Statements in which the resource exists as a subject.
PredicateObject
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: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