High impact information on 125I]iodo-

• All three forms of hGH had a similar ability to inhibit [125I]iodo-met-hGH 22K binding to 3T3-adipocytes [1].
• Visualization of [125I]iodo-alpha hANP-specific binding sites in APA and adjacent normal adrenal tissues by an in vitro receptor autoradiographic technique showed that these sites were localized only in normal adrenal tissue, but not in APA tissue [2].
• Specific binding of [125I]iodo human GH [( 125I]iodo hGH) was rapid, reversible, and time and temperature dependent [3].
• The partially purified activity competes with [125I]iodo-platelet-derived growth factor (PDGF) for binding to target cells, and the biological activity is neutralized with anti-PDGF IgG, suggesting shared domains in the two molecules [4].
• 2. Denervation by sciatic nerve section increased the number of [125I]iodo-alpha-bungarotoxin ([125I]BTX) binding sites from low, unmeasurable levels to 39 +/- 3 fmol of toxin bound per milligram muscle protein at 21 days [5].

Biological context of 125I]iodo-

• As part of a study concerning the mechanism of mammotroph autoregulation, the intracellular fate of [125I]iodo rat PRL, internalized by mammotrophs, was determined by quantitative electron microscope autoradiography [6].

Anatomical context of 125I]iodo-

• However, freeze-thawing of the cells fragmented the membranes, releasing [125I]iodo TSH binding as well as LATS/TSI absorbing activities into the soluble (cell sap) fraction [7].
• The granulosa cells degrade rat [125I]iodo high density lipoprotein (HDL) to acid-soluble products, mainly monoiodotyrosine [8].
• An enzyme hydrolysing [125I]iodo-insulin B chain was enriched in preparations of intestinal microvilli [9].
• Membranes purified from thyroid homogenates or isolated thyroid cells absorbed LATS/TSI activities and specifically bound [125I]iodo TSH [7].
• Time- and temperature-dependent specific binding of [125I]iodo-insulin to kidney cell membranes was demonstrated [10].

Associations of 125I]iodo- with other chemical compounds

• In contrast to the ability of FSH to induce luteinizing hormone (LH) receptor formation, treatment with VIP did not increase [125I]iodo-human chorionic gonadotropin (hCG) binding to granulosa cells [11].
• The divalent cations magnesium, calcium and manganese, and the monovalent cation, potassium, but not sodium, enhance binding of [125I]iodo-porcine follicle-stimulating hormone to follicle-stimulating hormone (FSH) receptors in membranes of porcine granulosa cells via an increase in the apparent number of binding sites [12].

Gene context of 125I]iodo-

• Purified thyroglobulin, nuclei, mitochondria and ribosomes did not bind [125I]iodo TSH nor did they absorb LATS/TSI activities [7].
• That this regulation was partly produced by uptake of secreted PRL from the medium was demonstrated by supplementing the medium with [125I]iodo-rat PRL [13].
• Concomitant treatment with FSH and T4 (10(-7) M) markedly increased FSH-stimulated induction of [125I]iodo-human CG binding to cultured granulosa cells obtained from small follicles [14].
• Whereas native hCG displayed negligible binding potency when compared with that of ovine FSH in competition with [125I]iodo-human FSH for ovarian receptors, AHF-hCG bound to FSH receptors with about 5% of the binding affinity of ovine FSH [15].
• The beta-subunits of hFSH, hTSH and hLH did not inhibit binding of [125I]iodo-beta hCG to the antibody at up to 250 ng/tube [16].

Analytical, diagnostic and therapeutic context of 125I]iodo-

• Like the latter, PP12 bound somatomedin (insulin-like growth factor I) as demonstrated in gel chromatography by a shift in the elution pattern of [125I]iodo-insulin-like growth factor I after incubation with PP12 [17].
• Autoradiography revealed rat [125I]iodo CGRP binding associated with the intima and media of the aorta, the coronary arteries and the heart valves, and the red pulp of the spleen [18].

References