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Budding uninhibited by benzimidazoles 3 homolog

Bub3, Bub3p, hBUB3
This gene encodes a protein involved in spindle checkpoint function. The encoded protein contains four WD repeat domains and has sequence similarity with the yeast BUB3 protein. Alternate transcriptional splice variants, encoding different isoforms, have been characterized. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Bub1, Mad2, Mad3, CAN, Smad1
Papers using Bub3 antibodies
Preclinical activity of a novel multiple tyrosine kinase and aurora kinase inhibitor, ENMD-2076, against multiple myeloma.
Lydon John P., In PLoS ONE, 2009
... The anti-MAD2 and anti-BUBR1 antibodies were from BD-biosciences, the anti-CDC20, anti-BUB3 and anti-KNTC1 from Santa Cruz Biotechnology, the anti-αtubulin from Oncogene ...
Papers on Bub3
Cellular and molecular markers in monitoring the fate of lymphoid cell culture from Penaeus monodon Fabricius (1798).
Singh et al., Cochin, India. In Fish Shellfish Immunol, Dec 2015
Cdc2, CycA, CycB, EF-1α and BUB3 genes involved in cell cycle were studied in both the cells and tissue, of which EF-1α showed an elevated expression in cells in vitro (∼19.7%).
Dissecting the roles of human BUB1 in the spindle assembly checkpoint.
Kops et al., Utrecht, Netherlands. In J Cell Sci, Sep 2015
Unattached kinetochores catalyze the formation of a diffusible APC/C(CDC20) inhibitor that comprises BUBR1 (also known as BUB1B), BUB3, MAD2 (also known as MAD2L1) and a second molecule of CDC20.
Widespread Recurrent Patterns of Rapid Repeat Evolution in the Kinetochore Scaffold KNL1.
Kops et al., Utrecht, Netherlands. In Genome Biol Evol, Aug 2015
When phosphorylated, these motifs form docking sites for the BUB1-BUB3 dimer that regulates chromosome biorientation and the spindle assembly checkpoint.
In situ carcinoma developed over oral lichen planus: a case report with analysis of BUB3, p16, p53, Ki67 and SOX4 expression.
Amorim et al., Brasília, Brazil. In J Appl Oral Sci, Jul 2015
There was strong nuclear BUB3 staining in both OLP and ISOC areas.
A motif from Lys216 to Lys222 in human BUB3 protein is a nuclear localization signal and critical for BUB3 function in mitotic checkpoint.
Kang et al., Shanghai, China. In J Biol Chem, Jun 2015
Human BUB3 is a key mitotic checkpoint factor that recognizes centromeric components and recruits other mitotic checkpoint molecules to the unattached kinetochore.
Sequential multisite phospho-regulation of KNL1-BUB3 interfaces at mitotic kinetochores.
Kops et al., Utrecht, Netherlands. In Mol Cell, Apr 2015
Regulated recruitment of the kinase-adaptor complex BUB1/BUB3 to kinetochores is crucial for correcting faulty chromosome-spindle attachments and for spindle assembly checkpoint (SAC) signaling.
The role of BUB and CDC proteins in low-grade breast cancers.
Ellis et al., Nottingham, United Kingdom. In Lancet, Mar 2015
METHODS: The Nottingham Tenovus Primary Breast Cancer Series (n=1858) microarrays were immunostained for BUB (BUB1, BUB1B, BUB3) and CDC proteins (CDC2, CDC42) and expression correlated with clinicopathological and molecular variables and patient outcome (SPSS, version 22).
Three BUB1 and BUBR1/MAD3-related spindle assembly checkpoint proteins are required for accurate mitosis in Arabidopsis.
Favery et al., Antibes, France. In New Phytol, 2015
We show that Arabidopsis SAC proteins BUB3.1, MAD2, BUBR1/MAD3s and BRK1 interact with each other and with MAP65-3.
Genetic variation in the major mitotic checkpoint genes and risk of breast cancer: a multigenic study on cancer susceptibility.
Zhao et al., Hangzhou, China. In Tumour Biol, 2014
We conducted this hospital-based case-control study to investigate whether genetic variants in three major spindle checkpoint genes (BUB3, MAD2L1, and BUB1) had any bearing on an individual risk of breast cancer (BC).
Novel downstream molecular targets of SIRT1 in melanoma: a quantitative proteomics approach.
Ahmad et al., Madison, United States. In Oncotarget, 2014
Real-Time qRT-PCR validation showed that five of these (PSAP, MYO1B, MOCOS, HIS1H4A and BUB3) were differentially expressed at mRNA levels.
