Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0017636 (glioblastoma)
 18,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have re-examined whether pp60c-src, the normal cellular homologue of the transforming protein of Rous sarcoma virus, is present in human T cells. By in vitro immune-complex kinase assay or Western blotting with the anti-pp60c-src mAbs 327 or GD11, pp60c-src was found to be present in lysates of T cell lines, including the Jurkat T cell line. The 327 and GD11 mAbs have been reported to be specific for pp60c-src and not to cross-react with other src family members or other kinases. Furthermore, the size of the pp60c-src bands present on Western blotting and in vitro kinase assay were clearly different from those of p56lck or p59fyn. In addition, pp60c-src is detected in the HTLV-I-derived T cell lines S1T and C8, which lack expression of p56lck and p59fyn. RNase protection assays confirmed that pp60c-src mRNA is present in Jurkat T cells. We also found pp60c-src protein to be constitutively present in freshly isolated thymocytes. In contrast, pp60c-src was absent, or present at extremely low levels, in normal, resting peripheral blood T lymphocytes, which is in agreement with previous findings. However, after stimulation of resting T cells with the mitogenic lectin PHA or with Ab to the TCR complex, pp60c-src expression is induced in both CD4+ and CD8+ T cell subsets, with peak expression detectable 12 to 24 h after T cell activation. The levels of pp60c-src are low in all T cells except Jurkat, where levels of pp60c-src are comparable to levels found in a glioblastoma cell line (T98G). Nevertheless, significant levels of pp60c-src kinase activity are readily detectable in thymocytes and activated normal T cells as well as in T cell lines. The finding that pp60c-src is inducible following activation through the TCR suggests that pp60c-src may play a specific role in the normal T cell activation pathway.
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PMID:pp60c-src expression is induced by activation of normal human T lymphocytes. 753 11

Characterization of the cellular transcription factors interacting with the human T cell lymphotropic virus type I (HTLV-I) long terminal repeat (LTR) is essential to dissecting the mechanisms involved in viral transcription that may be pertinent to the oncogenic and neuropathogenic processes associated with HTLV-I infection in both the immune and nervous systems. Electrophoretic mobility shift (EMS) analyses utilizing oligonucleotides homologous to each of the 21 bp repeat elements reacted with nuclear extracts derived from cell lines of lymphocytic, monocytic, neuronal, and glial cell origin have demonstrated differential binding of cellular factors to the three 21 bp repeats (1-4). ATF/CREB and Sp family members interacted with the 21 bp repeats to form DNA-protein complexes common to all cell types examined. However, a unique DNA-protein complex was detected when the promoter central 21 bp repeat was reacted with nuclear extracts derived from either the U-373 MG glioblastoma cell line or the THP-1 mature monocytic cell line. Based on nucleotide sequence requirements and immunoreactivity, we demonstrate that this DNA-protein complex is comprised of the AP-1 components, Fos and Jun.
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PMID:AP-1 derived from mature monocytes and astrocytes preferentially interacts with the HTLV-I promoter central 21 bp repeat. 920 84