low levels have been shown to reduce inflammation. This suggests that HIVEP3 may play a role in the regulation of inflammation and may be a potential biomarker for inflammatory diseases.

Finally, HIVEP3 has also been shown to play a role in the regulation of cellular processes such as cell adhesion and migration. High levels of HIVEP3 have been shown to increase cell adhesion and migration, while low levels have been shown to decrease these processes. This suggests that HIVEP3 may play a role in the regulation of cellular processes and may be a potential drug target for a variety of diseases.

In conclusion, HIVEP3 is a protein that is expressed in various tissues of the body and is thought to play a role in a variety of physiological processes. Its functions include blood pressure regulation, inflammation, and fibrosis. As a result, HIVEP3 has potential as a drug target or biomarker and may be a valuable tool for the study of these processes. Further research is needed to fully understand the role of HIVEP3 in these processes and to determine its potential as a drug or biomarker.

Protein Name: HIVEP Zinc Finger 3

Functions: Plays a role of transcription factor; binds to recognition signal sequences (Rss heptamer) for somatic recombination of immunoglobulin and T-cell receptor gene segments; Binds also to the kappa-B motif of gene such as S100A4, involved in cell progression and differentiation. Kappa-B motif is a gene regulatory element found in promoters and enhancers of genes involved in immunity, inflammation, and growth and that responds to viral antigens, mitogens, and cytokines. Involvement of HIVEP3 in cell growth is strengthened by the fact that its down-regulation promotes cell cycle progression with ultimate formation of multinucleated giant cells. Strongly inhibits TNF-alpha-induced NF-kappa-B activation; Interferes with nuclear factor NF-kappa-B by several mechanisms: as transcription factor, by competing for Kappa-B motif and by repressing transcription in the nucleus; through a non transcriptional process, by inhibiting nuclear translocation of RELA by association with TRAF2, an adapter molecule in the tumor necrosis factor signaling, which blocks the formation of IKK complex. Interaction with TRAF proteins inhibits both NF-Kappa-B-mediated and c-Jun N-terminal kinase/JNK-mediated responses that include apoptosis and pro-inflammatory cytokine gene expression. Positively regulates the expression of IL2 in T-cell. Essential regulator of adult bone formation

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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;
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•   related combination drugs;
•   pharmacochemistry experiments;
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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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