KIF5A: A Potential Drug Target and Biomarker (G3798)

Target Name: KIF5A

NCBI ID: G3798

KIF5A

KIF5A: A Potential Drug Target and Biomarker

The Kinesin family is an important protein family responsible for protein transport in cells, among which KIF5A plays a key role in cells. Mutations in KIF5A can cause a variety of genetic diseases, so the study of KIF5A is of great significance for understanding cellular transport mechanisms and developing drugs.

This article will introduce the structure, function, biology and application of KIF5A in drug research.

structure

KIF5A is a 21 kDa protein consisting of 114 amino acids. KIF5A has five structural domains: an N-terminal 伪-helix, a central 尾-page, a C-terminal 伪-helix, and two C-terminal 尾-pages (Figure 1). Both the N- and C-termini of KIF5A contain 伪-helices, while the central region contains a 尾-sheet and a helix-turn. These structures enable KIF5A to transport different types of proteins within a variety of cells.

Function

KIF5A plays a critical transport role within cells. KIF5A is transported within cells mainly by binding to proteins, lipids, nucleic acids and other substances. KIF5A can bind DNA and participate in DNA packaging and transportation. In addition, KIF5A can also bind to proteins and participate in the modification and transport of proteins within cells. The main proteins transported by KIF5A within cells include histones, non-histone proteins, ribonucleic acid (RNA) and lipids.

Mutations in KIF5A can cause a variety of genetic diseases, suggesting that KIF5A plays an important role in intracellular trafficking. Since KIF5A plays a key transport role within cells, studying the function and structure of KIF5A is of great significance for understanding cellular transport mechanisms and developing drugs.

biology

KIF5A plays an important role in various cancers. Studies have found that mutations in KIF5A are related to the occurrence of various cancers, including leukemia, liver cancer, breast cancer, and kidney cancer. Variations in KIF5A are also associated with cancer's resistance to chemotherapy and the rate of progression. Therefore, studying the biological functions and mutation mechanisms of KIF5A is of great significance for the development of new cancer treatment strategies.

In drug research, KIF5A is also regarded as a potential drug target. Mutations in KIF5A can cause a variety of diseases, so studying the biological functions and drug targets of KIF5A is of great significance for the development of new treatment strategies. Currently, some drugs targeting KIF5A have entered clinical research. These drugs mainly work by inhibiting the function of KIF5A.

Protein Name: Kinesin Family Member 5A

Functions: Microtubule-dependent motor required for slow axonal transport of neurofilament proteins (NFH, NFM and NFL). Can induce formation of neurite-like membrane protrusions in non-neuronal cells in a ZFYVE27-dependent manner. The ZFYVE27-KIF5A complex contributes to the vesicular transport of VAPA, VAPB, SURF4, RAB11A, RAB11B and RTN3 proteins in neurons. Required for anterograde axonal transportation of MAPK8IP3/JIP3 which is essential for MAPK8IP3/JIP3 function in axon elongation

The "KIF5A 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 KIF5A 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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