pubmed-article:7939633 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:7939633 | lifeskim:mentions | umls-concept:C0033684 | lld:lifeskim |
pubmed-article:7939633 | lifeskim:mentions | umls-concept:C0033640 | lld:lifeskim |
pubmed-article:7939633 | lifeskim:mentions | umls-concept:C1337047 | lld:lifeskim |
pubmed-article:7939633 | lifeskim:mentions | umls-concept:C0004083 | lld:lifeskim |
pubmed-article:7939633 | pubmed:issue | 5182 | lld:pubmed |
pubmed-article:7939633 | pubmed:dateCreated | 1994-11-8 | lld:pubmed |
pubmed-article:7939633 | pubmed:abstractText | In this study, a protein that interacts with sequences encoded by the first exon of the protein kinase Bcr was cloned. The Bcr-associated protein 1 (Bap-1) is a member of the 14-3-3 family of proteins. Bap-1 interacts with full-length c-Bcr and with the chimeric Bcr-Abl tyrosine kinase of Philadelphia chromosome (Ph1)-positive human leukemias. Bap-1 is a substrate for the Bcr serine-threonine kinase and is also phosphorylated on tyrosine by Bcr-Abl but not by c-Abl. Bap-1 may function in the regulation of c-Bcr and may contribute to the transforming activity of Bcr-Abl in vivo. 14-3-3 proteins are essential for cell proliferation and have a role in determining the timing of mitosis in yeast. Through direct binding to sequences present in Bcr and in other proteins implicated in signaling, the mammalian 14-3-3 proteins may link specific signaling protein components to mitogenic and cell-cycle control pathways. | lld:pubmed |
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pubmed-article:7939633 | pubmed:language | eng | lld:pubmed |
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pubmed-article:7939633 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:7939633 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:7939633 | pubmed:month | Oct | lld:pubmed |
pubmed-article:7939633 | pubmed:issn | 0036-8075 | lld:pubmed |
pubmed-article:7939633 | pubmed:author | pubmed-author:CollierR JRJ | lld:pubmed |
pubmed-article:7939633 | pubmed:author | pubmed-author:CripeL DLD | lld:pubmed |
pubmed-article:7939633 | pubmed:author | pubmed-author:GIEE | lld:pubmed |
pubmed-article:7939633 | pubmed:author | pubmed-author:PendergastA... | lld:pubmed |
pubmed-article:7939633 | pubmed:author | pubmed-author:ReutherG WGW | lld:pubmed |
pubmed-article:7939633 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:7939633 | pubmed:day | 7 | lld:pubmed |
pubmed-article:7939633 | pubmed:volume | 266 | lld:pubmed |
pubmed-article:7939633 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:7939633 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:7939633 | pubmed:pagination | 129-33 | lld:pubmed |
pubmed-article:7939633 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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pubmed-article:7939633 | pubmed:year | 1994 | lld:pubmed |
pubmed-article:7939633 | pubmed:articleTitle | Association of the protein kinases c-Bcr and Bcr-Abl with proteins of the 14-3-3 family. | lld:pubmed |
pubmed-article:7939633 | pubmed:affiliation | Department of Pharmacology, Duke University Medical Center, Durham, NC 27710. | lld:pubmed |
pubmed-article:7939633 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:7939633 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:7939633 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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