The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

Links

 

Gene Review

ARID3A  -  AT rich interactive domain 3A (BRIGHT-like)

Homo sapiens

Synonyms: ARID domain-containing protein 3A, AT-rich interactive domain-containing protein 3A, B-cell regulator of IgH transcription, BRIGHT, Bright, ...
 
 
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.
 

Disease relevance of ARID3A

  • Analysis of those genes most commonly compromized in tumours has led to the identification of the transcription factor p53 and the E2F binding protein Retinoblastoma (Rb), as key regulators of these processes [1].
  • The human dead ringer/bright homolog, DRIL1: cDNA cloning, gene structure, and mapping to D19S886, a marker on 19p13.3 that is strictly linked to the Peutz-Jeghers syndrome [2].
  • Within a few years of its occurrence, American clinicians became aware of the discovery by Bright in 1827 that albuminuria in edematous patients was associated with granular degeneration of the kidney [3].
  • He was strongly influenced by the previous work of Richard Bright on kidney disease at his own hospital (Guy's Hospital in London) and by the contemporary pathological studies of Gull and Sutton on arteriolar changes in persons with high blood pressure [4].
  • Three years later, he published a study of apoplexy in Bright's disease, in which he pointed clearly to the role of raised intra-arterial tension in the causation of arterial disease, a point that had eluded Bright, Johnson, and other contemporaries [5].
 

Psychiatry related information on ARID3A

  • BACKGROUND: Bright light therapy is the recommended treatment for winter seasonal affective disorder (SAD) [6].
  • Effects of four conditions (Dim Light-Placebo, Dim Light-Caffeine, Bright Light-Placebo and Bright Light-Caffeine) on alertness, and performance were studied during the night-time hours across 45.5 h of sleep deprivation [7].
  • CONCLUSIONS: Bright light exposure was effective in reducing daytime sleep in nursing home patients with dementia; this finding is possibly related to bright light's acute alerting effects [8].
  • 1. Bright light exposure has been demonstrated as an effective treatment for circadian rhythm sleep disorders [9].
  • PURPOSE: Pediatricians are encouraged by the American Academy of Pediatrics and Bright Futures guidelines to use well-child care as an opportunity to promote learning and development, encourage positive parenting practices, help children acquire behavioral self-control, and enhance the well-being of children and their families [10].
 

High impact information on ARID3A

 

Chemical compound and disease context of ARID3A

 

Biological context of ARID3A

  • Although E2FBP1 lacks the transactivation domain, it stimulates E2F site-dependent transcription in cooperation with E2F-1 [15].
  • One of the clones encodes E2FBP1 which has the helix-loop-helix (HLH) motif, but lacks the basic domain and the zipper structure usually found at N- and C-terminal sides to the HLH motif, respectively [15].
  • Here we show a novel connection between E2FBP1/DRIL1 and the p53 tumor suppressor, a key regulator of growth arrest or apoptosis in response to cellular stress [16].
  • E2FBP1/DRIL1was induced by p53 and up-regulated following DNA damage caused by UV radiation or doxorubicin treatment in a manner dependent on endogenous p53 [16].
  • Leptomycin B, chromosome region maintenance 1 (CRM1) overexpression, and heterokaryon experiments indicate that Bright actively shuttles between the nucleus and the cytoplasm in a CRM1-dependent manner [17].
 

Anatomical context of ARID3A

  • Bright/ARID3a/Dril1, a member of the ARID family of transcription factors, is expressed in a highly regulated fashion in B lymphocytes, where it enhances immunoglobulin transcription three- to sixfold [18].
  • For IgH transactivation, Bright binds to nuclear matrix association regions upstream of certain variable region promoters and flanking the IgH intronic enhancer [17].
  • However, an immunoglobulin M monoclonal antibody with specificity for the p73 LPS receptor in murine splenocytes (S. W. Bright, T.-Y. Chen, L. M. Flebbe, M.-G. Lei, and D. C. Morrison, J. Immunol. 145:1-7, 1990) inhibited 125I-ASD-PT labeling of the 70-kDa species in Jurkat cells [19].
  • At the end of each experimental period, MRI was performed using 7-T magnet Bruker Avance DRX 300 (Bruker, Wissembourg); T1-weighted MRI acquisition parameters were applied to show predominantly muscle fibers [20].
  • After a 0.038 Magic Torque wire (Boston Scientific/Medi-Tech, Watertown, MA) was anchored with the tip of the wire in the distal left occipital artery, a 7-French (outer diameter) Vista Bright guiding sheath (Cordis, Miami, FL) was successfully positioned in the mid left common carotid artery, with an MPA catheter (Cordis) used as guiding support [21].
 

