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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Pre B cell leukemia homeobox 3

Top mentioned proteins: Meis1, HOXA9, miR, MLL, p21
Papers on PBX3
PBX3 and MEIS1 cooperate in hematopoietic cells to drive acute myeloid leukemias characterized by a core transcriptome of the MLL-rearranged disease.
Chen et al., Chapel Hill, United States. In Cancer Res, Feb 2016
UNASSIGNED: Overexpression of HOXA/MEIS1/PBX3 homeobox genes is the hallmark of mixed lineage leukemia (MLL)-rearranged acute myeloid leukemia (AML).
EWSR1-PBX3: a novel gene fusion in myoepithelial tumors.
Antonescu et al., New York City, United States. In Genes Chromosomes Cancer, Feb 2015
We investigated by RNA sequencing an index case of EWSR1-rearranged ME of the tibia, lacking a known fusion partner, and identified a novel EWSR1-PBX3 fusion.
PBX3 promotes migration and invasion of colorectal cancer cells via activation of MAPK/ERK signaling pathway.
Zhang et al., Beijing, China. In World J Gastroenterol, 2015
METHODS: We detected PBX3 expression in five cell lines and surgical specimens from 111 patients with CRC using real-time reverse transcription-polymerase chain reaction.
PBX3 is targeted by multiple miRNAs and is essential for liver tumour-initiating cells.
Zhang et al., Beijing, China. In Nat Commun, 2014
Interestingly, all the four miRNAs synergistically target PBX3, which is sufficient and necessary for the acquisition and maintenance of TIC properties.
Fusion of the genes EWSR1 and PBX3 in retroperitoneal leiomyoma with t(9;22)(q33;q12).
Heim et al., Oslo, Norway. In Plos One, 2014
The translocation resulted in an EWSR1-PBX3 fusion gene in which exon 9 of EWSR1 (nucleotide 1320 accession number NM_013986 version 3) was in-frame fused to exon 5 of PBX3 (nucleotide 824 accession number NM_006195 version 5).
The miR-302 cluster transcriptionally regulated by POUV, SOX and STAT5B controls the undifferentiated state through the post-transcriptional repression of PBX3 and E2F7 in early chick development.
Byun et al., Suwŏn, South Korea. In Mol Reprod Dev, 2014
For example, microRNAs from the miR-302 cluster can bind to PBX3 and E2F7 transcripts, thus acting as a post-transcriptional regulator that maintains the undifferentiated state of blastodermal cells by balancing the expression of genes related to pluripotency and differentiation.
PU.1 is essential for MLL leukemia partially via crosstalk with the MEIS/HOX pathway.
Wang et al., Beijing, China. In Leukemia, 2014
We further identified a PU.1-governed 15-gene signature, which contains key regulators in the MEIS-HOX program (MEIS1, PBX3, FLT3, and c-KIT).
PBX3 is overexpressed in gastric cancer and regulates cell proliferation.
Xu et al., Shenyang, China. In Tumour Biol, 2014
The pre-leukemia transcription factor 3 (PBX3) is a member of the PBX family of transcription factors, which is known to increase DNA-binding/transcriptional activity of HOX proteins and regulate genes involved in development.
CBFB-MYH11 hypomethylation signature and PBX3 differential methylation revealed by targeted bisulfite sequencing in patients with acute myeloid leukemia.
Beneš et al., In J Hematol Oncol, 2013
Further, by comparing all targeted methylation and microarray expression data, PBX3 differential methylation was found to correlate with its gene expression.
HOXA/PBX3 knockdown impairs growth and sensitizes cytogenetically normal acute myeloid leukemia cells to chemotherapy.
Thompson et al., Belfast, United Kingdom. In Haematologica, 2013
An 11 HOXA/TALE code identified in an intermediate-risk group of patients (n=315) compared to a group with a favorable risk (n=105) was reduced to a four-gene signature of HOXA6, HOXA9, PBX3 and MEIS1 by iterative analysis of independent platforms.
