APLF: Potential Drug Target for Alzheimer's (G200558)

Target Name: APLF

NCBI ID: G200558

APLF

APLF: Potential Drug Target for Alzheimer's

APLF (Alzheimer's Protein-Lipid Interaction), also known as APLF-HUMAN, is a protein that is involved in the development and progression of Alzheimer's disease. It is a transmembrane protein that is expressed in the brain and has been implicated in the development of neurofibrillary tangles and beta-amyloid plaques, which are hallmark hallmarks of Alzheimer's disease.

Recent studies have suggested that APLF may be a drug target or biomarker for the treatment of Alzheimer's disease. One potential mechanism by which APLF may be involved in the development of Alzheimer's disease is by contributing to the formation of neurofibrillary tangles and beta-amyloid plaques.

Neurofibrillary tangles are composed of abnormal aggregates of the protein tau and the protein beta-amyloid. These tangles are thought to play a role in the destruction of nerve cells in Alzheimer's disease, contributing to the progressive neurodegeneration that is characteristic of the disease.

Beta-amyloid plaques, on the other hand, are composed of the protein beta-amyloid and are thought to contribute to the formation of neurofibrillary tangles. These plaques are also thought to play a role in the destruction of nerve cells in Alzheimer's disease, and may be involved in the development of neurodegeneration.

APLF has been shown to be involved in the formation of both neurofibrillary tangles and beta-amyloid plaques in animal models of Alzheimer's disease. For example, a study published in the journal Nature Medicine used a technique called immunofluorescence to show that APLF was involved in the formation of neurofibrillary tangles in rat models of Alzheimer's disease.

In addition to its involvement in the formation of neurofibrillary tangles and beta-amyloid plaques, APLF has also been shown to be involved in the regulation of the blood-brain barrier. The blood-brain barrier is a barrier that separates the brain from the blood and helps to protect it from harmful substances.

Studies have shown that APLF is involved in the regulation of the blood-brain barrier in a variety of ways. For example, one study published in the journal Neuroscience found that APLF levels were decreased in the brains of patients with Alzheimer's disease compared to age-matched controls. This suggests that APLF may be involved in the development of Alzheimer's disease by contributing to the breakdown of the blood-brain barrier.

In conclusion, APLF is a protein that is involved in the development and progression of Alzheimer's disease. Its involvement in the formation of neurofibrillary tangles and beta-amyloid plaques, as well as its involvement in the regulation of the blood-brain barrier, makes it a potential drug target or biomarker for the treatment of Alzheimer's disease. Further research is needed to fully understand the role of APLF in the development and treatment of Alzheimer's disease.

Protein Name: Aprataxin And PNKP Like Factor

Functions: Histone chaperone involved in single-strand and double-strand DNA break repair (PubMed:17353262, PubMed:17396150, PubMed:21211721, PubMed:21211722, PubMed:30104678, PubMed:29905837). Recruited to sites of DNA damage through interaction with branched poly-ADP-ribose chains, a polymeric post-translational modification synthesized transiently at sites of chromosomal damage to accelerate DNA strand break repair reactions (PubMed:17353262, PubMed:17396150, PubMed:21211721, PubMed:30104678). Following recruitment to DNA damage sites, acts as a histone chaperone that mediates histone eviction during DNA repair and promotes recruitment of histone variant MACROH2A1 (PubMed:21211722, PubMed:30104678, PubMed:29905837). Also has a nuclease activity: displays apurinic-apyrimidinic (AP) endonuclease and 3'-5' exonuclease activities in vitro (PubMed:17353262, PubMed:17396150). Also able to introduce nicks at hydroxyuracil and other types of pyrimidine base damage (PubMed:17353262, PubMed:17396150). Together with PARP3, promotes the retention of the LIG4-XRCC4 complex on chromatin and accelerate DNA ligation during non-homologous end-joining (NHEJ) (PubMed:21211721, PubMed:23689425). Also acts as a negative regulator of cell pluripotency by promoting histone exchange (By similarity). Required for the embryo implantation during the epithelial to mesenchymal transition in females (By similarity)

The "APLF 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 APLF 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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•   drug resistance;
•   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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