Associations of ARID3A with chemical compounds

  • The flavoenzyme D-amino acid oxidase (Eo) is rapidly chlorinated by N-chloro-D-leucine (Rudie, N.G., Porter, D.J.T., and Bright, H.J. (1980) J. Biol. Chem. 255, 498-508) [22].
  • Using a new and simplified technique for covalent immobilization of adenine nucleotides [Fuller, C. W. and Bright, H. J., J. Biol. Chem. 252, 6631 (1977)], we have prepared immobilized NADH using two water-soluble polymers and tested these preparations for activity with several dehydrogenases [23].
  • RESULTS: Bright light delayed the nocturnal melatonin peak by 2 hours and resulted in a decrease in cortisol concentrations [24].
  • Further, the combined treatment of caffeine and all-night bright light (Bright Light-Caffeine) enhanced performance to a larger degree than either the Dim Light-Caffeine or the Bright Light-Placebo condition [7].
  • Further, FTIR (which provides information about the changes in the surface groups of the HU) and DRX (which shows the formation of possible crystalline phases on the HU surface) were used to determine the specific interactions of Cu(II) cations with the surface reactive groups of HU [25].
 

Regulatory relationships of ARID3A

  • A novel E2F binding protein with Myc-type HLH motif stimulates E2F-dependent transcription by forming a heterodimer [15].
  • Because so little is known about human Bright, we sought to determine where human Bright is expressed in normal B cell differentiation and whether it also forms complexes with Btk [26].
 

Other interactions of ARID3A

 

