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Gene Review

Fosl2  -  fos-like antigen 2

Rattus norvegicus

Synonyms: FRA-2, Fos-related antigen 2, Fra-2, Fra2
 
 
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Psychiatry related information on Fosl2

 

High impact information on Fosl2

 

Biological context of Fosl2

 

Anatomical context of Fosl2

  • Fos-related antigen 2 controls protein kinase A-induced CCAAT/enhancer-binding protein beta expression in osteoblasts [4].
  • Withdrawal studies demonstrated robust induction of several known acute Fras, including c-Fos, FosB, Fra-1, Fra-2, and delta FosB, at 6 hr after naltrexone precipitation of withdrawal in the striatum, nucleus accumbens, and several other brain regions [10].
  • These data show that pineal AP-1 binding activity, which results from Fra-2 expression, can be modulated by light and serotonin through the suprachiasmatic nucleus according to a "phase dependence" that is characteristic of the rhythm of clock sensitivity to both zeitgebers [11].
  • JunB, c-Jun, c-Fos, and Fra2 were rapidly but transiently induced by FSH in immature granulosa cells [12].
  • Fra-2 and JunD are found in mature osteoclasts as well [13].
 

Associations of Fosl2 with chemical compounds

  • By contrast, OA and dbcAMP equally stimulated the accumulation of the mRNAs of Fra-2 and JunB [6].
  • Therefore, the regulatory role of pineal serine/threonine phosphatases in adrenergically stimulated AA-NAT expression probably does not depend on ICER or Fra-2 [14].
  • Consistent with these findings, over-expression of Fra-2 significantly increased C/EBPbeta promoter activity in PGE2-induced osteoblasts, whereas expression of Fra-2 lacking its activation domain had a dominant negative inhibitory effect [4].
  • Exposure to light during subjective night and administration of a serotonin 5-HT(1A)/5-HT(7) receptor agonist during subjective day, respectively, induced a 50% decrease and a 50% increase in both AP-1 and Fra-2 expression [11].
  • JunD and Fra2 were induced by LH and maintained as granulosa cells terminally differentiated into luteal cells [12].
 

Physical interactions of Fosl2

  • Together, these results demonstrate that TGF-beta 1 responsiveness of the rat osteocalcin gene in ROS 17/2.8 cells is mediated through an activator protein-1 like cis-acting element that interacts with Fra-2 [15].
  • These findings suggest that prolonged alterations in Fra-2 and subsequent increases in Fra-2/JunD binding to AP-1 and CREB response elements common among many gene promoters could serve to trigger broadly an NGF-specific program of gene expression [16].
 

Enzymatic interactions of Fosl2

  • Our results demonstrate that Fra-2 is hyperphosphorylated upon TGF-beta 1 treatment of ROS 17/2.8 cells [15].
 

Regulatory relationships of Fosl2

 

Other interactions of Fosl2

  • Studies are presented that indicate this 42/46-kDa Fra is Fra-2, a poorly understood member of the Fos family of transcription factors [17].
  • This set of observations extends the number of pineal genes that are known to be regulated by Fra-2, and also provides the first indication that a member of the NGFI-B group of nuclear receptors is involved in controlling gene expression in the pineal gland [18].
  • Repeated IMO triggered increased phosphorylation and levels of CREB along with transient induction of c-Fos and increased Fra-2 expression [19].
  • While in the caudate-putamen the increase in AP-1 DNA binding was mainly due to an elevation of the c-Fos and FosB proteins, the same phenomenon depended on the FosB, Fra-1 and Fra-2 peptides in the cingulate cortex [20].
  • Pretreatment of rats with the AT(1) receptor antagonist candesartan for 14 days prior to isolation completely prevented the stress-induced stimulation of catecholamine synthesis, decreasing tyrosine hydroxylase transcription by preventing the expression of the transcriptional factor, Fos-related antigen 2 (Fra-2) [21].
 

Analytical, diagnostic and therapeutic context of Fosl2

  • Both Fra-2 mRNA and protein are absent during the day and increase robustly at night on a circadian basis; organ culture studies indicate that regulation is mediated by an adrenergic-->cyclic AMP mechanism [17].
  • Fra-2 cDNA generated from rat osteoblasts by reverse transcriptase PCR was 95% homologous to human Fra-2, and PGE2 rapidly induced Fra-2 mRNA and protein expression [4].
  • Supershift EMSA and Western blot studies identified JunD, Fra2, and FosB as potential components of the HMAP-1 [22].
  • Differential expression of fos-related antigen-2 and growth arrest and DNA damage-inducible protein-45 were further confirmed at the protein level by immunohistochemistry [23].
  • In contrast, transcripts of fos-related antigen-2, growth arrest and DNA damage-inducible protein-45, and signal transducer and activator of transcription-3 were significantly increased in the LPs of T + E2-treated animals, but the increases were reversed by cotreatment with ICI [23].

