By Derek Leroith
Traditionally the sector of endocrine examine has consistently been on the vanguard of medical endeavors. The investigators of those very important breakthroughs in study were rewarded by way of a variety of Nobel awards. within the box of diabetes by myself, Nobel prizes were provided to researchers who stumbled on insulin, characterised the protein and invented radioimmunoassays utilizing insulin as a paradigm. now not unusually, biomedical researchers have consistently been attracted via the endocrine process and different related structures of intercellular verbal exchange. over the last twenty years, endocrine learn has built swiftly and tailored glossy molecular and mobile biology suggestions for its particular use. those adjustments have allowed researchers within the box to keep up their aspect. therefore, endocrine disease-related genes were characterised and mutations in those genes have helped clarify universal and much less universal endocrine problems. Our knowing of the legislation of gene expression has been vastly improved through molecular options. In an try to deliver investigators modern with the hot advances during this exploding box we've got determined to post a sequence entitled Advances in Molecular and mobile Endocrinology. the world over recognized investigators have agreed to take part and their contributions are favored. quantity 1 has fascinated by features of the hypothalamic-pituitary axis together with GnRH and GH gene rules, molecular points of insulin, insulin-like development components and glucagon. moreover, reports at the lately cloned calcium receptor and steroid receptor interactions with DNA are provided.
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Extra info for Advances in Molecular and Cellular Endocrinology, Vol. 1
1995) in the GT1 cells, but the precise mechanism of calcium action in these neurons is not yet known. Since the hypothalamic neuron releases GnRH in a pulsatile manner, as does the GT1 cells, the effects of the numerous signal transduction pathways already shown to affect GnRH secretion and expression may change the frequency and/or amplitude of the GnRH pulses. Many diverse signals and pathways may be necessary to generate the preovulatory surge of GnRH and may account for the fact that numerous signal transduction pathways change GnRH gene expression in the hypothalamic neuron.
Saunders, Philadelphia. L. (1991). Complex regulatory pathway of GnRH gene transcripts by forskolin, ionomycin and phorbol esters in the GT1 cell line. Soc. Neurosci. ). L. (1993). Transcriptional and post-transcriptional regulation of gonadotropin releasing hormone gene expression by the activation of protein kinase C pathway in a mouse hypothalamic GT1 cell line. Soc. Neurosci. ). L. (1994). Second messenger regulation of mouse gonadotropin-releasing hormone gene expression in immortalized mouse hypothalamic GTI-3 cells.
Targets of Signal Transduction Pathways The signaling molecules that cause acute stimulation of GnRH secretion have also been consistently found to repress GnRH gene expression over the longer term. A specific example is the induction of GnRH secretion by NMDA or NO and a repression of gene expression by these same neurotransmitters. This apparent GnRH Gene Expression 23 paradox can be viewed as an endocrine damping mechanism. Many signals that are normally received intermittently or as short pulses, when applied for long periods (hours), will downregulate the system at a fundamental level to protect cells from overstimulation.
Advances in Molecular and Cellular Endocrinology, Vol. 1 by Derek Leroith