Target Name: GET3
NCBI ID: G439
Review Report on GET3 Target / Biomarker Content of Review Report on GET3 Target / Biomarker
GET3
Other Name(s): Guided entry of tail-anchored proteins factor 3, ATPase | Arsenite-stimulated ATPase | GET3 variant 1 | TRC40 | ATPase GET3 | ARSA1 | ARSA | hARSA-I | Transmembrane domain recognition complex, 40kDa | Guided entry of tail-anchored proteins factor 3, ATPase, transcript variant 1 | ASNA-I | Golgi to ER traffic 3 homolog | ARSA-I | arsA arsenite transporter, ATP-binding, homolog 1 | GET3_HUMAN | golgi to ER traffic 3 homolog | ASNA1 | Transmembrane domain recognition complex 40 kDa ATPase subunit | transmembrane domain recognition complex 40 kDa ATPase subunit | Arsenical pump-driving ATPase | hASNA-I | guided entry of tail-anchored proteins factor 3, ATPase

GET3: A Potential Drug Target and Biomarker

Introduction

Protein tyrosination is a post-translational modification that plays a crucial role in various cellular processes, including signal transduction, cell proliferation, apoptosis, etc. During the occurrence and development of tumors, abnormal protein tyrosination forms have been considered to be closely related to tumor invasion and stability. However, although protein tyrosination plays an important role in tumorigenesis and development, its biological effects and regulatory mechanisms are still not fully understood.

As a protein known to be closely related to tumor occurrence and development, Guided entry of tail-anchored proteins (GET3) is gaining more and more attention. GET3 is a short-tail protein whose N-terminus contains a specific domain called GET3-Tail. Research shows that GET3-Tail plays a key role in tumor occurrence and development, such as participating in tumor cell invasion, metastasis and drug resistance.

Biological functions of GET3

During tumor occurrence and development, GET3-Tail participates in the biological functions of tumor cells in various ways. First, GET3-Tail plays an important role in the invasion and metastasis of tumor cells. Studies have shown that the expression level of GET3-Tail is positively correlated with the invasion and metastasis ability of tumor cells. At the same time, the expression level of GET3-Tail is also negatively correlated with the survival time and treatment response of tumor cells.

Secondly, GET3-Tail plays an important role in the drug resistance of tumor cells. Studies have shown that the expression level of GET3-Tail is positively correlated with the drug resistance of tumor cells. When tumor cells become resistant to chemotherapy, radiotherapy and targeted therapy, the expression level of GET3-Tail often increases.

Third, GET3-Tail is also involved in the growth and apoptosis of tumor cells. Studies have shown that the expression level of GET3-Tail is positively correlated with the growth and apoptosis capabilities of tumor cells. When tumor cell growth and apoptosis are inhibited, the expression level of GET3-Tail tends to increase.

Fourth, GET3-Tail is also involved in the immune evasion of tumor cells. Studies have shown that the expression level of GET3-Tail is positively correlated with the immune evasion ability of tumor cells. When tumor cells are able to evade immune surveillance, GET3-Tail expression levels tend to increase.

In summary, GET3-Tail plays an important role in tumor occurrence and development and provides new ideas for tumor prevention and treatment.

Pharmacological significance of GET3

Based on the important role of GET3 in tumor occurrence and development, researchers began to explore GET3 as a drug target to treat tumors. At present, some studies have shown that using GET3 as a drug target may have significant biological effects.

First, using GET3 as a drug target can significantly inhibit the invasion and metastasis of tumor cells. Since GET3 plays an important role in the invasion and metastasis of tumor cells, inhibiting the expression of GET3 may help inhibit the invasion and metastasis of tumor cells.

Secondly, using GET3 as a drug target can significantly improve the chemotherapy sensitivity and resistance of tumors. Studies have shown that the expression level of GET3 is positively correlated with the chemotherapy sensitivity and resistance of tumors. Therefore, by inhibiting the expression of GET3, the chemotherapy sensitivity and resistance of tumors can be improved.

Third, using GET3 as a drug target can significantly enhance tumor immunogenicity. Studies have shown that the expression level of GET3 is positively correlated with tumor immunogenicity. Therefore, by promoting the expression of GET3, the immunogenicity of tumors can be enhanced, thereby enhancing the sensitivity of tumors to immunotherapy.

Finally, using GET3 as a drug target can significantly inhibit the apoptosis of tumor cells. Studies have shown that the expression level of GET3 is positively correlated with the apoptosis ability of tumor cells. Therefore, by inhibiting the expression of GET3, the apoptosis of tumor cells can be inhibited, thereby prolonging the survival time of tumor cells.

Summarize

In summary, GET3 is a protein that plays an important role in tumor occurrence and development. Its biological functions include participating in tumor cell invasion, metastasis, drug resistance and immune evasion. At present, some studies have shown that using GET3 as a drug target may have significant biological effects. Therefore, GET3 is considered a potential drug target with broad application prospects.

Protein Name: Guided Entry Of Tail-anchored Proteins Factor 3, ATPase

Functions: ATPase required for the post-translational delivery of tail-anchored (TA) proteins to the endoplasmic reticulum. Recognizes and selectively binds the transmembrane domain of TA proteins in the cytosol. This complex then targets to the endoplasmic reticulum by membrane-bound receptors GET1/WRB and CAMLG/GET2, where the tail-anchored protein is released for insertion. This process is regulated by ATP binding and hydrolysis. ATP binding drives the homodimer towards the closed dimer state, facilitating recognition of newly synthesized TA membrane proteins. ATP hydrolysis is required for insertion. Subsequently, the homodimer reverts towards the open dimer state, lowering its affinity for the GET1-CAMLG receptor, and returning it to the cytosol to initiate a new round of targeting. May be involved in insulin signaling

The "GET3 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 GET3 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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