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Paired box 5

Pax5, BSAP
This gene encodes a member of the paired box (PAX) family of transcription factors. The central feature of this gene family is a novel, highly conserved DNA-binding motif, known as the paired box. PAX proteins are important regulators in early development, and alterations in the expression of their genes are thought to contribute to neoplastic transformation. This gene encodes the B-cell lineage specific activator protein that is expressed at early, but not late stages of B-cell differentiation. Its expression has also been detected in developing CNS and testis and so the encoded protein may also play a role in neural development and spermatogenesis. This gene is located at 9p13, which is involved in t(9;14)(p13;q32) translocations recurring in small lymphocytic lymphomas of the plasmacytoid subtype, and in derived large-cell lymphomas. This translocation brings the potent E-mu enhancer of the IgH gene into close proximity of the PAX5 promoter, suggesting that the deregulation of transcription of this gene contributes to the pathogenesis of these lymphomas. Alternatively spliced transcript variants encoding different isoforms have been described but their biological validity has not been determined. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: CAN, CD20, HAD, CD19, CD30
Papers using Pax5 antibodies
Dimerization-induced corepressor binding and relaxed DNA-binding specificity are critical for PML/RARA-induced immortalization
Koeffler H. Phillip et al., In Oncogene, 2005
... Transcription factor Pax5 activates the chromatin of key genes involved in B-cell signaling, adhesion, migration, and immune ...
Aberrant promoter methylation of the transcription factor genes PAX5 alpha and beta in human cancers
Macon William R et al., In Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc, 2002
... 8.0 for 30 min at 97°C (PT Module; Lab Vision, Fremont, CA) and staining for PAX5 (1:200, clone 24, BD Bioscience) on a Dako (Carpinteria, CA) autostainer using ...
Skeletal complications in hairy cell leukemia: diagnosis and therapy
Sohani Aliyah R. et al., In Journal of Hematopathology, 1987
Papers on Pax5
High-resolution antibody array analysis of childhood acute leukemia cells.
Kalina et al., Praha, Czech Republic. In Mol Cell Proteomics, Feb 2016
From non-CD markers, we found DBN1, PAX5, or PTK2 overexpressed in B-cell precursor acute lymphoblastic leukemias, LAT, SH2D1A, or STAT5A overexpressed in T-cell acute lymphoblastic leukemias, and HCK, GLUD1, or SYK overexpressed in acute myeloid leukemias.
Intrafollicular Epstein-Barr virus-positive large B cell lymphoma. A variant of "germinotropic" lymphoproliferative disorder.
Facchetti et al., Brescia, Italy. In Virchows Arch, Feb 2016
FISH analysis was performed in two cases and showed no translocations of BCL2, BCL6, MYC, and PAX5 genes.
[Detection of copy number variations in pediatric ETV6/RUNX1-positive acute lymphoblastic leukemia with multiplex ligation-dependent probe amplification].
Zhu et al., Tianjin, China. In Zhongguo Dang Dai Er Ke Za Zhi, Jan 2016
The CNVs of EBF1, CDKN2A/2B, PAX5, ETV6, RB1, and BTG1 were detected in more than 10% of all the patients.
GEMMs addressing Pax5 loss-of-function in childhood pB-ALL.
Hauer et al., Düsseldorf, Germany. In Eur J Med Genet, Dec 2015
This review focuses on PAX5 loss-of-function and summarizes techniques of murine model generation, available GEMMs, which mimic Pax5 loss-of-function in leukemia development and discusses the challenges and drawbacks of these models.
Non-coding recurrent mutations in chronic lymphocytic leukaemia.
Campo et al., Oviedo, Spain. In Nature, Nov 2015
In addition, mutations in an enhancer located on chromosome 9p13 result in reduced expression of the B-cell-specific transcription factor PAX5.
Genomics and drug profiling of fatal TCF3-HLF-positive acute lymphoblastic leukemia identifies recurrent mutation patterns and therapeutic options.
Yaspo et al., Düsseldorf, Germany. In Nat Genet, Sep 2015
We identified recurrent intragenic deletions of PAX5 or VPREB1 in constellation with the fusion of TCF3 and HLF.
A robust in vivo model for B cell precursor acute lymphoblastic leukemia.
Aplan et al., In J Clin Invest, Sep 2015
In this issue of the JCI, Duque-Afonso et al. develop an accurate in vivo model for BCP ALL that recapitulates the key features of human disease, including acquired mutations in genes encoding PAX5 and components of the JAK/STAT pathway.
Transcription factor networks in B-cell differentiation link development to acute lymphoid leukemia.
