Unlocking the Potential of ACTL6A as a Drug Target and Biomarker

Target Name: ACTL6A

NCBI ID: G86

ACTL6A

Unlocking the Potential of ACTL6A as a Drug Target and Biomarker

Abstract:

Actl6a (BRG1-associated factor 53A) is a protein that has been identified as a potential drug target and biomarker for various diseases, including cancer, neurodegenerative disorders, and autoimmune diseases. This article reviews the current research on ACTL6a, including its structure, function, and potential as a drug target and biomarker.

Introduction:

Actl6a (BRG1-associated factor 53A) is a protein that is expressed in various tissues and cells, including neurons, glial cells, and immune cells. It has been identified as a potential drug target and biomarker for various diseases, including cancer, neurodegenerative disorders, and autoimmune diseases. In this article, we will review the current research on ACTL6a and its potential as a drug target and biomarker.

Structure and Function:

The protein ACTL6a is characterized by its unique structure and biology. It has a molecular weight of 42 kDa and consists of 106 amino acid residues. The protein has a monomeric structure and is expressed in various tissues and cells, including neurons, glial cells, and immune cells.

One of the unique features of ACTL6a is its association with the BRG1 protein. BRG1 is a non-coding RNA-protein hybrid that has been shown to play a role in various cellular processes, including cell growth, differentiation, and survival. The association between ACTL6a and BRG1 suggests that ACTL6a may be a regulatory protein that is influenced by BRG1 activity.

In addition to its association with BRG1, ACTL6a has been shown to play a role in various cellular processes, including cell adhesion, migration, and survival. It has also been shown to be involved in the regulation of various signaling pathways, including the TGF-β pathway, the Wnt pathway, and the NF-kappa-B pathway.

Potential as a Drug Target:

The potential of ACTL6a as a drug target is based on its involvement in various cellular processes that are associated with the development and progression of various diseases. One of the primary targets of ACTL6a is the TGF-β pathway, which is involved in cell growth, differentiation, and survival. Activation of the TGF-β pathway has been shown to promote the development and progression of various diseases, including cancer, neurodegenerative disorders, and autoimmune diseases.

Actl6a has also been shown to play a role in the regulation of the Wnt pathway, which is involved in cell-to-cell signaling and the development of various tissues. The Wnt pathway has been shown to be involved in the development and maintenance of tissues, including brain, and has been implicated in the development of neurodegenerative disorders.

In addition to its involvement in the TGF-β and Wnt pathways, ACTL6a has also been shown to play a role in the regulation of the NF-kappa-B pathway, which is involved in inflammation and cellular signaling. Activation of the NF-kappa-B pathway has been implicated in the development and progression of various diseases, including cancer and autoimmune diseases.

Potential as a Biomarker:

The potential of ACTL6a as a biomarker for various diseases is based on its association with the development and progression of these diseases and its involvement in various cellular processes that are associated with these diseases. One of the primary biomarkers for cancer is the expression ofactl6a, as it has been shown to be involved in the regulation of various cellular processes that are associated with cancer development, including cell growth, differentiation, and survival.

In addition to its association with cancer, ACTL6a has also been shown to be involved in the regulation of neurodegenerative disorders, including Alzheimer's disease, Parkinson's disease, and Huntington's disease. The regulation of these disorders is associated with the dysfunction of various cellular processes, including the TGF-β pathway, the Wnt pathway, and the NF-kappa-B pathway.

In addition to its involvement in neurodegenerative disorders, ACTL6a has also been shown to be involved in the regulation of autoimmune diseases, including rheumatoid arthritis, lupus, and multiple sclerosis. The regulation of these diseases is associated with the dysfunction of various cellular processes, including the TGF-β pathway, the Wnt pathway, and the NF-kappa-B pathway.

Conclusion:

In conclusion, ACTL6a is a protein that has been identified as a potential drug target and biomarker for various diseases, including cancer, neurodegenerative disorders, and autoimmune diseases. Its unique structure and biology, as well as its association with the BRG1 protein, suggest that ACTL6a may be a regulatory protein that is influenced by BRG1 activity. Further research is needed to fully understand the potential of ACTL6a as a drug target and biomarker for various diseases.

Protein Name: Actin Like 6A

Functions: Involved in transcriptional activation and repression of select genes by chromatin remodeling (alteration of DNA-nucleosome topology). Component of SWI/SNF chromatin remodeling complexes that carry out key enzymatic activities, changing chromatin structure by altering DNA-histone contacts within a nucleosome in an ATP-dependent manner. Required for maximal ATPase activity of SMARCA4/BRG1/BAF190A and for association of the SMARCA4/BRG1/BAF190A containing remodeling complex BAF with chromatin/nuclear matrix. Belongs to the neural progenitors-specific chromatin remodeling complex (npBAF complex) and is required for the proliferation of neural progenitors. During neural development a switch from a stem/progenitor to a postmitotic chromatin remodeling mechanism occurs as neurons exit the cell cycle and become committed to their adult state. The transition from proliferating neural stem/progenitor cells to postmitotic neurons requires a switch in subunit composition of the npBAF and nBAF complexes. As neural progenitors exit mitosis and differentiate into neurons, npBAF complexes which contain ACTL6A/BAF53A and PHF10/BAF45A, are exchanged for homologous alternative ACTL6B/BAF53B and DPF1/BAF45B or DPF3/BAF45C subunits in neuron-specific complexes (nBAF). The npBAF complex is essential for the self-renewal/proliferative capacity of the multipotent neural stem cells. The nBAF complex along with CREST plays a role regulating the activity of genes essential for dendrite growth (By similarity). Component of the NuA4 histone acetyltransferase (HAT) complex which is involved in transcriptional activation of select genes principally by acetylation of nucleosomal histones H4 and H2A. This modification may both alter nucleosome - DNA interactions and promote interaction of the modified histones with other proteins which positively regulate transcription. This complex may be required for the activation of transcriptional programs associated with oncogene and proto-oncogene mediated growth induction, tumor suppressor mediated growth arrest and replicative senescence, apoptosis, and DNA repair. NuA4 may also play a direct role in DNA repair when recruited to sites of DNA damage. Putative core component of the chromatin remodeling INO80 complex which is involved in transcriptional regulation, DNA replication and probably DNA repair

The "ACTL6A 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 ACTL6A 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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