Synonyms for aurka or Related words with aurka

aurkb              cenpa              cenpf              cflar              gmnn              tagln              ccnf              ctsl              ncaph              mycn              ywhab              nfkbia              aurkc              ldhc              prkcb              anln              ikbke              ptprd              ywhae              mdfic              nucks              prkaca              tyms              cenpi              cenpe              ptprk              ptprg              cenph              ptgds              ptprt              zwilch              rybp              hnrpd              ywhaz              cenpj              cebpa              zwint              melk              pdgfrl              prkx              ptprm              dpyd              heph              palld              mylk              hmmr              inhba              sdcbp              farsla              paics             



Examples of "aurka"
ARAF; ATM; ATR; AURKA; AURKB; AURKC; AXL; BCKDK; BLK; BMP2K; BMPR1A; BMPR1B; BMPR2; BMX;
Aurora kinase A also known as serine/threonine-protein kinase 6 is an enzyme that in humans is encoded by the "AURKA" gene.
JUB proteins contribute to cell fate determination and regulate cell proliferation and differentiation. Plays an important role in regulation of the kinase activity of AURKA/Aurora-A for mitotic commitment.
CASS4 has been reported to play a modifying role in cystic fibrosis severity, progression and comorbid conditions. The CAS family member NEDD9 has also been shown to interact directly with AURKA (encoding Aurora-A kinase) to regulate cell cycle and ciliary resorption; it is possible that CASS4 may similarly interact with aurora-A kinase.
The kinase itself has been identified as a possible route for generating pluripotent stem cells. Researchers have been trying to inhibit kinases, which were activated by the gene manipulation used to generate pluripotent stem cells. The inhibition of ITP3K, AurkA, and P38 expedited the method used to make these induced pluripotent stem cells (iPSC). The potential in this field could possibly find treatments for many types of cancers and neurodegenerative disorders.
NEDD9 binds directly to the Aurora-A mitotic kinase at the centrosome, and promotes its activity, allowing cells to enter mitosis. Degradation of NEDD9 at the end of mitosis contributes to timely Aurora-A degradation. Cell overexpressing NEDD9 exhibit deficient cytokinesis resulting in accumulation of multipolar mitotic spindles and abnormal numbers of centrosomes. On the other hand, cells with depleted NEDD9 have prematurely separated centrosomes and are deficient in microtubule organizing activity at mitosis leading to abundance of monopolar or asymmetric spindles, preventing cells from entering mitosis. NEDD9 also regulates Aurora-A activation at the basal body of cilia as cells resorb cilia during early G1. Cilia are small organelles that protrude from the surface of adherent cells that are the obligate site of action for proteins such as Hedgehog, and the polycystins: by influencing ciliary stability, NEDD9 is positioned to affect these signaling systems. Interaction of NEDD9 with Aurora A kinase may also play a role in tumor invasion. NEDD9 binds to and regulates acetylation of cortactin (CTTN) in an Aurora A kinase (AURKA)/HDAC6–dependent manner. The knockdown of NEDD9 or AURKA results in an increase in the amount of acetylated CTTN and a decrease in the binding of CTTN to F-actin. Overexpression of the deacetylation mimicking (9KR) mutant of CTTN is sufficient to restore actin dynamics at the leading edge and migration proficiency of the tumor cells. Inhibition of AURKA and HDAC6 activity by alisertib and tubastatin A in xenograft models of breast cancer leads to a decrease in the number of pulmonary metastases.
The main function of the DREAM complex is to repress gene expression during quiescence (G). One of the genes repressed is the proto-oncogene Myc. Entry into G causes the dissociation of p130 from the complex, which prevents E2F4/5 from binding gene promoters. BMYB, which is repressed by the DREAM complex during G is expressed during G and it subsequently binds to MuvB during S phase to promote the expression of key G/M phase genes such as CDK1 and CCNB1. FOXM1 is then recruited in G to further promote gene expression (e.g. AURKA). During late S phase BMYB is degraded via CUL1 (SCF complex), while FOXM1 is degraded during mitosis by the APC/C. The DREAM complex regulates cytokinesis through GAS2L3.