| pubmed-article:16778138 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16778138 | lifeskim:mentions | umls-concept:C0007587 | lld:lifeskim |
| pubmed-article:16778138 | lifeskim:mentions | umls-concept:C0085249 | lld:lifeskim |
| pubmed-article:16778138 | lifeskim:mentions | umls-concept:C2936267 | lld:lifeskim |
| pubmed-article:16778138 | lifeskim:mentions | umls-concept:C0332325 | lld:lifeskim |
| pubmed-article:16778138 | lifeskim:mentions | umls-concept:C0883208 | lld:lifeskim |
| pubmed-article:16778138 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:16778138 | pubmed:dateCreated | 2006-9-21 | lld:pubmed |
| pubmed-article:16778138 | pubmed:abstractText | Neoplastic T cells in mycosis fungoides (MF) are resistant to apoptotic agents, including galectin-1 that is abundant in skin. Although MF cells are typically CD7-, and thus galectin-1 resistant, CD7+ HH cells, derived from a patient with MF, were also resistant to galectin-1. HH cells demonstrate altered cell surface glycosylation, with loss of core 2 O-glycan ligands for galectin-1 created by core 2 beta1,6-N-acetylglucosaminyltransferase (C2GnT-I). Loss of core 2 O-glycans on tumor cells was also seen in primary CD7+ MF lesions. Surprisingly, HH cells are heterozygous for a C2GnT-I point mutation, yet this mutation resulted in a dramatic reduction in cellular glycosyltransferase activity. Expression of wild-type C2GnT-I in human HH cells, or murine lymphoma cells that lack C2GnT-I, restored core 2 O-glycan expression and susceptibility to galectin-1, whereas mutant enzyme lacked activity and did not restore core 2 O-glycan expression or susceptibility to galectin-1. Mutant enzyme did not have a dominant negative effect by affecting dimerization or activity of wild-type enzyme; rather, C2GnT-I haploinsufficiency is sufficient for loss of core 2 O-glycan expression and galectin-1 resistance. Thus, glycosyltransferase haploinsufficiency results in altered cellular glycosylation and resistance to cell death, identifying a new survival mechanism for T-lymphoma cells. | lld:pubmed |
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| pubmed-article:16778138 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16778138 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16778138 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:16778138 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16778138 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:16778138 | pubmed:issn | 0006-4971 | lld:pubmed |
| pubmed-article:16778138 | pubmed:author | pubmed-author:FukudaMinoruM | lld:pubmed |
| pubmed-article:16778138 | pubmed:author | pubmed-author:BaumLinda GLG | lld:pubmed |
| pubmed-article:16778138 | pubmed:author | pubmed-author:SaidJonathanJ | lld:pubmed |
| pubmed-article:16778138 | pubmed:author | pubmed-author:ChanJessicaJ | lld:pubmed |
| pubmed-article:16778138 | pubmed:author | pubmed-author:CabreraPaula... | lld:pubmed |
| pubmed-article:16778138 | pubmed:author | pubmed-author:AmanoMahoM | lld:pubmed |
| pubmed-article:16778138 | pubmed:author | pubmed-author:MitomaJunyaJ | lld:pubmed |
| pubmed-article:16778138 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16778138 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:16778138 | pubmed:volume | 108 | lld:pubmed |
| pubmed-article:16778138 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16778138 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16778138 | pubmed:pagination | 2399-406 | lld:pubmed |
| pubmed-article:16778138 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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