Expression of three mammalian cDNAs that interfere with RAS function in Saccharomyces cerevisiae.

Colicelli, John; Nicolette, Charles A.; Birchmeier, Carmen; Rodgers, Linda; Riggs, Michael; Wigler, Michael

doi:10.1073/pnas.88.7.2913

Cited by 103 publications

(78 citation statements)

References 41 publications

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“…Here we demonstrate the cloning of a mammalian eDNA encoding choline kinase by complementation of the yeast cki mutation from a human glioblastoma eDNA library constructed by Colicelli et al [11]. The results raises the possibility that other mammalian ¢DNAs involved in phospholipid metabolism would also be available through yeast eomplementation (for yeast phospholipid metabolism mutants, see review [13]).…”

Section: Introductionmentioning

confidence: 75%

“…The composition of the inositol-free minimum medium (M-i medium) was as described previously [16]. The human glioblastoma eDNA library [11] was a gift from M, Wiglet (Cold Spring Harbor Laboratory) to J.N.…”

Section: Yeast Strains Attd Edna Librarymentioning

confidence: 99%

“…Competent ceils were prepared and transformed with a human glioblastoma eDNA library [I 1] by the method of Ito et al [18]. The library had been constructed on yeast expression vector pADANS [11] containing the ADH1 promoter and 14 amino acids derived from ADHI, and the Notl cloning site. Thus the cDNAs ture were incubated at 30°C for the indicated times with shaking.…”

Section: Cloning Of a Human Edna Capable Of Complementmentioning

confidence: 99%

“…Recently, several mammalian eDNAs were successfully cloned by complementation of the corresponding yeast mutations [7][8][9][10][11][12], but so far no successful cloning of eDNAs for phospholipid metabolism has been reported. Here we demonstrate the cloning of a mammalian eDNA encoding choline kinase by complementation of the yeast cki mutation from a human glioblastoma eDNA library constructed by Colicelli et al [11].…”

Section: Introductionmentioning

confidence: 99%

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Cloning of a human choline kinase cDNA by complementation of the yeast cki mutation

et al. 1992

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A human choline kinase eDNA was cloned by complementation of the yeast choline kina~ mutation, cki, from a human glioblastoma eDNA expression library. The deduced sequence of the human enzyme comprised 456 amino acids with a calculated relative molecular mass of 52.065. The human enzyme resembled the rat liver enzyme over the entire se,4uen¢~. It also resembled the yeast enzyme in the carbox~-terminal region, but not much in the amino-terminal region.

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Section: Introductionmentioning

confidence: 75%

Section: Yeast Strains Attd Edna Librarymentioning

confidence: 99%

Section: Cloning Of a Human Edna Capable Of Complementmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Cloning of a human choline kinase cDNA by complementation of the yeast cki mutation

et al. 1992

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“…Despite this ubiquity, it has until recently been poorly studied, and its mechanisms of action remain unclear. It was originally described as a gene product that modulated RAS function in Saccharomyces cerevisiae (9). Later, a yeast two-hybrid screen of a Schizosaccharomyces pombe cDNA library identified an apparent ortholog of the Avo1 gene that binds the StyI/Spc1, stress-activated MAP kinase (SAPK) (10).…”

mentioning

confidence: 99%

A link between SIN1 (MAPKAP1) and poly(rC) binding protein 2 (PCBP2) in counteracting environmental stress