PBX3 is an important cofactor of HOXA9 in leukemogenesis.
Chen et al., Chicago, United States. In Blood, 2013
Although PBX proteins are known to increase DNA-binding/transcriptional activity of HOX proteins through their direct binding, the functional importance of their interaction in leukemogenesis is unclear.We recently reported that overexpression of a 4-homeobox-gene signature (ie, PBX3/HOXA7/HOXA9/HOXA11) is an independent predictor of poor survival in patients with cytogenetically abnormal acute myeloid leukemia (CA-AML).
MicroRNA profiling in pediatric pilocytic astrocytoma reveals biologically relevant targets, including PBX3, NFIB, and METAP2.
Rodriguez et al., Baltimore, United States. In Neuro Oncol, 2013
Predicted targets with increased expression at the mRNA and/or protein level in PA included PBX3, METAP2, and NFIB.
Down-regulation of miR-181c in imatinib-resistant chronic myeloid leukemia.
Knuutila et al., Helsinki, Finland. In Mol Cytogenet, 2012
Some miR-181c target genes such as PBX3, HSP90B1, NMT2 and RAD21 have been associated with drug response.
MiR-495 is a tumor-suppressor microRNA down-regulated in MLL-rearranged leukemia.
Chen et al., Chicago, United States. In Proc Natl Acad Sci U S A, 2012
Furthermore, our studies demonstrate that PBX3 and MEIS1 are two direct target genes of miR-495, and forced expression of either of them can reverse the effects of miR-495 overexpression on inhibiting cell viability and promoting apoptosis of human MLL-rearranged leukemic cells.
Clinical, immunophenotypic, cytogenetic, and molecular genetic features in 117 adult patients with mixed-phenotype acute leukemia defined by WHO-2008 classification.
Chen et al., Suzhou, China. In Haematologica, 2012
Array-CGH revealed genomic deletions of CDKN2A (4 of 12), IKZF1 (3 of 12), MEF2C (2 of 12), BTG1 (2 of 12), together with BCOR, EBF1, K-RAS, LEF1, MBNL1, PBX3, and RUNX1 (one of 12 each).
Non-synonymous variants in pre-B cell leukemia homeobox (PBX) genes are associated with congenital heart defects.
Bowles et al., Salt Lake City, United States. In Eur J Med Genet, 2012
The Pbx3 Ala136Val variant is a modifier or risk allele for congenital heart defects.
Up-regulation of a HOXA-PBX3 homeobox-gene signature following down-regulation of miR-181 is associated with adverse prognosis in patients with cytogenetically abnormal AML.
Chen et al., Chicago, United States. In Blood, 2012
Data show that up-regulation of the HOXA7, HOXA9, HOXA11, and PBX3 resulting from the down-regulation of miR-181 family members probably contribute to the poor prognosis of patients with nonfavorable cytogenetically abnormal AML (CA-AML).
Regulation of PBX3 expression by androgen and Let-7d in prostate cancer.
Taskén et al., Oslo, Norway. In Mol Cancer, 2010
PBX3 is up-regulated in prostate cancer and post- transcriptionally regulated by androgen through Let-7d.
Lack of replication of celiac disease risk variants reported in a Spanish population using an independent Spanish sample.
Núñez et al., Madrid, Spain. In Genes Immun, 2009
our results seem to discard the role of the previously described polymorphisms in SERPINE2, PPP6C and PBX3 in celiac disease susceptibility.
Pbx/Meis deficiencies demonstrate multigenetic origins of congenital heart disease.
Chang et al., Stanford, United States. In Circ Res, 2008
Reduction or absence of Pbx2 or Pbx3 leads to Pbx1 haploinsufficiency and specific malformations that resemble tetralogy of Fallot, overriding aorta with ventricular septal defect, and bicuspid aortic valves.
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