High-resolution antibody array analysis of childhood acute leukemia cells.
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.
GEMMs addressing Pax5 loss-of-function in childhood pB-ALL.
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.
EBV noncoding RNA binds nascent RNA to drive host PAX5 to viral DNA.
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.
Genes and childhood leukemia.
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.
Germline PAX5 mutations and B cell leukemia.
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).