Sigvardsson et al., Linköping, Sweden. In Blood, Aug 2015
Over the last few years, high-resolution analysis of genetic changes in leukemia has revealed that several key regulators of normal B-cell development, including IKZF1, TCF3, EBF1, and PAX5, are genetically altered in a large portion of the human B-lineage acute leukemias.
EBV noncoding RNA binds nascent RNA to drive host PAX5 to viral DNA.
Steitz et al., New Haven, United States. In Cell, Mar 2015
Probing its possible chromatin localization by CHART revealed EBER2's presence at the terminal repeats (TRs) of the latent EBV genome, overlapping previously identified binding sites for the B cell transcription factor PAX5. EBER2 interacts with PAX5 and is required for the localization of PAX5 to the TRs.
The role of Pax5 in leukemia: diagnosis and prognosis significance.
Saki et al., Tehrān, Iran. In Med Oncol, 2015
Pax5 transcription factor, also known as B-cell specific activator protein (BSAP), plays a dual role in the hematopoietic system.
Cytogenetic Study and Analysis of Protein Expression in Plasma Cell Myeloma with t(11;14)(q13;q32): Absence of BCL6 and SOX11, and Infrequent Expression of CD20 and PAX5.
Miura et al., In J Clin Exp Hematop, 2014
PAX5 is an essential transcriptional factor involved in B-cell development and commitment, and is down-regulated upon plasma cell differentiation.
Genes and childhood leukemia.
Januszkiewicz-Lewandowska et al., Poznań, Poland. In Postepy Hig Med Dosw (online), 2014
Common lesions include translocations to T cell receptor (TCR) loci in T-lineage acute lymphoblastic leukemia (T-ALL), mutations of transcription factors regulating B-lineage development and cell maturation in B-lineage acute lymphoblastic leukemia (B-ALL) (PAX5, TCF3, EBF1, etc.), aberrational disruption of genes coding for transcription factors and coactivators in acute myeloid leukemia (AML) (e.g.
One missense mutation in exon 2 of the PAX5 gene in Iran.
Jaseb et al., Ahvāz, Iran. In Genet Mol Res, 2014
The PAX5 gene, which encodes the B-cell specific activator protein, is one of the most important factors in determination of B-cell development.
A recurrent germline PAX5 mutation confers susceptibility to pre-B cell acute lymphoblastic leukemia.
Offit et al., New York City, United States. In Nat Genet, 2013
Somatic alterations of the lymphoid transcription factor gene PAX5 (also known as BSAP) are a hallmark of B cell precursor acute lymphoblastic leukemia (B-ALL), but inherited mutations of PAX5 have not previously been described.
Germline PAX5 mutations and B cell leukemia.
Liu et al., Bethesda, United States. In Nat Genet, 2013
The transcription factor PAX5 is required for normal B cell development and is frequently mutated or deleted in B cell precursor acute lymphoblastic leukemia (B-ALL).
PAX5-AUTS2: a recurrent fusion gene in childhood B-cell precursor acute lymphoblastic leukemia.
Strehl et al., Vienna, Austria. In Leuk Res, 2012
PAX5-AUTS2: a recurrent fusion gene in childhood B-cell precursor acute lymphoblastic leukemia.
The B-cell identity factor Pax5 regulates distinct transcriptional programmes in early and late B lymphopoiesis.
Busslinger et al., Vienna, Austria. In Embo J, 2012
Pax5 controls B-cell identity and function by regulating distinct target genes in early and late B lymphopoiesis.
B cell receptor-ERK1/2 signal cancels PAX5-dependent repression of BLIMP1 through PAX5 phosphorylation: a mechanism of antigen-triggering plasma cell differentiation.
Naoe et al., Nagoya, Japan. In J Immunol, 2012
These data imply that PAX5 phosphorylation by the B-cell receptor signal is the initial event in plasma cell differentiation
Sequential array comparative genomic hybridization analysis identifies copy number changes during blastic transformation of chronic myeloid leukemia.
Kim et al., Seoul, South Korea. In Leuk Res, 2012
we identified a novel fusion gene consisted of PAX5 and MLLT3 during progression from chronic phase to blastic phase in chronic myeloid leukemia
Genome-wide association study of intelligence: additive effects of novel brain expressed genes.
Nelson et al., Los Angeles, United States. In J Am Acad Child Adolesc Psychiatry, 2012
Genome-wide significance in genes involved in synaptic signaling (KIF16B; p = 1.27E-08) and neurodevelopment (PAX5; p = 3.58E-08).
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