Analytical, diagnostic and therapeutic context of ARID3A

References

  1. PML interaction with p53 and its role in apoptosis and replicative senescence. Pearson, M., Pelicci, P.G. Oncogene (2001) [Pubmed]
  2. The human dead ringer/bright homolog, DRIL1: cDNA cloning, gene structure, and mapping to D19S886, a marker on 19p13.3 that is strictly linked to the Peutz-Jeghers syndrome. Kortschak, R.D., Reimann, H., Zimmer, M., Eyre, H.J., Saint, R., Jenne, D.E. Genomics (1998) [Pubmed]
  3. The origins of American nephrology (1800-1850). Maher, J.F. J. Am. Soc. Nephrol. (1991) [Pubmed]
  4. Frederick Akbar Mahomed. O'Rourke, M.F. Hypertension (1992) [Pubmed]
  5. High blood pressure and the kidney: the forgotten contribution of William Senhouse Kirkes. Cameron, J.S., Hicks, J. Kidney Int. (2000) [Pubmed]
  6. Bright light treatment of winter depression: a placebo-controlled trial. Eastman, C.I., Young, M.A., Fogg, L.F., Liu, L., Meaden, P.M. Arch. Gen. Psychiatry (1998) [Pubmed]
  7. Combination of bright light and caffeine as a countermeasure for impaired alertness and performance during extended sleep deprivation. Wright, K.P., Badia, P., Myers, B.L., Plenzler, S.C. Journal of sleep research. (1997) [Pubmed]
  8. Bright-light treatment reduces actigraphic-measured daytime sleep in nursing home patients with dementia: a pilot study. Fetveit, A., Bjorvatn, B. The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry. (2005) [Pubmed]
  9. Light mask 500 lux treatment for delayed sleep phase syndrome. Ando, K., Kripke, D.F., Cole, R.J., Elliott, J.A. Prog. Neuropsychopharmacol. Biol. Psychiatry (1999) [Pubmed]
  10. Brief approaches to educating patients and parents in primary care. Glascoe, F.P., Oberklaid, F., Dworkin, P.H., Trimm, F. Pediatrics (1998) [Pubmed]
  11. A functional screen identifies hDRIL1 as an oncogene that rescues RAS-induced senescence. Peeper, D.S., Shvarts, A., Brummelkamp, T., Douma, S., Koh, E.Y., Daley, G.Q., Bernards, R. Nat. Cell Biol. (2002) [Pubmed]
  12. Regulation of matrix attachment region-dependent, lymphocyte-restricted transcription through differential localization within promyelocytic leukemia nuclear bodies. Zong, R.T., Das, C., Tucker, P.W. EMBO J. (2000) [Pubmed]
  13. Immunohistochemical localization of ganciclovir in the human retina. Park, S.S., Girard, B., Font, R.L., Hauw, J.J., Young, L.H. Curr. Eye Res. (1998) [Pubmed]
  14. Domenico Cotugno, a pioneer in neurosciences. Manni, E., Petrosini, L. Journal of the history of the neurosciences. (1997) [Pubmed]
  15. A novel E2F binding protein with Myc-type HLH motif stimulates E2F-dependent transcription by forming a heterodimer. Suzuki, M., Okuyama, S., Okamoto, S., Shirasuna, K., Nakajima, T., Hachiya, T., Nojima, H., Sekiya, S., Oda, K. Oncogene (1998) [Pubmed]
  16. E2FBP1/DRIL1, an AT-rich interaction domain-family transcription factor, is regulated by p53. Ma, K., Araki, K., Ichwan, S.J., Suganuma, T., Tamamori-Adachi, M., Ikeda, M.A. Mol. Cancer Res. (2003) [Pubmed]
  17. A regulated nucleocytoplasmic shuttle contributes to Bright's function as a transcriptional activator of immunoglobulin genes. Kim, D., Tucker, P.W. Mol. Cell. Biol. (2006) [Pubmed]
  18. Induction of immunoglobulin heavy-chain transcription through the transcription factor Bright requires TFII-I. Rajaiya, J., Nixon, J.C., Ayers, N., Desgranges, Z.P., Roy, A.L., Webb, C.F. Mol. Cell. Biol. (2006) [Pubmed]
  19. The 70-kilodalton pertussis toxin-binding protein in Jurkat cells. Armstrong, G.D., Clark, C.G., Heerze, L.D. Infect. Immun. (1994) [Pubmed]
  20. Texture analysis of magnetic resonance images of rat muscles during atrophy and regeneration. Mahmoud-Ghoneim, D., Cherel, Y., Lemaire, L., de Certaines, J.D., Maniere, A. Magnetic resonance imaging. (2006) [Pubmed]
  21. Transaxillary carotid stenting: technical case report. Wang, H., Swischuk, J.L., Fraser, K., Alvernia, J., Lanzino, G. Neurosurgery (2005) [Pubmed]
  22. An active site-tyrosine-containing heptapeptide from D-amino acid oxidase. Ronchi, S., Galliano, M., Minchiotti, L., Curti, B., Rudie, N.G., Porter, D.J., Bright, H.J. J. Biol. Chem. (1980) [Pubmed]
  23. A simple procedure for covalent immobilization of NADH in a soluble and enzymically active form. Fuller, C.W., Rubin, J.R., Bright, H.J. Eur. J. Biochem. (1980) [Pubmed]
  24. Bright light exposure and pituitary hormone secretion. Kostoglou-Athanassiou, I., Treacher, D.F., Wheeler, M.J., Forsling, M.L. Clin. Endocrinol. (Oxf) (1998) [Pubmed]
  25. Modeling the adsorption and precipitation processes of Cu(II) on humin. Alvarez-Puebla, R.A., Valenzuela-Calahorro, C., Garrido, J.J. Journal of colloid and interface science. (2004) [Pubmed]
  26. The transcription factor, Bright, is not expressed in all human B lymphocyte subpopulations. Nixon, J.C., Rajaiya, J.B., Ayers, N., Evetts, S., Webb, C.F. Cell. Immunol. (2004) [Pubmed]
  27. E2FBP1/hDril1 modulates cell growth through downregulation of promyelocytic leukemia bodies. Fukuyo, Y., Mogi, K., Tsunematsu, Y., Nakajima, T. Cell Death Differ. (2004) [Pubmed]
  28. Application of stable isotopes to identify problems in large-scale water transfer in Grand Canyon National Park. Ingraham, N.L., Zukosky, K., Kreamer, D.K. Environ. Sci. Technol. (2001) [Pubmed]
  29. HDAC-3 participates in the repression of e2f-dependent gene transcription in primary differentiated neurons. Panteleeva, I., Rouaux, C., Larmet, Y., Boutillier, S., Loeffler, J.P., Boutillier, A.L. Ann. N. Y. Acad. Sci. (2004) [Pubmed]
  30. Carotid endarterectomy. Bright light at the end of the tunnel. Reinmuth, O.M., Dyken, M.L. Stroke (1991) [Pubmed]
  31. Impaired micturition reflex caused by acute selective dorsal or ventral root(s) rhizotomy in anesthetized rats. Liao, J.M., Cheng, C.L., Lee, S.D., Chen, G.D., Chen, K.J., Yang, C.H., Pan, S.F., Chen, M.J., Huang, P.C., Lin, T.B. Neurourology and urodynamics. (2006) [Pubmed]
  32. Strategies for predicting and treating access induced ischemic steal syndrome. Tynan-Cuisinier, G.S., Berman, S.S. European journal of vascular and endovascular surgery : the official journal of the European Society for Vascular Surgery. (2006) [Pubmed]
  33. The bright liver syndrome. Prevalence and determinants of a "bright" liver echopattern. Lonardo, A., Bellini, M., Tartoni, P., Tondelli, E. Italian journal of gastroenterology and hepatology. (1997) [Pubmed]
 
WikiGenes - Universities