rdf:type |
|
lifeskim:mentions |
|
pubmed:issue |
6 Pt 1
|
pubmed:dateCreated |
1991-3-1
|
pubmed:abstractText |
We have demonstrated a requirement for cellular ATP in the receptor-mediated endocytosis of transferrin. This has been accomplished using a novel assay for endocytosis based on acquisition of resistance to the membrane impermeable reducing agent, glutathione (GSH). Diferric-transferrin was conjugated to biotin via a cleavable disulfide bond and iodinated. Internalization of 125I-biotin-S-S-transferrin (125I-BSST) was quantitated by adsorption to avidin-Sepharose after treatment of cells with GSH. Receptor-mediated endocytosis of 125I-BSST was severely inhibited in ATP-depleted cells. Similar results were obtained when ATP was depleted by incubation of cells either under a N2-atmosphere or in the presence of NaN3 and NaF. The latter treatment, alone, also resulted in a loss of surface transferrin receptors which could not be correlated to reductions in cellular ATP. In contrast to the acquisition of GSH resistance, the apparent internalization of 125I-BSST as assessed by inaccessibility to antitransferrin antibodies reached control levels in ATP-depleted cells. Our biochemical and morphological data suggested that, although ATP is required for receptor-mediated endocytosis, in ATP-depleted cells ligands can become efficiently sequestered into deeply invaginated pits that are inaccessible to large probes such as antibodies, but remain accessible to small molecules such as GSH.
|
pubmed:grant |
|
pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-1104607,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-2180149,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-2527741,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-2545438,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-2557061,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-2564003,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-2565904,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-2575616,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-2576383,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-2857182,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-2864349,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-2881559,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-2883727,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-2885011,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-2887575,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-2890644,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-2892842,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-2897244,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-2900073,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-2904698,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-2905261,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-3009438,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-3021750,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-3028771,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-3204117,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-3243274,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-332066,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-3356185,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-3360775,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-3469657,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-3554220,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-3955657,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-3965443,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-4055891,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-6137595,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-6138359,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-6146630,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-6169759,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-6243633,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-6251452,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2126013-6309781
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Dec
|
pubmed:issn |
0021-9525
|
pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:volume |
111
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
2307-18
|
pubmed:dateRevised |
2011-11-17
|
pubmed:meshHeading |
pubmed-meshheading:2126013-Adenosine Triphosphate,
pubmed-meshheading:2126013-Anaerobiosis,
pubmed-meshheading:2126013-Azides,
pubmed-meshheading:2126013-Biotin,
pubmed-meshheading:2126013-Cell Line,
pubmed-meshheading:2126013-Coated Pits, Cell-Membrane,
pubmed-meshheading:2126013-Endocytosis,
pubmed-meshheading:2126013-Glutathione,
pubmed-meshheading:2126013-HeLa Cells,
pubmed-meshheading:2126013-Humans,
pubmed-meshheading:2126013-Kinetics,
pubmed-meshheading:2126013-Receptors, Transferrin,
pubmed-meshheading:2126013-Sodium Azide,
pubmed-meshheading:2126013-Sodium Fluoride,
pubmed-meshheading:2126013-Transferrin
|
pubmed:year |
1990
|
pubmed:articleTitle |
ATP is required for receptor-mediated endocytosis in intact cells.
|
pubmed:affiliation |
Department of Molecular Biology, Research Institute of Scripps Clinic, La Jolla, California 92037.
|
pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|