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anti-Human Aurora Kinase C Anticorps:
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Cow (Bovine) Polyclonal Aurora Kinase C Primary Antibody pour WB - ABIN2785453
Lee, Lim, Park, Lee, Han, Kim, Cheang, Lee, Lee, Ko, Jang, Kim, Miniaci, Bartsch, Kim, Bailey, Kandel, Kaang: Nuclear translocation of CAM-associated protein activates transcription for long-term facilitation in Aplysia. dans Cell 2007
Show all 2 Pubmed References
Human Polyclonal Aurora Kinase C Primary Antibody pour ELISA, WB - ABIN4282476
Dieterich, Zouari, Harbuz, Vialard, Martinez, Bellayou, Prisant, Zoghmar, Guichaoua, Koscinski, Kharouf, Noruzinia, Nadifi, Sefiani, Lornage, Zahi, Viville, Sèle, Jouk, Jacob, Escalier, Nikas et al.: The Aurora Kinase C c.144delC mutation causes meiosis I arrest in men and is frequent in the North African population. ... dans Human molecular genetics 2009
Human Monoclonal Aurora Kinase C Primary Antibody pour IF, IHC - ABIN2716477
Woo Seo, Yeop You, Chung, Cho, Kim, Su Oh: Zwint-1 is required for spindle assembly checkpoint function and kinetochore-microtubule attachment during oocyte meiosis. dans Scientific reports 2015
Human Polyclonal Aurora Kinase C Primary Antibody pour WB - ABIN4890463
Doyle, Lee, Selesniemi, Styer, Rueda: The impact of vitrification on murine germinal vesicle oocyte In vitro maturation and aurora kinase A protein expression. dans Journal of assisted reproduction and genetics 2014
This study showed the role of Lactobacilli in down-regulation of TSGA10, AURKC, OIP5 and AKAP4 genes. Such expression change might be involved in the anticancer effects of these Lactobacilli. The underlying mechanisms of these observations are not clear but epigenetic modulatory mechanisms may participate in this process.
These results further support the important role of AURKC in male infertility and guide the practitioner in optimal decision making for patients with macrozoospermia.
Teratozoospermia is not correlated with c.144delC mutation in the AURKC gene in the men of the Sichuan area. Therefore, large-scale genotyping of the AURKC gene may not be necessary clinically among Chinese patients with idiopathic teratozoospermia.
The epigenetic targets AURKB, AURKC and DNMT3B, and the global DNA methylation profile are regulated during HIV-1 replication in CD4+ T cells, and this regulation can be influenced by the activation state of the cell at the time of infection.
The data suggest that AKA is the vertebrate ancestral gene, and that AKB and AKC resulted from gene duplication in placental mammals.
Two novel DMRs, located in RPS6KA4/MIR1237 and the AURKC promoter, were found to be hypermethylated in WT
Identification and characterization of AURKB and AURKC variants associated with maternal aneuploidy has been reported.
Aurora-C interactions with members of the Chromosome Passenger Complex (CPC), Survivin and Inner Centromere Protein (INCENP) in reference to known Aurora-B 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.
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.
may play an important role in the development of colorectal cancer
Data indicate that the selective Aurora A, B, and C inhibitor SAR156497 showed antineoplastic activity in HCT116 cell xenograft model.
This review will describe the functions of each Aurora kinase which include Aurora A (AURKA), Aurora B (AURKB) 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.
The immunoreactivity profile of AURKA, AURKB and AURKC in this study showed a significantly reduced expression in PCa cases compared to BPH cases.
expression of AURKC, OIP5, PIWIL2 and TAF7L differed between patients with Acute myeloid leukemia, myelodysplastic syndrome and healthy controls in a gender-dependent manner
in the absence of AURKC, AURKA localizes to chromosomes in a CPC-dependent manner. These data suggest that AURKC prevents AURKA from localizing to chromosomes by competing for CPC binding. This competition is important for adequate spindle length to support meiosis I. There is also a unique requirement for AURKB to negatively regulate AURKC to prevent aneuploidy.
findings demonstrate that maternal RNAs regulate AURKC localization and activity in mouse oocytes
The high sequence similarity among the AURK family members has made discerning the individual kinase functions in meiosis challenging. Technical limitations in specifically targeting AURKB or AURKC using small-molecule inhibitors and compensatory abilities in single-knockout animals add to this challenge...proper regulation of AURKA expression is crucial for spindle formation in meiosis
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 through differences in both message recruitment and protein stability.
Overexpressed Aurora-C (aurkc) is an oncogene. 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 phosphorylation in the cytokinetic process
INCENP recruits Aurora-C (or some other factor(s) recruit INCENP 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.
AURK may be an oocyte histone-H3 kinase capable of regulating chromatin remodeling throughout oocyte meiosis.
AURKB, AURKC, and Thr-phosphorylated AURKA 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)