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Data indicate ARID3a(+) B cells as a type of effector B cell, and link ARID3a expression in B lymphocytes to interferon alpha (IFNa)-associated inflammatory responses in systemic lupus erythematosus (SLE).
results suggest that appropriate regulation of ARID3a is critical for normal development of both myeloid and B lineage pathways.
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.
Systemic lupus erythematosus (SLE) patients had increased ARID3a+ B cells compared to healthy controls. ARID3a was not expressed in naive B cells of controls, but was abundant in SLE patients. Number of ARID3a+ B cells correlated with disease activity.
miR-125b can act as an oncogene in B-cell acute lymphoblastic leukemia by targeting ARID3a and mediating its repression.
These findings support the hypothesis that Epstein-Barr virus EBNA1 initiates transcription at the C promoter via interactions between multiple EBNA1 homodimers and cellular transcription such as E2F1, ARID3A and Oct-2.
These results indicate both cooperative and interdependent roles for ARID3A and p53 in the transcriptional activation of p21(WAF1) in response to DNA damage.
functions as a critical antagonist to the p16(INK4A)-Rb tumor suppressor machinery by regulating promyelocytic leukemia protein stability
report that E2FBP1 inhibits accumulation of ICP0 RNA and, at the same time, is degraded via ICP0's herpes ubiquitin ligase 2 (HUL-2) activity upon HSV-1 infection.
Bright/ARID3a inhibition causes increased developmental plasticity in mouse and human cells.
Solution NMR structure of the ARID domain of human ARID3A.
Results show that DRIL1 disrupts cellular protection against RAS(V12)-induced proliferation downstream of the p19(ARF)/p53 pathway.
role in p53 regulatory pathway.(E2FBP1)
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.
a putative p53-binding site was found, which specifically responded to p53, in the second intron of the E2FBP1/DRIL1 gene
E2FBP1 modulates cell growth through down-regulation of promyelocytic leukemia bodies.
Bright is not expressed in all human B lymphocyte subpopulations.
TFII-I directly interacts with Bright through amino acids in Bright's protein interaction domain
identify Bright as a contributor to accessibility of the IgH enhancer
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.
Here, the authors show that adam13 interacts with the arid3a/dril1/Bright transcription factor. This interaction promotes a proteolytic cleavage of arid3a and its translocation to the nucleus where it regulates another transcription factor: tfap2alpha. Tfap2alpha in turn activates multiple genes including the protocadherin pcdh8l (PCNS).
dril1 is a novel regulator of TGF(beta) signaling and a vital component of mesodermal patterning and embryonic morphogenesis.
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.
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.
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.
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
These data suggest a novel role for Bright in the normal development of mature B cell subsets and in autoantibody production
these results place Bright/Arid3a on a select list of transcriptional regulators required to program both hematopoietic stem cell and lineage-specific differentiation.
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)
identify regions within Bright that are required for the DNA binding activity of Bright and for its function as a transcription factor
The ability of Bright to enhance immunoglobulin transcription critically requires functional Bruton's tyrosine kinase .
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.
Bright functions in a subset of Bruton's tyrosine kinase-dependent pathways in vivo, particularly those responses dominated by B1 B cells.
A palmitoylated pool of Bright is diverted to lipid rafts of resting B cells where it associates with signalosome components.
This gene encodes a member of the ARID (AT-rich interaction domain) family of DNA binding proteins. It was found by homology to the Drosophila dead ringer gene, which is important for normal embryogenesis. Other ARID family members have roles in embryonic patterning, cell lineage gene regulation, cell cycle control, transcriptional regulation, and possibly in chromatin structure modification.
AT rich interactive domain 3A (BRIGHT-like)
, AT-rich interactive domain-containing protein 3A-like
, AT-rich interactive domain-containing protein 3A
, dead ringer homolog 1
, ARID domain-containing 3A
, ARID domain-containing protein 3A
, AT rich interactive domain 3A (BRIGHT- like) protein
, B-cell regulator of IgH transcription
, E2F-binding protein 1
, dead ringer-like 1
, dead ringer-like protein 1
, bright homolog
, AT rich interactive domain 3A (Bright like)