Target Name: APBB1IP
NCBI ID: G54518
Review Report on APBB1IP Target / Biomarker Content of Review Report on APBB1IP Target / Biomarker
APBB1IP
Other Name(s): MLLT10/APBB1IP reciprocal fusion | PREL1 | APBB1-interacting protein 1 | amyloid beta precursor protein binding family B member 1 interacting protein | Retinoic acid-responsive proline-rich protein 1 | AB1IP_HUMAN | retinoic acid-responsive proline-rich protein 1 | PREL-1 | Amyloid beta precursor protein binding family B member 1 interacting protein | RARP1 | rap1-GTP-interacting adapter molecule | Proline rich EVH1 ligand 1 | proline rich EVH1 ligand 1 | proline-rich protein 73 | INAG1 | Rap1-GTP-interacting adapter molecule | Rap1-interacting adaptor molecule | Proline-rich EVH1 ligand 1 | Amyloid beta A4 precursor protein-binding family B member 1-interacting protein | RIAM | Proline-rich protein 73 | MLLT10/APBB1IP reciprocal fusion protein | Rap1-GTP-interacting adaptor molecule | RARP-1

APBB1IP: A Promising Drug Target / Biomarker

Apoptosis (programmed cell death) is a natural process that occurs in all living organisms to remove damaged or dysfunctional cells. It is a critical mechanism for maintaining tissue homeostasis and has been implicated in a wide range of diseases, including cancer, neurodegenerative diseases, and autoimmune disorders. The anti-apoptosis protein Bcl-2 (Bcl-2) is a key regulator of apoptosis and has been implicated in many of these diseases. However, despite its potential as a drug target, Bcl-2 has not yet been approved for use in humans.

The Bcl-2 protein is a member of the Bcl-2 family of proteins, which are known for their ability to regulate apoptosis. The Bcl-2 family includes at least seven different proteins, each with distinct differences in their sequence and function. Bcl-2 is the most well-studied member of the family and is widely expressed in many different tissues, including tissues of the central nervous system, immune system, and organs.

Bcl-2 functions as an anti-apoptosis protein by inhibiting the execution of the apoptosis-associated DNA damage response (ADDR). The ADDR is a series of genes that are expressed in response to DNA damage and play a critical role in the regulation of apoptosis. Bcl-2 works by binding to the protein BAD1, which is a key component of the ADDR complex, and preventing it from binding to the target protein Bax. This inhibition of BAD1 binding to Bax allows the ADDR to be removed, thereby preventing the formation of the DNA damage-inducible apoptosis-associated protein complex (ADP-ribosome complex) and the subsequent execution of apoptosis.

Despite its potential as a drug target, Bcl-2 has not yet been approved for use in humans. There are several reasons for this. First, the safety and efficacy of Bcl-2 have not been fully established in animal models of the disease. Second, the structure and function of Bcl-2 are not well understood, which can make it difficult to design and synthesize effective small molecules that interact with it. Finally, the development of new drugs that specifically target Bcl-2 may be difficult due to the large number of different isoforms of Bcl-2 that exist in the body.

In this article, we will discuss the potential of Bcl-2 as a drug target and the challenges and opportunities in the development of new treatments for diseases associated with Bcl-2.

Potential Therapeutics

Bcl-2 has the potential to be a powerful drug target due to its involvement in the regulation of apoptosis. By inhibiting the execution of the ADDR and preventing the formation of the ADP-ribosome complex, Bcl-2 can be used to treat a wide range of diseases associated with apoptosis. Some potential therapies that may target Bcl-2 include:

1. Anticancer agents: Bcl-2 has been shown to be involved in the regulation of apoptosis in cancer cells, and inhibiting its activity may be a useful strategy for the treatment of cancer. Anticancer agents such as taxanes and topotecan have been shown to be effective in inhibiting Bcl-2 activity and have been used in the treatment of various cancers.
2. neurodegenerative diseases: Bcl-2 has been implicated in the development and progression of neurodegenerative diseases, including Alzheimer's disease and Parkinson's disease. In these diseases, the loss of Bcl-2 activity may contribute to the development and progression of neurodegeneration.
3. autoimmune disorders: Bcl-2 has been implicated in the development and maintenance of autoimmune disorders, such as rheumatoid arthritis and multiple sclerosis. In these disorders, Bcl-2 may play a role in the regulation of apoptosis and the immune response.

Developing New Treatments

The development of new treatments for diseases associated with Bcl-2 will require a combination of research and

Protein Name: Amyloid Beta Precursor Protein Binding Family B Member 1 Interacting Protein

Functions: Appears to function in the signal transduction from Ras activation to actin cytoskeletal remodeling. Suppresses insulin-induced promoter activities through AP1 and SRE. Mediates Rap1-induced adhesion

The "APBB1IP 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 APBB1IP 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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APBB2 | APBB3 | APC | APC2 | APCDD1 | APCDD1L | APCDD1L-DT | APCS | APEH | APELA | APEX1 | APEX2 | APH1A | APH1B | API5 | APIP | APLF | APLN | APLNR | APLP1 | APLP2 | APMAP | APOA1 | APOA1-AS | APOA2 | APOA4 | APOA5 | APOB | APOBEC1 | APOBEC2 | APOBEC3A | APOBEC3A_B | APOBEC3B | APOBEC3B-AS1 | APOBEC3C | APOBEC3D | APOBEC3F | APOBEC3G | APOBEC3H | APOBEC4 | APOBR | APOC1 | APOC1P1 | APOC2 | APOC3 | APOC4 | APOC4-APOC2 | APOD | APOE | APOF | APOH | APOL1 | APOL2 | APOL3 | APOL4 | APOL5 | APOL6 | APOLD1 | Apolipoprotein B mRNA editing complex | APOM | APOO | APOOL | APOOP2 | APOOP5 | APP | APPAT | APPBP2 | APPL1 | APPL2 | APRG1 | APRT | APTR | APTX | AQP1 | AQP10 | AQP11 | AQP12A | AQP12B | AQP2 | AQP3 | AQP4 | AQP4-AS1 | AQP5 | AQP6 | AQP7 | AQP7P1 | AQP7P2 | AQP7P3 | AQP7P5 | AQP8 | AQP9 | AQR | AR | ARAF | ARAP1 | ARAP1-AS2 | ARAP2 | ARAP3 | ARC | ARCN1