Cordyceps cicadae induces G2/M cell cycle arrest in MHCC97H human hepatocellular carcinoma cells: a proteomic study.
Wan et al., Hong Kong, Hong Kong. In Chin Med, 2013
Meanwhile, the proteins with downregulated expression were 14-3-3 gamma, BUB3, microtubule-associated protein RP/EB family member 1, thioredoxin-like protein, chloride intracellular channel protein 1, ectonucleoside triphosphate diphosphohydrolase 5, xaa-Pro dipeptidase, enoyl-CoA delta isomerase 1, protein-disulfide isomerase-related chaperone Erp29, hnRNP 2H9B, peroxiredoxin 1, WD-40 repeat protein, and serine/threonine kinase receptor-associated protein.
Bub3p facilitates spindle checkpoint silencing in fission yeast.
Hardwick et al., Edinburgh, United Kingdom. In Mol Biol Cell, 2009
Spindle checkpoint proteins are severely depleted from unattached kinetochores in fission yeast cells lacking Bub3p.
Bub1 and Bub3 promote the conversion from monopolar to bipolar chromosome attachment independently of shugoshin.
Hauf et al., Tübingen, Germany. In Embo Rep, 2009
find that Bub3 is also dispensable for shugoshin localization to the centromeres, which is the second known function of Bub1.
TAp73alpha binds the kinetochore proteins Bub1 and Bub3 resulting in polyploidy.
De Laurenzi et al., Roma, Italy. In Cell Cycle, 2009
Results suggest a novel molecular mechanism leading to aneuploidy involving interference of TAp73alpha with Bub1 and Bub3 resulting in an altered mitotic checkpoint.
Bub3 is a spindle assembly checkpoint protein regulating chromosome segregation during mouse oocyte meiosis.
Sun et al., Beijing, China. In Plos One, 2008
as a member of the spindle assembly checkpoint, Bub3 is required for regulation of both meiosis I and II, and is potentially involved in kinetochore-microtubule attachment in mammalian oocytes
Schizosaccharomyces pombe Bub3 is dispensable for mitotic arrest following perturbed spindle formation.
Niwa et al., Kisarazu, Japan. In Genetics, 2008
the bub3 mutation only weakly affected the stability of minichromosome Ch16 compared with other spindle assembly checkpoint mutants
Willmar Schwabe Award 2006: antiplasmodial and antitumor activity of artemisinin--from bench to bedside.
Efferth, Heidelberg, Germany. In Planta Med, 2007
The identified genes are from classes with diverse biological functions; for example, regulation of proliferation (BUB3, cyclins, CDC25A), angiogenesis (vascular endothelial growth factor and its receptor, matrix metalloproteinase-9, angiostatin, thrombospondin-1) or apoptosis (BCL-2, BAX, NF-kappaB).
Genomic models of metastatic cancer: functional analysis of death-from-cancer signature genes reveals aneuploid, anoikis-resistant, metastasis-enabling phenotype with altered cell cycle control and activated Polycomb Group (PcG) protein chromatin silencing pathway.
Glinsky, Albany, United States. In Cell Cycle, 2006
This analysis predicts that cancer cells manifesting a stem cell-like expression profile of a death-from-cancer signature would exhibit the following features: a concomitantly increased expression of certain members of inhibitor of apoptosis protein (IAP) family (Survivin and XIAP); activation of mitotic spindle check point proteins (BUB1, BUB3, KNTC2, Mad2, PLK1, PLK4, STK6/Aurora A); and elevated levels of certain cell cycle control/marker proteins (CCNB1, CCNB2, CCND1, CCNA2, CDC2, CDC25, Ki67, USP22).
Mechanistic perspectives for 1,2,4-trioxanes in anti-cancer therapy.
Efferth, Heidelberg, Germany. In Drug Resist Updat, 2005
These genes are from classes with different biological function; for example, regulation of proliferation (BUB3, cyclins, CDC25A), angiogenesis (vascular endothelial growth factor and its receptor, matrix metalloproteinase-9, angiostatin, thrombospondin-1) or apoptosis (BCL-2, BAX).
Suppression of spontaneous chromosomal rearrangements by S phase checkpoint functions in Saccharomyces cerevisiae.
Kolodner et al., San Diego, United States. In Cell, 2001
Mutations in Saccharomyces cerevisiae RFC5, DPB11, MEC1, DDC2 MEC3, RAD53, CHK1, PDS1, and DUN1 increased the rate of genome rearrangements up to 200-fold whereas mutations in RAD9, RAD17, RAD24, BUB3, and MAD3 had little effect.
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