Linked Life Data

16373497

Source:http://linkedlifedata.com/resource/pubmed/id/16373497

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2005-12-23
pubmed:abstractText
A regulated shift from the production of membrane to secretory forms of Immunoglobulin M (IgM) mRNA occurs during B cell differentiation due to the activation of an upstream secretory poly(A) site. U1A plays a key role in inhibiting the expression of the secretory poly(A) site by inhibiting both cleavage at the poly(A) site and subsequent poly(A) tail addition. However, how the inhibitory effect of U1A is alleviated in differentiated cells, which express the secretory poly(A) site, is not known. Using B cell lines representing different stages of B cell differentiation, we show that the amount of U1A available to inhibit the secretory poly(A) site is reduced in differentiated cells. Undifferentiated B cells have more total U1A than differentiated cells and a greater proportion of this is not associated with the U1snRNP. We show that this is available to inhibit poly(A) addition at the secretory poly(A) site using cold competitor RNA oligos to de-repress poly(A) addition in nuclear extracts from the respective cell lines. In addition, endogenous non-snRNP associated U1A-immunopurified from the different cell lines-inhibits poly(A) polymerase activity proportional to U1A recovered, suggesting that available U1A level alone is responsible for changes in its inhibitory effect at the secretory IgM poly (A) site.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/16373497-10688667, http://linkedlifedata.com/resource/pubmed/commentcorrection/16373497-11343899, http://linkedlifedata.com/resource/pubmed/commentcorrection/16373497-11707415, http://linkedlifedata.com/resource/pubmed/commentcorrection/16373497-12617996, http://linkedlifedata.com/resource/pubmed/commentcorrection/16373497-12670951, http://linkedlifedata.com/resource/pubmed/commentcorrection/16373497-1361868, http://linkedlifedata.com/resource/pubmed/commentcorrection/16373497-15226420, http://linkedlifedata.com/resource/pubmed/commentcorrection/16373497-1618898, http://linkedlifedata.com/resource/pubmed/commentcorrection/16373497-1826045, http://linkedlifedata.com/resource/pubmed/commentcorrection/16373497-2481270, http://linkedlifedata.com/resource/pubmed/commentcorrection/16373497-2565533, http://linkedlifedata.com/resource/pubmed/commentcorrection/16373497-2900759, http://linkedlifedata.com/resource/pubmed/commentcorrection/16373497-310843, http://linkedlifedata.com/resource/pubmed/commentcorrection/16373497-3119424, http://linkedlifedata.com/resource/pubmed/commentcorrection/16373497-3128787, http://linkedlifedata.com/resource/pubmed/commentcorrection/16373497-3139489, http://linkedlifedata.com/resource/pubmed/commentcorrection/16373497-3924411, http://linkedlifedata.com/resource/pubmed/commentcorrection/16373497-6091052, http://linkedlifedata.com/resource/pubmed/commentcorrection/16373497-6206193, http://linkedlifedata.com/resource/pubmed/commentcorrection/16373497-6402777, http://linkedlifedata.com/resource/pubmed/commentcorrection/16373497-6771018, http://linkedlifedata.com/resource/pubmed/commentcorrection/16373497-6771020, http://linkedlifedata.com/resource/pubmed/commentcorrection/16373497-6828386, http://linkedlifedata.com/resource/pubmed/commentcorrection/16373497-8232294, http://linkedlifedata.com/resource/pubmed/commentcorrection/16373497-8945520, http://linkedlifedata.com/resource/pubmed/commentcorrection/16373497-8977316, http://linkedlifedata.com/resource/pubmed/commentcorrection/16373497-9087430, http://linkedlifedata.com/resource/pubmed/commentcorrection/16373497-9171084, http://linkedlifedata.com/resource/pubmed/commentcorrection/16373497-9404895, http://linkedlifedata.com/resource/pubmed/commentcorrection/16373497-9659922, http://linkedlifedata.com/resource/pubmed/commentcorrection/16373497-9848648
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1355-8382
pubmed:author
pubmed:issnType
Print
pubmed:volume
12
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
122-32
pubmed:dateRevised
2011-10-26
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Non-snRNP U1A levels decrease during mammalian B-cell differentiation and release the IgM secretory poly(A) site from repression.
pubmed:affiliation
Rutgers University, Department of Molecular Biology and Biochemistry, Nelson Laboratories, Room A322, 604 Allison Road, Piscataway, NJ 08854, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, N.I.H., Extramural