Mullerian inhibiting substance binding and uptake

Catlin, Elizabeth A.; Ezzell, Robert M.; Donahoe, Patricia K.; Manganaro, Thomas F.; Ebb, R. G.; MacLaughlin, David T.

doi:10.1002/aja.1001930402

Cited by 12 publications

(4 citation statements)

References 14 publications

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“…Samples were examined with a Bio-Rad MRC 600 Scanning Confocal Imaging System which revealed punctate surface fluorescence, temporally succeeded by cytosolic and nuclear accumulation of immunoreactive rhMIS ( Fig. 10; Catlin et al, 1992). These data support the hypothesis that MIS exists as a ligand for its own receptor and that this binding species is present in the fetal rat lung.…”

Section: Sex Specific Lung Ontogeny and Missupporting

confidence: 62%

Müllerian inhibiting substance: New perspectives and future directions

Catlin

MacLaughlin

Donahoe

1993

Microscopy Res & Technique

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MIS, as a differentiate and antiproliferative agent, is precisely regulated, for example, at the transcriptional level by such transacting factors as SRY, and posttranslationally by testosterone. Processing of MIS most likely requires an as yet unknown in vivo protease which probably serves to control cleavage of MIS and hence its activation at specific sites wherein a localized program of cell death is initiated via a receptor mediated event. Progress has been made in understanding the molecular domains of MIS; current efforts are focused on characterizing the wild type MIS receptor as well as cloning and expressing the MIS receptor. We need now to understand how to target and efficiently activate MIS at its projected site of action. We must focus, after structural analysis of its receptor, on elucidating the MIS initiated intracellular signals which result in localized cell inhibition. Understanding of these mechanisms will permit design of antitumor agents and therapeutic strategies. Similarly, understanding regulation of MIS expression may lead to therapeutic induction of expression in those states where depressed expression is associated with tumorigenesis, sexual ambiguity, or infertility.

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Section: Sex Specific Lung Ontogeny and Missupporting

confidence: 62%

Müllerian inhibiting substance: New perspectives and future directions

Catlin

MacLaughlin

Donahoe

1993

Microscopy Res & Technique

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“…Müllerian Inhibiting Substance (MIS), the initiator of Müllerian duct regression, acts through the MIS type II receptor (reviewed by Teixeira et al, 2001), which is expressed in the mesenchymal cells surrounding the MDE in the male after E15.5 in the rat (Catlin et al, 1992; Teixeira et al, 1996; Zhan et al, 2006; Arango et al, 2008), resulting in subsequent apoptosis or epithelial–mesenchymal transformation of MDE cells (Dyche, 1979; Trelstad et al, 1982; Allard et al, 2000). To elicit MIS signaling, some mesenchymal–epithelial interaction must occur (Roberts et al, 1999), which may block the PI3K pathway in the MDE.…”

Section: Discussionmentioning

confidence: 99%

Cell migration and activated PI3K/AKT-directed elongation in the developing rat Müllerian duct

Fujino

Arango²,

Zhan³

et al. 2009

Developmental Biology

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In vertebrates, the Müllerian duct elongates along the Wolffian duct, a mesonephric structure that is required for Müllerian duct formation. Recently, several genes required for initial Müllerian duct formation have been identified. However, the precise mechanism of Müllerian duct elongation remains to be elucidated. In this study, we investigated dynamic morphological changes in the elongating Müllerian duct in rat urogenital ridges in organ culture manipulated by microincision and/or chemical inhibitors. Mechanical division of the developing Müllerian duct showed that epithelial cells of the Müllerian duct actively migrate along the anterior–posterior axis independent of the proliferative expansion of the anterior portion of the duct. We found that the PI3K/AKT signaling pathway is activated in the Müllerian duct epithelium and is required for elongation of the tip of the duct; however, migration of Müllerian duct epithelial cells proximal to the tip remains intact when PI3K/AKT is inactivated. Although much is known about the molecular and cellular mechanisms leading to Müllerian duct regression, the present findings provide a fuller understanding of the mechanisms contributing to Müllerian duct formation and to the general process of early tubulogenesis.

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“…Fur-thermore, now that sufficient radioiodinated recombinant human MIS (rhMIS) is available, it was possible to demonstrate competition for rhMIS binding to A-431 membranes by the anti-idiotypic antibody, again indicating that the antibody and MIS itself bind to the same sites. Further support for the existence of specific MIS membrane binding sites is the recent demonstration of adsorptive endocytosis of rhMIS as visualized by a fluorescing antibody sandwich in fetal target tissue (Catlin, Ezzell, Donahoe, Manganaro, Ebb and MacLaughlin 1992).…”

Section: Discussionmentioning

confidence: 96%

Identification of Müllerian Inhibiting Substance Specific Binding in Human Cell Lines

MacLaughlin

Levin²,

Catlin³

et al. 1992

Horm Metab Res

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The receptor for Müllerian Inhibiting Substance (MIS), a gonadal glycoprotein hormone, has not been previously identified. Plasma membranes from MIS-sensitive human tumor cell lines (HTB-111, endometrial carcinoma; and A-431, vulvar squamous carcinoma) were detergent extracted and incubated with 125I-labeled MIS anti-idiotypic antibody, or radioiodinated human recombinant MIS (125I rhMIS), with and without unlabeled competitors. 125I anti-idiotypic MIS antibody bound to HTB-111 membrane extracts was displaceable by unlabeled anti-idiotypic antibody, but not by anti-isotypic antibody prior to cross-linking. Specific binding of the anti-idiotypic MIS antibody to endometrial carcinoma cells was verified using fluorescence activated cell analysis and fluoresceinated antibody. Furthermore, unlabeled anti-idiotypic MIS antibody competed for 125I rhMIS binding to A-431 vulvar carcinoma membranes. The labeled anti-idiotypic MIS antibody binding complex could be separated from 32P labeled EGF receptor in the A-431 membranes, indicating that EGF, a natural inhibitor of MIS activity, and MIS itself bind to different receptors. These studies demonstrate a specific, displaceable binder for MIS in the plasmalemmae of two human tumor lines. Purification of this cell surface receptor protein will be greatly aided by using the MIS anti-idiotypic antibody.

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Mullerian inhibiting substance binding and uptake

Cited by 12 publications

References 14 publications

Müllerian inhibiting substance: New perspectives and future directions

Müllerian inhibiting substance: New perspectives and future directions

Cell migration and activated PI3K/AKT-directed elongation in the developing rat Müllerian duct

Identification of Müllerian Inhibiting Substance Specific Binding in Human Cell Lines

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