GOLGA7B: A Potential Drug Target and Biomarker for Golgi-Initiative Differentiation and Maintenance

Target Name: GOLGA7B

NCBI ID: G401647

GOLGA7B

GOLGA7B: A Potential Drug Target and Biomarker for Golgi-Initiative Differentiation and Maintenance

Golgi-initiation differentiated cells (GIDCs) are a subset of human cancer stem cells that have been identified as a promising therapeutic target in various diseases, including cancer. GIDCs are characterized by the loss of cell surface antigens, such as CD11b, CD33, and PDGFR伪, and the expression of various transcription factors, including ID4, which encodes the transcription factor PDGFR伪.

One of the hallmarks of GIDCs is the loss of the Golgi system, which is a complex network of organelles responsible for the synthesis, processing, and degradation of proteins. The Golgi system is composed of several components, including the endoplasmic reticulum (ER), the trans-endosomal system (TES), and the Golgi themselves. The loss of the Golgi system in GIDCs has been observed in various cellular and tissue samples, and it has been associated with the increased invasiveness and metastatic potential of these cells.

Golgin subfamily A member 7B (GOLGA7B) is a gene that has been identified as a potential drug target and biomarker in GIDCs. GOLGA7B is a member of the Golgin family, which includes several genes that encode proteins involved in the Golgi system. GOLGA7B is characterized by the loss of several key Golgi components, including the trans-endosomal system (TES), the endoplasmic reticulum (ER), and the mitochondria. These loss of events are consistent with the observed loss of the Golgi system in GIDCs.

GOLGA7B has been shown to be involved in the regulation of cellular processes that are critical for cancer progression, including cell survival, angiogenesis, and immune evasion. For example, GOLGA7B has been shown to be involved in the regulation of the PI3K/Akt signaling pathway, which is a critical pathway involved in the regulation of cell survival and angiogenesis. GOLGA7B has also been shown to be involved in the regulation of the TGF-β pathway, which is involved in cell growth, differentiation, and angiogenesis.

In addition to its role in cellular processes, GOLGA7B has also been shown to be involved in the regulation of the immune response. GOLGA7B has been shown to be involved in the regulation of the output of the T-cell receptor (TCR), which is the critical receptor responsible for recognizing and responding to foreign antigens. GOLGA7B has also been shown to be involved in the regulation of the activation and proliferation of T-cells, which are critical for immune surveillance against cancer cells.

GOLGA7B has been shown to be involved in the regulation of cellular processes that are critical for cancer progression, including cell survival, angiogenesis, and immune evasion. Therefore, GOLGA7B is a potential drug target and biomarker for cancer. Further studies are needed to determine the specific mechanisms by which GOLGA7B contributes to the regulation of these processes and to determine its potential as a drug target.

Protein Name: Golgin A7 Family Member B

Functions: Play a role in cell adhesion by regulating the plasma membrane localization of the palmitoyltransferase ZDHHC5 (PubMed:31402609). May be involved in protein transport from Golgi to cell surface

The "GOLGA7B 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 GOLGA7B comprehensively, including but not limited to:
•   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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•   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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