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Aurora-C interactions with members of the Chromosome Passenger Complex (CPC), Survivin (show BIRC5 ELISA Kits) and Inner Centromere Protein (INCENP (show INCENP ELISA Kits)) in reference to known Aurora-B (show AURKB ELISA Kits) interactions to understand the functional significance of Aurora-C overexpression in human cancer cells, is reported.
Patients presenting with a monomorphic teratozoospermia such as globozoospermia or macrospermia with more than 85% of the spermatozoa presenting this specific abnormality have been analyzed permitting to identify several key genes for spermatogenesis such as AURKC and DPY19L2 (show DPY19L2 ELISA Kits).
Homozygous c.144delC mutation in AURKC gene in infertile men with macrozoospermia in the Tunisian population
AURKC mutations are more frequent than Klinefelter syndrome and constitute the leading genetic cause of infertility in North African men.
Low AURKC expression is associated with cancer.
Overexpression of AURKC is associated with breast tumors.
Data indicate that the selective Aurora A (show AURKA ELISA Kits), B, and C inhibitor SAR156497 showed antineoplastic activity in HCT116 cell xenograft model.
This review will describe the functions of each Aurora kinase (show AURKA ELISA Kits) which include Aurora A (AURKA (show AURKA ELISA Kits)), Aurora B (AURKB (show AURKB ELISA Kits)) and Aurora C (AURKC summarize their involvement in leukemia and discuss inhibitor development and efficacy in leukemia clinical trials
Aberrantly expressed Aurora-C in somatic cancer cells may impair spindle checkpoint assembly by displacing the centromeric localization of chromosomal passenger complexes.
Our data indicate that the AURKC c.144delC mutation has a relatively high carrier frequency in the Moroccan population.
Three of these mutations AURKC c.144delC (AURKC p.L49Wfs22), AURKC c.686G > A (AURKC p.C229Y) and AURKC c.744C > G (AURKC p.Y248*) are the focus of this study. AURKC p.L49Wfs22 is a loss-of-function mutant that perturbs localization of the chromosomal passenger complex (CPC), AURKC p.C229Y is a hypomorph that cannot fully support cell-cycle progression, and AURKC p.Y248* fails to support chromosome segregation.
These data uncover a role for haspin as a regulator of bipolar spindle assembly by regulating AURKC function at acentriolar microtubule-organizing centers in oocytes.
these data suggest that mammalian oocytes contain AURKC to efficiently execute meiosis I and ensure high-quality eggs necessary for sexual reproduction.
These findings suggest a model for the presence of AURKC in oocytes: that AURKC compensates for loss of AURKB (show AURKB ELISA Kits) through differences in both message recruitment and protein stability.
Overexpressed Aurora-C (aurkc) is an oncogene (show RAB1A ELISA Kits). Overexpression of Aurora-C induces abnormal cell division resulting in centrosome amplification and multinucleation. Cells overexpressing active Aurora-C induced tumour formation.
Conditional deletion of aurora B in somatic cells that do not express aurora C results in chromosomal misalignment and lack of chromosome segregation.
Aurora-C, but not Aurora-B, plays essential roles in female mouse meiosis.
role in regulating the cleavage furrow-specific vimentin (show VIM ELISA Kits) phosphorylation in the cytokinetic process
INCENP (show INCENP ELISA Kits) recruits Aurora-C (or some other factor(s) recruit INCENP (show INCENP ELISA Kits) and Aurora-C) to meiotic chromosomes, while Aurora-C may either work alone or cooperate with Aurora-B to regulate chromosome segregation during male meiosis
Aurora-B and Aurora-C serve specialized functions in mammalian spermatogenesis.
AURKB (show AURKB ELISA Kits), AURKC, and Thr (show TRH ELISA Kits)-phosphorylated AURKA (show AURKA ELISA Kits) were detected at a contractile ring/midbody during the first polar body extrusion.
This gene encodes a member of the Aurora subfamily of serine/threonine protein kinases. The encoded protein is a chromosomal passenger protein that forms complexes with Aurora-B and inner centromere proteins and may play a role in organizing microtubules in relation to centrosome/spindle function during mitosis. This gene is overexpressed in several cancer cell lines, suggesting an involvement in oncogenic signal transduction. Alternative splicing results in multiple transcript variants.
aurora kinase C
, aurora 3
, aurora-related kinase 3
, aurora/IPL1-related kinase 3
, aurora/IPL1/EG2 protein 2
, serine/threonine kinase 13 (aurora/IPL1-like)
, serine/threonine-protein kinase 13
, serine/threonine-protein kinase aurora-C
, aurora B
, aurora/Ipl1/Eg2 protein 1
, serine/threonine kinase 13 (aurora/IPL-like)