| A+T rich interaction domain protein 3a (Arid3a) impairs Mertk-mediated efferocytosis in cholestasis. | A+T rich interaction domain protein 3a (Arid3a) impairs Mertk-mediated efferocytosis in cholestasis.
Chen R, Huang B, Lian M, Wei Y, Miao Q, Liang J, Ou Y, Liang X, Zhang H, Li Y, Xiao X, Wang Q, You Z, Chai J, Gershwin ME, Tang R, Ma X. | 01/31/2024 |
| Comprehensive analysis identified a reduction in ATP1A2 mediated by ARID3A in abdominal aortic aneurysm. | Comprehensive analysis identified a reduction in ATP1A2 mediated by ARID3A in abdominal aortic aneurysm.
Wang Q, Li N, Guo X, Huo B, Li R, Feng X, Fang Z, Zhu XH, Wang Y, Yi X, Wei X, Jiang DS., Free PMC Article | 05/21/2022 |
| Crucial Role of Increased Arid3a at the Pre-B and Immature B Cell Stages for B1a Cell Generation. | Crucial Role of Increased Arid3a at the Pre-B and Immature B Cell Stages for B1a Cell Generation.
Hayakawa K, Li YS, Shinton SA, Bandi SR, Formica AM, Brill-Dashoff J, Hardy RR., Free PMC Article | 09/5/2020 |
| Our data show that signals provided by thymic epithelial cells control thymic B cell development by up-regulating Let-7, suppressing Arid3a expression in intrathymic progenitor B cells to limit their proliferation during the neonatal to adult transition. | Thymic epithelial cell-derived signals control B progenitor formation and proliferation in the thymus by regulating Let-7 and Arid3a.
Xiao S, Zhang W, Manley NR., Free PMC Article | 05/26/2018 |
| ARID3A is required for normal murine trophoblast development in vivo. The results reveal an essential, conserved function for ARID3A in mammalian placental development through regulation of both intrinsic and extrinsic developmental programs. | ARID3A is required for mammalian placenta development.
Rhee C, Edwards M, Dang C, Harris J, Brown M, Kim J, Tucker HO., Free PMC Article | 06/3/2017 |
| identify the Arid3a transcription factor as a key target of Let-7, whose ectopic expression is sufficient to induce B-1 development in adult pro-B cells and whose silencing by knockdown blocks B-1 development in fetal pro-B cells. | Lin28b promotes fetal B lymphopoiesis through the transcription factor Arid3a.
Zhou Y, Li YS, Bandi SR, Tang L, Shinton SA, Hayakawa K, Hardy RR., Free PMC Article | 06/20/2015 |
| These data reveal new functions for ARID3a in early hematopoiesis and suggest that knowledge regarding ARID3a levels in HSPCs could be informative for applications requiring transplantation of those cells. | Differential expression of the transcription factor ARID3a in lupus patient hematopoietic progenitor cells.
Ratliff ML, Ward JM, Merrill JT, James JA, Webb CF., Free PMC Article | 04/18/2015 |
| identify Arid3a as a critical regulator of TE and placental development through execution of the commitment and differentiation phases of the first cell fate decision | Arid3a is essential to execution of the first cell fate decision via direct embryonic and extraembryonic transcriptional regulation.
Rhee C, Lee BK, Beck S, Anjum A, Cook KR, Popowski M, Tucker HO, Kim J., Free PMC Article | 12/20/2014 |
| These data suggest a novel role for Bright in the normal development of mature B cell subsets and in autoantibody production | The transcription factor Bright plays a role in marginal zone B lymphocyte development and autoantibody production.
Oldham AL, Miner CA, Wang HC, Webb CF., Free PMC Article | 12/24/2011 |
| these results place Bright/Arid3a on a select list of transcriptional regulators required to program both hematopoietic stem cell and lineage-specific differentiation. | The ARID family transcription factor bright is required for both hematopoietic stem cell and B lineage development.
Webb CF, Bryant J, Popowski M, Allred L, Kim D, Harriss J, Schmidt C, Miner CA, Rose K, Cheng HL, Griffin C, Tucker PW., Free PMC Article | 04/9/2011 |
| Id1 inhibited DNA binding by Dril1, and the two proteins co-localized in vitro and in vivo, providing a potential mechanism for suppression of fibrosis by Id1 through inhibition of the profibrotic function of Dril1.(Dril1) | Cross talk between Id1 and its interactive protein Dril1 mediate fibroblast responses to transforming growth factor-beta in pulmonary fibrosis.
Lin L, Zhou Z, Zheng L, Alber S, Watkins S, Ray P, Kaminski N, Zhang Y, Morse D., Free PMC Article | 03/9/2011 |
| Bright/ARID3a inhibition causes increased developmental plasticity in mouse and human cells. | Loss of Bright/ARID3a function promotes developmental plasticity.
An G, Miner CA, Nixon JC, Kincade PW, Bryant J, Tucker PW, Webb CF., Free PMC Article | 11/13/2010 |
| A palmitoylated pool of Bright is diverted to lipid rafts of resting B cells where it associates with signalosome components. | Signalling of the BCR is regulated by a lipid rafts-localised transcription factor, Bright.
Schmidt C, Kim D, Ippolito GC, Naqvi HR, Probst L, Mathur S, Rosas-Acosta G, Wilson VG, Oldham AL, Poenie M, Webb CF, Tucker PW., Free PMC Article | 01/21/2010 |
| Bright functions in a subset of Bruton's tyrosine kinase-dependent pathways in vivo, particularly those responses dominated by B1 B cells. | Transgenic mice expressing dominant-negative bright exhibit defects in B1 B cells.
Nixon JC, Ferrell S, Miner C, Oldham AL, Hochgeschwender U, Webb CF., Free PMC Article | 01/21/2010 |
| identify regions within Bright that are required for the DNA binding activity of Bright and for its function as a transcription factor | Mutations in the DNA-binding domain of the transcription factor Bright act as dominant negative proteins and interfere with immunoglobulin transactivation.
Nixon JC, Rajaiya J, Webb CF. | 01/21/2010 |
| Variations in Bright binding and matrix attachment region activity contribute to localized control of accessibility and therefore nonrandom gene use during V(D)J recombination. | High frequency of matrix attachment regions and cut-like protein x/CCAAT-displacement protein and B cell regulator of IgH transcription binding sites flanking Ig V region genes.
Goebel P, Montalbano A, Ayers N, Kompfner E, Dickinson L, Webb CF, Feeney AJ. | 01/21/2010 |
| The ability of Bright to enhance immunoglobulin transcription critically requires functional Bruton's tyrosine kinase . | Bruton's tyrosine kinase regulates immunoglobulin promoter activation in association with the transcription factor Bright.
Rajaiya J, Hatfield M, Nixon JC, Rawlings DJ, Webb CF., Free PMC Article | 01/21/2010 |
| For IgH transactivation, Bright binds to nuclear matrix association regions.Bright actively shuttles between the nucleus and the cytoplasm, regulation of Bright's cellular localization appears to be required for its function. | A regulated nucleocytoplasmic shuttle contributes to Bright's function as a transcriptional activator of immunoglobulin genes.
Kim D, Tucker PW., Free PMC Article | 01/21/2010 |