The promoter of the CD19 gene is a target for the B-cell-specific transcription factor BSAP.

Kozmík, Zbyněk; Wang, Shirley; Dörfler, P; Adams, Ben; Busslinger, Meinrad

doi:10.1128/mcb.12.6.2662

Cited by 315 publications

(208 citation statements)

References 38 publications

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“…The specific binding of PAX5 to the human CD19 promoter was shown in a previous study (Kozmik et al, 1992). In a subsequent study we showed that PAX5 binds to both, the promoter and enhancer, of the mouse Cd19 gene loci (Walter et al, 2008).…”

Section: Pax5 Binds To the Cd19 Promoter And Enhancer In B Cellssupporting

confidence: 68%

Aberrant expression of CD19 in AML with t(8;21) involves a poised chromatin structure and PAX5

et al. 2010

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Correct hematopoietic differentiation requires the tightly regulated execution of lineage-specific and stage-restricted gene expression programs. This process is disturbed in hematological malignancies that typically show incomplete differentiation but often also display a mixed lineage phenotype. Co-expression of lymphoid and myeloid molecules is a well-known feature of acute myeloblastic leukemia (AML) with t(8;21). These cells consistently express the B-cell-specific transcription factor PAX5, and the B-cell-specific cell surface protein CD19. However, the functional consequences of PAX5 expression are unknown. To address this question, we studied the chromatin features of CD19, which is a direct target of PAX5 in cells with and without the t(8;21) chromosomal translocation. We show that CD19 chromatin exists in a poised configuration in myeloid progenitors and that this poised chromatin structure facilitates PAX5-dependent CD19 activation. Our results also show a positive correlation between PAX5 and CD19 expression in t(8;21)-positive AML cells and demonstrate that PAX5 binds to the promoter and enhancer of CD19 gene and remodels chromatin structure at the promoter. This study shows that expression of PAX5 in leukemic cells has functional consequences and points to an important role of a progenitor-specific chromatin configuration in myeloid leukemia.

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Section: Pax5 Binds To the Cd19 Promoter And Enhancer In B Cellssupporting

confidence: 68%

Aberrant expression of CD19 in AML with t(8;21) involves a poised chromatin structure and PAX5

et al. 2010

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“…Four SNPs were detected in the promoter region, but these sites are not considered to be binding sites for the important transcription factors such as B cell lineage-specific antigen promoter (BSAP, Pax5). 52 In conclusion, this study demonstrated a number of polymorphisms within human CD19. Association of CD19 3'UTR dinucleotide repeat polymorphism, or another gene in linkage disequilibrium with it, with susceptibility to SLE was suggested.…”

Section: Genes and Immunity Antinuclear Antibodies (Sato S Personal mentioning

confidence: 57%

Polymorphisms of human CD19 gene: possible association with susceptibility to systemic lupus erythematosus in Japanese

et al. 2002

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CD19 regulates the signaling for B lymphocyte development, activation and proliferation. In mice, CD19 deficiency and overexpression were shown to result in hypogammaglobulinemia and autoantibody production, respectively. In the present study, we screened for the polymorphisms of CD19 , and examined the detected polymorphisms for the association with rheumatoid arthritis (RA), Crohn's disease and systemic lupus erythematosus (SLE). Two SNPs, were decreased (P = 0.0096 and P = 0.028, respectively), in SLE. A GT repeat polymorphism, c.*132(GT) [12][13][14][15][16][17][18] , was detected within the 3'-untranslated region, and individuals with у15 times repeat was significantly increased in the independent two groups of Japanese SLE patients (P = 0.011 and P = 0.035, respectively); the overall difference between total SLE and controls was striking (P = 0. [15][16][17][18] alleles compared with those without these alleles, both in controls and in SLE patients; however, the difference did not reach statistical significance. These results suggested that either the slight reduction in the CD19 mRNA level associated with the elongation of GT repeat, or an allele of another locus in linkage disquilibrium with CD19 (GT) [15][16][17][18] , may be associated with susceptibility to SLE in Japanese. 0061). No association was observed for RA and Crohn's disease. In addition, no variations other than the common polymorphisms were detected in four patients with common variable immunodeficiency, the phenotype of which resembles CD19 deficient mice. In Caucasian SLE families, this GT repeat polymorphism was rare. CD19 mRNA level in the isolated peripheral blood B lymphocytes was lower in individuals possessing (GT)

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“…The Tg vector, pCD19-FLIP, encoding Flag-muFLIP under the control of the B cell-specific CD19 promoter was constructed in the pBSKS II(-) vector and contained (a) in the NotI site, a 6.4-kb EagI fragment of vector CD19 XS (containing nucleotides -6435 to -15 of hCD19) [46]; (b) in the BamHI/XhoI sites, nucleotides 421-1592 of rabbit g -globin (comprising the end of exon 2, intron 2, exon 3 and the poly A addition signal) [4]; (c) in the blunted EcoRI site of the g -globin sequence, a 1525-nucleotide sequence encoding Flag-mouse FLIP L (MDYKDDDDKEFGL followed by amino acid residues 2-481 of mouse FLIP L ) [20]. Tg mice were generated by microinjection of the BssHII fragment of pCD19-FLIP into fertilized (C57BL/6×DBA/2) F2 oocytes, and screened by PCR using oligonucleotides JT1822 5'-TCA-AGAGTGAGGCGGTTTGACC-3' and JT1823 5'-TCCTGAT-TCCTGGATGGATGTC-3'.…”

Section: Transgenic Micementioning

confidence: 99%

The anti‐apoptotic factor Bcl‐2 can functionally substitute for the B cell survival but not for the marginal zone B cell differentiation activity of BAFF

et al. 2004

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The TNF family ligand B cell-activating factor (BAFF, BLyS, TALL-1) is an essential factor for B cell development. BAFF binds to three receptors, BAFF-R, transmembrane activator and CAML interactor (TACI), and B cell maturation antigen (BCMA), but only BAFF-R is required for successful survival and maturation of splenic B cells. To test whether the effect of BAFF is due to the up-regulation of anti-apoptotic factors, TACI-Ig-transgenic mice, in which BAFF function is inhibited, were crossed with transgenic mice expressing FLICE-inhibitory protein (FLIP) or Bcl-2 in the B cell compartment. FLIP expression did not rescue B cells, while enforced Bcl-2 expression restored peripheral B cells and the ability to mount T-dependent antibody responses. However, many B cells retained immaturity markers and failed to express normal amounts of CD21. Marginal zone B cells were not restored and the Tindependent IgG3, but not IgM, response was impaired in the TACI-Ig×Bcl-2 mice. These results suggest that BAFF is required not only to inhibit apoptosis of maturating B cells, but also to promote differentiation events, in particular those leading to the generation of marginal zone B cells.

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The promoter of the CD19 gene is a target for the B-cell-specific transcription factor BSAP.

Cited by 315 publications

References 38 publications

Aberrant expression of CD19 in AML with t(8;21) involves a poised chromatin structure and PAX5

Aberrant expression of CD19 in AML with t(8;21) involves a poised chromatin structure and PAX5

Polymorphisms of human CD19 gene: possible association with susceptibility to systemic lupus erythematosus in Japanese

The anti‐apoptotic factor Bcl‐2 can functionally substitute for the B cell survival but not for the marginal zone B cell differentiation activity of BAFF

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