Ghosh¹,

Srivastava²,

Xu³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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When SIN1 (MAPKAP1) was used as the bait in a two-hybrid screen of a human bone marrow cDNA library, its most frequent partner was poly(rC) binding protein 2 (PCBP2/hnRNP-E2), which associates with the N-terminal domain of SIN1 and can be coimmunoprecipitated with SIN1 and the cytoplasmic domain of the IFN receptor IFNAR2 from HeLa cells. SIN1, but not PCBP2, also associates with the receptors that bind TNF␣. PCBP2 is known to bind pyrimidinerich repeats within the 3 UTR of mRNAs and has been implicated in control of RNA stability and translation and selective capindependent transcription. RNAi silencing of either SIN1 or PCBP2 renders cells sensitive to basal and stress-induced apoptosis. Stress in the form of TNF␣ and H2O2 treatments rapidly raises the cell content of SIN1 and PCBP2, an effect reversible by inhibiting MAPK14. A meta analysis of human microarray information with an algorithm that discerns similarities in gene-regulatory profiles shows that SIN1 and PCBP2 are generally coregulated with large numbers of genes implicated in both cell survival and death and in cellular stress responses, including RNA translation and processing. We predict that SIN1 is a scaffold protein that organizes antiapoptotic responses in stressed cells, whereas PCBP2, its binding partner, provides for the selective expression of cell survival factors through posttranslational events.apoptosis ͉ interferon ͉ stress kinase-interacting protein 1 ͉ yeast two-hybrid assay W hen faced with environmental stressors such as reactive oxygen species, inflammatory shock, or viral infection, cells may react by either boosting protective mechanisms or undergoing programmed cell death. A delicate balance is maintained between pathways that promote survival or death, and this balance can be affected by a number of cytokines, including members of the IL, IFN, and TNF families (1). The type 1 IFN in particular have the ability to promote (2, 3) or prevent (4) cell death depending on the circumstances. Exposure of cells to stress induces compensatory activation of multiple intracellular signaling pathways, among which is the one controlled by p38 MAPK (MAPK14), also known as stress-activated protein kinase (5).We previously used yeast two-hybrid genetic screens to identify stress kinase-interacting protein 1 (SIN1; MAPKAP1) as a factor that associates with the IFN receptor subunit IFNAR2 (6). Cells in which the SIN1 gene has been ablated or where gene expression had been knocked down by RNAi silencing are susceptible to stress (7,8). SIN1 is represented as a single gene in all metazoan species and fungi so far examined, is highly conserved in vertebrates, and is expressed in most, if not all, tissues of the mouse (6). Despite this ubiquity, it has until recently been poorly studied, and its mechanisms of action remain unclear. It was originally described as a gene product that modulated RAS function in Saccharomyces cerevisiae (9). Later, a yeast two-hybrid screen of a Schizosaccharomyces pombe cDNA library identified an apparent ortholog of t...

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A consistent pattern ofRIN1 rearrangements in oral squamous cell carcinoma cell lines supports a breakage-fusion-bridge cycle model for 11q13 amplification

Shuster

Han²,

Beau

et al. 2000

Genes Chromosom. Cancer

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Gene amplification is a common feature of tumors. Overexpression of some amplified genes plays a role in tumor progression. Gene amplification can occur either extrachromosomally as double‐minute chromosomes (dmin) or intrachromosomally in the form of homogeneously staining regions (hsrs). Approximately one‐half of our oral squamous cell carcinomas (OSCCs) are characterized by amplification of band 11q13, usually as an hsr located entopically (occurring or situated at the normal chromosomal site, as opposed to ectopically). Using chromosomal fluorescence in situ hybridization (FISH), we confirmed the amplification of the cyclin D1 (CCNDx1/PRAD1) and fibroblast growth factor types 3 and 4 (FGF3/INT2 and FGF4/HSTF1) genes within the 11q13 amplicon in our series of primary OSCCs and derived cell lines. The human RIN1 gene was isolated as an RAS interaction/interference protein in a genetic selection in yeast and has been described as a putative effector of both the RAS and ABL oncogenes. We mapped RIN1 to 11q13.2. FISH analysis of 10 11q13‐amplified OSCC cell lines revealed high‐level RIN1 amplification in two cell lines. Three additional cell lines have what appear to be duplications and/or low‐level amplification of RIN1, visible in both interphase and metaphase cells. The hybridization pattern of RIN1 on the metaphase chromosomes is particularly revealing; RIN1 signals flank the 11q13 hsr, possibly as a result of an inverted duplication. The gene amplification model of Coquelle et al. (1997) predicted that gene amplification occurs by breakage‐fusion‐bridge (BFB) cycles involving fragile sites. Our data suggest that the pattern of gene amplification at 11q13 in OSCC cell lines is consistent with a BFB model. RIN1 appears to be a valuable probe for investigating the process of gene amplification in general and, specifically, 11q13 amplification in oral cancer. Genes Chromosomes Cancer 28:153–163, 2000. © 2000 Wiley‐Liss, Inc.

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Expression of three mammalian cDNAs that interfere with RAS function in Saccharomyces cerevisiae.

Cited by 103 publications

References 41 publications

Cloning of a human choline kinase cDNA by complementation of the yeast cki mutation

Cloning of a human choline kinase cDNA by complementation of the yeast cki mutation

A link between SIN1 (MAPKAP1) and poly(rC) binding protein 2 (PCBP2) in counteracting environmental stress

A consistent pattern ofRIN1 rearrangements in oral squamous cell carcinoma cell lines supports a breakage-fusion-bridge cycle model for 11q13 amplification

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