References

  1. Quinpirole attenuates the striatal immediate early gene expression, but not the hyperactivity, induced by the serotonin agonist RU-24969. Cook, D.F., Wirtshafter, D. Brain Res. (2000) [Pubmed]
  2. Tissue-specific transgenic knockdown of Fos-related antigen 2 (Fra-2) expression mediated by dominant negative Fra-2. Smith, M., Burke, Z., Humphries, A., Wells, T., Klein, D., Carter, D., Baler, R. Mol. Cell. Biol. (2001) [Pubmed]
  3. Fos-related antigen 2: potential mediator of the transcriptional activation in rat adrenal medulla evoked by repeated immobilization stress. Nankova, B.B., Rivkin, M., Kelz, M., Nestler, E.J., Sabban, E.L. J. Neurosci. (2000) [Pubmed]
  4. Fos-related antigen 2 controls protein kinase A-induced CCAAT/enhancer-binding protein beta expression in osteoblasts. Chang, W., Rewari, A., Centrella, M., McCarthy, T.L. J. Biol. Chem. (2004) [Pubmed]
  5. Adrenergic inducibility of AP-1 binding in the rat pineal gland depends on prior photoperiod. Guillaumond, F., Becquet, D., Bosler, O., François-Bellan, A.M. J. Neurochem. (2002) [Pubmed]
  6. A differential role of CREB phosphorylation in cAMP-inducible gene expression in the rat pineal. Spessert, R., Rapp, M., Jastrow, H., Karabul, N., Blum, F., Vollrath, L. Brain Res. (2000) [Pubmed]
  7. Differential regulation of fos family genes in the ventrolateral and dorsomedial subdivisions of the rat suprachiasmatic nucleus. Schwartz, W.J., Carpino, A., de la Iglesia, H.O., Baler, R., Klein, D.C., Nakabeppu, Y., Aronin, N. Neuroscience (2000) [Pubmed]
  8. Is light-regulated AP-1 binding in the rat suprachiasmatic nucleus gated by the circadian clock? François-Bellan, A.M., Guillaumond, F., Bosler, O., Becquet, D. Brain Res. Mol. Brain Res. (2000) [Pubmed]
  9. Interactions between Egr1 and AP1 factors in regulation of tyrosine hydroxylase transcription. Nakashima, A., Ota, A., Sabban, E.L. Brain Res. Mol. Brain Res. (2003) [Pubmed]
  10. Induction of chronic Fos-related antigens in rat brain by chronic morphine administration. Nye, H.E., Nestler, E.J. Mol. Pharmacol. (1996) [Pubmed]
  11. Circadian binding activity of AP-1, a regulator of the arylalkylamine N-acetyltransferase gene in the rat pineal gland, depends on circadian Fra-2, c-Jun, and Jun-D expression and is regulated by the clock's zeitgebers. Guillaumond, F., Sage, D., Deprez, P., Bosler, O., Becquet, D., François-Bellan, A.M. J. Neurochem. (2000) [Pubmed]
  12. Regulation of AP1 (Jun/Fos) factor expression and activation in ovarian granulosa cells. Relation of JunD and Fra2 to terminal differentiation. Sharma, S.C., Richards, J.S. J. Biol. Chem. (2000) [Pubmed]
  13. Carbonic anhydrase II is an AP-1 target gene in osteoclasts. David, J.P., Rincon, M., Neff, L., Horne, W.C., Baron, R. J. Cell. Physiol. (2001) [Pubmed]
  14. Serine/threonine phosphatase inhibitors decrease adrenergic arylalkylamine n-acetyltransferase induction in the rat pineal gland. Spessert, R., Rapp, M., Vollrath, L. J. Neuroendocrinol. (2001) [Pubmed]
  15. Transforming growth factor-beta 1 responsiveness of the rat osteocalcin gene is mediated by an activator protein-1 binding site. Banerjee, C., Stein, J.L., Van Wijnen, A.J., Frenkel, B., Lian, J.B., Stein, G.S. Endocrinology (1996) [Pubmed]
  16. Nerve growth factor, but not epidermal growth factor, increases Fra-2 expression and alters Fra-2/JunD binding to AP-1 and CREB binding elements in pheochromocytoma (PC12) cells. Boss, V., Roback, J.D., Young, A.N., Roback, L.J., Weisenhorn, D.M., Medina-Flores, R., Wainer, B.H. J. Neurosci. (2001) [Pubmed]
  17. Circadian expression of transcription factor Fra-2 in the rat pineal gland. Baler, R., Klein, D.C. J. Biol. Chem. (1995) [Pubmed]
  18. NGFI-B (Nurr77/Nr4a1) orphan nuclear receptor in rat pinealocytes: circadian expression involves an adrenergic-cyclic AMP mechanism. Humphries, A., Weller, J., Klein, D., Baler, R., Carter, D.A. J. Neurochem. (2004) [Pubmed]
  19. Single and repeated immobilization stress differentially trigger induction and phosphorylation of several transcription factors and mitogen-activated protein kinases in the rat locus coeruleus. Hebert, M.A., Serova, L.I., Sabban, E.L. J. Neurochem. (2005) [Pubmed]
  20. Delta9-tetrahydrocannabinol increases sequence-specific AP-1 DNA-binding activity and Fos-related antigens in the rat brain. Porcella, A., Gessa, G.L., Pani, L. Eur. J. Neurosci. (1998) [Pubmed]
  21. Angiotensin II AT1 and AT2 receptor types regulate basal and stress-induced adrenomedullary catecholamine production through transcriptional regulation of tyrosine hydroxylase. Armando, I., Jezova, M., Bregonzio, C., Baiardi, G., Saavedra, J.M. Ann. N. Y. Acad. Sci. (2004) [Pubmed]
  22. Control of the tissue inhibitor of metalloproteinases-1 promoter in culture-activated rat hepatic stellate cells: regulation by activator protein-1 DNA binding proteins. Bahr, M.J., Vincent, K.J., Arthur, M.J., Fowler, A.V., Smart, D.E., Wright, M.C., Clark, I.M., Benyon, R.C., Iredale, J.P., Mann, D.A. Hepatology (1999) [Pubmed]
  23. Gene expression profiling of testosterone and estradiol-17 beta-induced prostatic dysplasia in Noble rats and response to the antiestrogen ICI 182,780. Thompson, C.J., Tam, N.N., Joyce, J.M., Leav, I., Ho, S.M. Endocrinology (2002) [Pubmed]
 
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