Linked Life Data

7929123

Source:http://linkedlifedata.com/resource/pubmed/id/7929123

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
40
pubmed:dateCreated
1994-11-4
pubmed:abstractText
The role of RCC1-Ran/TC4 in nuclear protein import was examined in living cells using a temperature-sensitive RCC1 mutant cell line, tsBN2, and tsBN2 transformed with a RCC1 cDNA lacking the nuclear localization sequence domain, delta 8-29. Substrate, containing a small number of SV40 T antigen nuclear localization sequence peptides, injected into the cytoplasm of tsBN2 cells cultured at the non-permissive temperature of 39.5 degrees C did not accumulate efficiently in the nucleus. When the same substrate was injected into the cytoplasm of heterokaryons of tsBN2 and wild type BHK21 cells, import efficiency into the tsBN2 nuclei was not restored. Import into the BHK21 nuclei gradually decreased after fusion. In contrast, import efficiency into tsBN2 nuclei gradually recovered after fusion with tsBN2 cells transformed with delta 8-29 in which functional RCC1 was diffusely distributed in both the nuclei and cytoplasm. Substrate did not accumulate in the nuclei of digitonin-permeabilized tsBN2 cells cultured at 39.5 degrees C even in the presence of normal cytosol. These results suggest that loss of RCC1 function leads to the decline of import competence of the nucleus and accumulation of a factor in the cytoplasm that suppresses nuclear import. These results indicate that the RCC1-Ran/TC4 system may regulate nuclear import.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
7
pubmed:volume
269
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
24542-5
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Loss of RCC1 leads to suppression of nuclear protein import in living cells.
pubmed:affiliation
Department of Anatomy and Cell Biology, Osaka University Medical School, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't