Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recently the pH gradient evoked by a K+ diffusion potential was shown to translocate a synthetic monobasic amphipathic hexapeptide across the bilayer of lipid vesicles (De Kroon, A.I.P.M., Vogt, B., Van 't Hof, R., De Kruijff, B. and De Gier, J. (1991) Biophys. J. 60, in press). Here this observation is extended by studying the effect of a membrane potential on a set of bioactive peptides. The panel of peptides comprises the toxin mastoparan X, a tryptophan-containing analogue of the presequence of the mitochondrial protein cytochrome oxidase subunit IV (preCoxIV(1-25)W18), and the regulatory peptides ACTH(1-24), alpha-MSH, ACTH(1-10), dynorphin A, bombesin, and LHRH. The interaction of these peptides with phospholipid vesicles has been measured using the intrinsic tryptophan residue as fluorescent probe. In the absence of a K+ diffusion potential only mastoparan X and the presequence show considerable binding to vesicles consisting of phosphatidylcholine (PC). In contrast, under these conditions all peptides display affinity for vesicles consisting of the acidic phospholipid cardiolipin (CL), the extent of which depends on the net positive charge of the peptide. Application of a K+ diffusion potential to large unilamellar vesicles (LUV) consisting of PC results in a time dependent tryptophan fluorescence increase for mastoparan X, which is accelerated upon incorporating increasing amounts of CL into the LUV. A similar fluorescence increase in response to a K+ diffusion potential was observed for the above model peptide. Yet the mechanism resulting in the fluorescence increase of mastoparan X is completely different from that of the hexapeptide. Binding experiments indicate that a membrane potential-induced enhanced binding of the peptide to the outer surface of the vesicles contributes to the fluorescence increase. PreCoxIV(1-25)W18, dynorphin A, and ACTH(1-24) show fluorescence responses upon applying a membrane potential that are consistent with that of mastoparan X, whereas the other peptides tested do not respond up to a LUV CL content of 50%. The results tentatively suggest that the membrane potential only affects a peptide when it has the ability to adopt a stable membrane bound conformation.
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PMID:The effect of a membrane potential on the interaction of mastoparan X, a mitochondrial presequence, and several regulatory peptides with phospholipid vesicles. 168 Mar 97

Although women were welcomed into medical practice in increasing numbers by the close of the nineteenth century, it was not until the second quarter of the twentieth century that they were recognised as valuable collaborators and contributors in the nascent field of neuroendocrinology, wherein they soon made advances that have stood the test of time. Mary Pickford at Edinburgh measured the action of acetyl choline in the supraoptic nucleus of the hypothalamus and helped to establish that vasopressin and oxytocin are formed in separate and distinct neurons. Berta Scharrer, like her future husband Ernest Scharrer, was born in Munich. Their great contribution was the proof that the posterior pituitary is not a gland, but the location of the release into the circulation of vasopressin and oxytocin from fibres in the hypothalamico-hypophysial tract. Their work succeeded in establishing against high-powered, vehement opposition the value of histological evidence in elucidating synthesis, storage and release of secretion from neuro-endocrine cells. A Rockefeller travelling fellowship allowed Marthe Vogt to move from Berlin in 1932 to London and then to Cambridge. The relations between the cortex and medulla of the suprarenal gland and the control of adrenocorticotropin were her main concerns. Dora Jacobsohn emigrated to Sweden after graduating in Berlin in 1934. She investigated control of the anterior pituitary gland by the hypothalamus, and co-operated with Geoffrey Harris in establishing the role of the hypothalamico-hypophysial portal venous system that conveys the releasing factors that preside over anterior pituitary cells. Laboratory discoveries do not constitute the whole of science, for the interpretation of evidence and recognition of general principles deserve attention. Dorothy Price, from Aurora, Illinois, received her BS in 1922 at the University of Chicago, and was glad to find employment as a histology technician in the zoology laboratory, where she was quietly appropriated by Carl Moore (1892-1955), an investigator seeking the key to hormonal control of gonadal function. The burning question was the part played by what was (then) called hormone antagonism in the biology of the testis. Price recognised that the common factor in explaining the deleterious effects of oestrin and testosterone on the testes could be traced to the anterior pituitary: the pituitary controlled testicular secretion, and the male hormone in turn controlled gonadotropin release in the pituitary. This seesaw balance explained the problem, and was the first of many regulatory systems to be recognised as ensuring stability--and later became known as negative feedback. The contributions of these five women helped place neuro-endocrinology on a firm foundation for its later expansion.
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PMID:First ladies in laying the foundation of neuroendocrinology. 2258 Oct 99