An aberrant lck mRNA in two human T-cell lines

Vogel, Lee; Arthur, Richard; Fujita, Daishi

doi:10.1016/0167-4781(95)00162-a

Cited by 4 publications

(2 citation statements)

References 17 publications

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“…PCR primers pairs that amplify a product that crosses introns for reduced glyceraldehyde-phosphate dehydrogenase and p56lck were chosen from previous publications. 19,21 PCR was performed using previously published conditions for the primers. 19,21 Resultant products were electrophoresed, stained with ethidium bromide, and photographed under ultraviolet light.…”

Section: Rna Extraction and Rt-pcr For P56lck Expressionmentioning

confidence: 99%

Adenomatous Polyposis Coli Gene Mutation Alters Proliferation through its β-Catenin-Regulatory Function in Aggressive Fibromatosis (Desmoid Tumor)

Bapat

Alman

1998

The American Journal of Pathology

119

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Aggressive fibromatosis is a monoclonal proliferation of spindle (fibroblast-like) cells. A subset of lesions contain somatic truncating adenomatous polyposis coli (APC) gene mutations, and all of the lesions contain an elevated beta-catenin protein level. A major function of APC is to regulate beta-catenin protein level. Beta-catenin has a dual function in the cell: it is a member of the adherens junction, and it binds transcription factors in the tcf-lef family, transactivating transcription. Cell cultures from aggressive fibromatoses containing an APC mutation were studied. Transient transfection of the full-length APC gene caused decreased proliferation and beta-catenin protein level in these cultures. To determine whether beta-catenin protein level was responsible for the change in proliferation rate, stable transfections of deltaN89beta-catenin (a stabilized form that is not degraded by APC, but retains all other functions) were achieved in half of the cultures derived from each tumor, whereas the other half were transfected with an empty vector. Transfection of the full-length APC gene in cultures that were stably transfected with deltaN89beta-catenin did not result in a change in proliferation. The type I promotor of p56lck contains an HMG consensus region, to which members of the tcf-lef family can bind. p56lck was expressed in cultures not transfected with the full-length APC gene and in cultures transfected with the full-length APC gene and deltaN89beta-catenin, but not in cultures transfected with only the full-length APC gene. These data show that APC truncating mutations give aggressive fibromatosis cells a proliferative advantage through beta-catenin and suggest that beta-catenin acts to transactivate transcription.

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Section: Rna Extraction and Rt-pcr For P56lck Expressionmentioning

confidence: 99%

Adenomatous Polyposis Coli Gene Mutation Alters Proliferation through its β-Catenin-Regulatory Function in Aggressive Fibromatosis (Desmoid Tumor)

Bapat

Alman

1998

The American Journal of Pathology

119

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“…Src-associated substrate in mitosis of 68 kDa (Sam68), otherwise known as KHDRBS1, was first characterized as a mitotic target of Src tyrosine kinase in mouse NIH3T3 fibroblasts [ , ], and as a tyrosine phosphorylated protein associated with the T cell–specific Src kinase p56 lck in leukemic T-cell lines and mitogen-activated T lymphocytes [ ]. Sam68 belongs to the signal transducer and activator of the RNA (STAR) family of RNA-binding proteins that link signaling pathways to RNA processing and contain a heteronuclear ribonucleoprotein particle K homology (KH) domain [ ].…”

Section: Introductionmentioning

confidence: 99%

Sam68 is cleaved by caspases under apoptotic cell death induced by ionizing radiation

Cho

Choi

Nam

et al. 2015

Journal of Radiation Research

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The RNA-binding protein Sam68, a mitotic substrate of tyrosine kinases, has been reported to participate in the cell cycle, apoptosis, and signaling. In particular, overexpression of Sam68 protein is known to suppress cell growth and cell cycle progression in NIH3T3 cells. Although Sam68 is involved in many cellular activities, the function of Sam68, especially in response to apoptotic stimulation, is not well understood. In this study, we found that Sam68 protein is cleaved in immune cells undergoing apoptosis induced by γ-radiation. Moreover, we found that Sam68 cleavage was induced by apoptotic stimuli containing γ-radiation in a caspase-dependent manner. In particular, we showed that activated casepase-3, 7, 8 and 9 can directly cleave Sam68 protein through in vitro protease cleavage assay. Finally, we found that the knockdown of Sam68 attenuated γ-radiation–induced cell death and growth suppression. Conclusively, the cleavage of Sam68 is a new indicator for the cell damaging effects of ionizing radiation.

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Variable selection using probability density function similarity for support vector machine classification of high-dimensional microarray data

Tang

Jiang

Shen

et al. 2009

Talanta

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An aberrant lck mRNA in two human T-cell lines

Cited by 4 publications

References 17 publications

Adenomatous Polyposis Coli Gene Mutation Alters Proliferation through its β-Catenin-Regulatory Function in Aggressive Fibromatosis (Desmoid Tumor)

Adenomatous Polyposis Coli Gene Mutation Alters Proliferation through its β-Catenin-Regulatory Function in Aggressive Fibromatosis (Desmoid Tumor)

Sam68 is cleaved by caspases under apoptotic cell death induced by ionizing radiation

Variable selection using probability density function similarity for support vector machine classification of high-dimensional microarray data

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