Understanding AURKB: A Potential Drug Target and Biomarker (G9212)

Target Name: AURKB

NCBI ID: G9212

AURKB

Understanding AURKB: A Potential Drug Target and Biomarker

AURKB (AURKB_HUMAN) is a protein that is expressed in human tissues and has been identified as a potential drug target or biomarker. The protein is named after its discovery by researchers at the University of California, San Diego, and is derived from the human proteome.

AURKB is a protein that is expressed in a variety of human tissues, including muscle, liver, and brain. It is a 21-kDa protein that is composed of 156 amino acid residues. The protein is characterized by a N-terminus that is rich in amino acids that are involved in its stability and function. The C-terminus of the protein is also unique, as it is missing several amino acids that are typically present in the C-terminus of proteins.

One of the unique features of AURKB is its ability to interact with several different proteins, including the protein known as TrkB. TrkB is a G protein-coupled receptor that is involved in the regulation of cell growth, differentiation, and survival. AURKB has been shown to interact with TrkB and can modulate its activity.

Another potential drug target for AURKB is the protein known as p53. p53 is a tumor suppressor protein that is involved in the regulation of cell growth and apoptosis. AURKB has been shown to interact with p53 and can modulate its activity.

In addition to its potential drug target properties, AURKB has also been identified as a potential biomarker. The protein is expressed in a variety of human tissues and can be used as a protein biomarker for a variety of diseases, including cancer, neurodegenerative diseases, and cardiovascular disease.

One of the challenges in studying AURKB is its relatively small size and the limited amount of information that is available about its function. However, research into AURKB is ongoing and is expected to provide more insights into its potential role in human biology and disease.

In conclusion, AURKB is a protein that is expressed in human tissues and has been identified as a potential drug target or biomarker. Its unique structure and ability to interact with several different proteins make it an attractive target for research and potential therapeutic use. Further studies are needed to fully understand its function and potential in human biology and disease.

Protein Name: Aurora Kinase B

Functions: Serine/threonine-protein kinase component of the chromosomal passenger complex (CPC), a complex that acts as a key regulator of mitosis (PubMed:11516652, PubMed:12925766, PubMed:14610074, PubMed:14722118). The CPC complex has essential functions at the centromere in ensuring correct chromosome alignment and segregation and is required for chromatin-induced microtubule stabilization and spindle assembly (PubMed:11516652, PubMed:12925766, PubMed:14610074, PubMed:14722118, PubMed:26829474). Involved in the bipolar attachment of spindle microtubules to kinetochores and is a key regulator for the onset of cytokinesis during mitosis (PubMed:15249581). Required for central/midzone spindle assembly and cleavage furrow formation (PubMed:12458200, PubMed:12686604). Key component of the cytokinesis checkpoint, a process required to delay abscission to prevent both premature resolution of intercellular chromosome bridges and accumulation of DNA damage: phosphorylates CHMP4C, leading to retain abscission-competent VPS4 (VPS4A and/or VPS4B) at the midbody ring until abscission checkpoint signaling is terminated at late cytokinesis (PubMed:22422861, PubMed:24814515). AURKB phosphorylates the CPC complex subunits BIRC5/survivin, CDCA8/borealin and INCENP (PubMed:11516652, PubMed:12925766, PubMed:14610074). Phosphorylation of INCENP leads to increased AURKB activity (PubMed:11516652, PubMed:12925766, PubMed:14610074). Other known AURKB substrates involved in centromeric functions and mitosis are CENPA, DES/desmin, GPAF, KIF2C, NSUN2, RACGAP1, SEPTIN1, VIM/vimentin, HASPIN, and histone H3 (PubMed:11784863, PubMed:12689593, PubMed:14602875, PubMed:11856369, PubMed:16103226, PubMed:21658950, PubMed:11756469). A positive feedback loop involving HASPIN and AURKB contributes to localization of CPC to centromeres (PubMed:21658950). Phosphorylation of VIM controls vimentin filament segregation in cytokinetic process, whereas histone H3 is phosphorylated at 'Ser-10' and 'Ser-28' during mitosis (H3S10ph and H3S28ph, respectively) (PubMed:11784863, PubMed:11856369). AURKB is also required for kinetochore localization of BUB1 and SGO1 (PubMed:15020684, PubMed:17617734). Phosphorylation of p53/TP53 negatively regulates its transcriptional activity (PubMed:20959462). Key regulator of active promoters in resting B- and T-lymphocytes: acts by mediating phosphorylation of H3S28ph at active promoters in resting B-cells, inhibiting RNF2/RING1B-mediated ubiquitination of histone H2A and enhancing binding and activity of the USP16 deubiquitinase at transcribed genes (By similarity). Acts as an inhibitor of CGAS during mitosis: catalyzes phosphorylation of the N-terminus of CGAS during the G2-M transition, blocking CGAS liquid phase separation and activation, and thereby preventing CGAS-induced autoimmunity (PubMed:33542149). Phosphorylates KRT5 during anaphase and telophase (By similarity)

The "AURKB 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 AURKB 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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