@article{MTMT:2179455, title = {Novel mechanisms of estrogen action in the brain: New players in an old story}, url = {https://m2.mtmt.hu/api/publication/2179455}, author = {Toran-Allerand, CD and Singh, M and Sétáló, György (ifj.)}, doi = {10.1006/frne.1999.0177}, journal-iso = {FRONT NEUROENDOCRIN}, journal = {FRONTIERS IN NEUROENDOCRINOLOGY}, volume = {20}, unique-id = {2179455}, issn = {0091-3022}, abstract = {Estrogen elicits a selective enhancement of the growth and differentiation of axons and dendrites (neurites) in the developing brain. Widespread colocalization of estrogen and neurotrophin receptors (trk) within estrogen and neurotrophin targets, including neurons of the cerebral cortex, sensory ganglia, and PC12 cells, has been shown to result in differential and reciprocal transcriptional regulation of these receptors by their ligands. In addition, estrogen and neurotrophin receptor coexpression leads to convergence or cross-coupling of their signaling pathways, particularly at the level of the mitogen-activated protein (MAP) kinase cascade. 17beta-Estradiol elicits rapid (within 5-15 min) and sustained (at least 2 h) tyrosine phosphorylation and activation of the MAP kinases, extracellular-signal regulated kinase (ERK)1, and ERK2, which is successfully inhibited by the MAP kinase/ERK kinase 1 inhibitor PD98059, but not by the estrogen receptor (ER) antagonist ICI 182,780 and also does not appear to result from estradiol-induced activation of trk. Furthermore, the ability of estradiol to phosphorylate ERK persists even in ER-alpha knockout mice, implicating other estrogen receptors such as ER-beta in these actions of estradiol. The existence of an estrogen receptor-containing, multimeric complex consisting of hsp90, src, and B-Raf also suggests a direct link between the estrogen receptor and the MAP kinase signaling cascade. Collectively, these novel findings, coupled with our growing understanding of additional signaling substrates utilized by estrogen, provide alternative mechanisms for estrogen action in the developing brain which could explain not only some of the very rapid effects of estrogen, but also the ability of estrogen and neurotrophins to regulate the same broad array of cytoskeletal and growth-associated genes involved in neurite growth and differentiation. This review expands the usually restrictive view of estrogen action in the brain beyond the confines of sexual differentiation and reproductive neuroendocrine function. It considers the much broader question of estrogen as a neural growth factor with important influences on the development, survival, plasticity, regeneration, and aging of the mammalian brain and supports the view that the estrogen receptor is not only a ligand-induced transcriptional enhancer but also a mediator of rapid, nongenomic events.}, year = {1999}, eissn = {1095-6808}, pages = {97-121} } @article{MTMT:1904570, title = {Interactions and developmental effects of mutations at the 2B5 locus of Drosophila melanogaster.}, url = {https://m2.mtmt.hu/api/publication/1904570}, author = {Kiss, István and BEATON, AH and TARDIFF, J and FRISTROM, D and FRISTROM, JW}, journal-iso = {GENETICS}, journal = {GENETICS}, volume = {118}, unique-id = {1904570}, issn = {0016-6731}, year = {1988}, eissn = {1943-2631}, pages = {247-259} } @article{MTMT:1899746, title = {Cytogenetic analysis of the 2B3-4-2B11 region of the X chromosome of Drosophila melanogaster. I. Cytology of the region and mutant complementation groups.}, url = {https://m2.mtmt.hu/api/publication/1899746}, author = {BELYAEVA, ES and AIZENZON, MG and SEMESHIN, VF and Kiss, István and Koczka, Katalin and BARITCHEVA, EM and GOREM, D and ZHIMULEV, IF}, doi = {10.1007/BF00285954}, journal-iso = {CHROMOSOMA}, journal = {CHROMOSOMA}, volume = {81}, unique-id = {1899746}, issn = {0009-5915}, year = {1980}, eissn = {1432-0886}, pages = {281-306} } @article{MTMT:1900772, title = {Genetic and developmental analysis of puparium formation in Drosophila.}, url = {https://m2.mtmt.hu/api/publication/1900772}, author = {Kiss, István and Szabad, János and Major, J.}, doi = {10.1007/BF00267601}, journal-iso = {MOL GEN GENET}, journal = {MOLECULAR & GENERAL GENETICS}, volume = {164}, unique-id = {1900772}, issn = {0026-8925}, year = {1978}, eissn = {1432-1874}, pages = {77-83} }