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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 (Montrer IFNA Protéines))-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 (Montrer MLXIP Protéines)-125b can act as an oncogene (Montrer RAB1A Protéines) in B-cell acute lymphoblastic leukemia by targeting ARID3a and mediating its repression.
These findings support the hypothesis that Epstein-Barr virus EBNA1 (Montrer EBNA-1 Protéines) initiates transcription at the C promoter via interactions between multiple EBNA1 (Montrer EBNA-1 Protéines) homodimers and cellular transcription such as E2F1 (Montrer E2F1 Protéines), ARID3A and Oct-2.
These results indicate both cooperative and interdependent roles for ARID3A and p53 (Montrer TP53 Protéines) in the transcriptional activation of p21(WAF1 (Montrer CDKN1A Protéines)) in response to DNA damage.
functions as a critical antagonist to the p16(INK4A)-Rb tumor suppressor machinery by regulating promyelocytic leukemia protein (Montrer PML Protéines) 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.
Here, the authors show that adam13 (Montrer ADAM33 Protéines) 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 (Montrer TFAP2A Protéines). Tfap2alpha (Montrer TFAP2A Protéines) in turn activates multiple genes including the protocadherin pcdh8l (PCNS).
dril1 is a novel regulator of TGF(beta (Montrer TGFB1 Protéines)) 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 results place Bright/Arid3a on a select list of transcriptional regulators required to program both hematopoietic stem cell and lineage-specific differentiation.
Id1 (Montrer ID1 Protéines) 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 (Montrer ID1 Protéines) through inhibition of the profibrotic function of Dril1.(Dril1)
The ability of Bright to enhance immunoglobulin transcription critically requires functional Bruton's tyrosine kinase (Montrer BTK Protéines) .
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.
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)