Identification of amyloid β-peptide responsive genes by cDNA microarray technology: Involvement of RTP801 in amyloid β-peptide toxicity

Kim, Ki Wook; Lee, Myeong Soo; Chung, Henry; S, Kim; Baek, Seung‐Hoon; Kim, Jae‐Hun; Ys, Kim

doi:10.1038/emm.2003.53

Cited by 76 publications

(46 citation statements)

References 27 publications

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“…Although Ab is a secreted peptide, it has been proposed that intracellular Ab pools may regulate the p53 gene (Ohyagi et al 2005). Several studies have also reported RNA expression differences in a variety of models that are associated with overexpression of Ab peptides, ranging from lymphocytes (Kalman et al 2005) or other cell types from AD patients (Kim et al 2003;Maes et al 2007) to brains from APP transgenic mice (Reddy et al 2004) and Caenorhabditis elegans expressing Ab (Wu and Luo 2005). These studies have proposed that Ab expression causes misregulation of stress-response genes, cytoskeletal components, DNA repair, and transcription.…”

Section: Discussionmentioning

confidence: 99%

Identification of Novel Genes That Modify Phenotypes Induced by Alzheimer's β-Amyloid Overexpression in Drosophila

Cao

Song²,

Gangi

et al. 2008

Genetics

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Sustained increases in life expectancy have underscored the importance of managing diseases with a high incidence in late life, such as various neurodegenerative conditions. Alzheimer's disease (AD) is the most common among these, and consequently significant research effort is spent on studying it. Although a lot is known about the pathology of AD and the role of b-amyloid (Ab) peptides, the complete network of interactions regulating Ab metabolism and toxicity still eludes us. To address this, we have conducted genetic interaction screens using transgenic Drosophila expressing Ab and we have identified mutations that affect Ab metabolism and toxicity. These analyses highlight the involvement of various biochemical processes such as secretion, cholesterol homeostasis, and regulation of chromatin structure and function, among others, in mediating toxic Ab effects. Several of the mutations that we identified have not been linked to Ab toxicity before and thus constitute novel potential targets for AD intervention. We additionally tested these mutations for interactions with tau and expanded-polyglutamine overexpression and found a few candidate mutations that may mediate common mechanisms of neurodegeneration. Our data offer insight into the toxicity of Ab and open new areas for further study into AD pathogenesis

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Section: Discussionmentioning

confidence: 99%

Identification of Novel Genes That Modify Phenotypes Induced by Alzheimer's β-Amyloid Overexpression in Drosophila

Cao

Song²,

Gangi

et al. 2008

Genetics

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“…To validate the differential expressions of genes screened by cDNA microarray analysis, we used semi-quantitative RT-PCR (Kim et al, 2003b). The levels of amplified DNAs by RT-PCR were quantified using the UTHSCSA ImageTool program (developed at the University of Texas Health Science Center at San Antonio, Texas and available at http://ddsdx.uthscsa.edu/dig/itdesc.html).…”

Section: Semi-quantitative Reverse Transcription-polymerase Chain Reamentioning

confidence: 99%

Exploration of replicative senescence-associated genes in human dermal fibroblasts by cDNA microarray technology

Yoon

Kim

et al. 2004

Experimental Gerontology

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109

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“…1,2 Several recent reports showed that REDD1 is induced in response to hypoxia, energy stress, and DNA damage. [3][4][5] In addition, abnormal expression of REDD1 is involved in the pathogenesis of multiple diseases, including Alzheimer's disease, 6 ischemic proliferative retinopathy 7 and others. 8 Cellular response to hypoxia plays an important role not only in biological processes such as hematopoiesis, 9 wound healing, 10 ischemic stroke, myocardial infarction, and retinopathy but also in carcinogenesis.…”

Section: Introductionmentioning

confidence: 99%

REDD1 is required for RAS-mediated transformation of human ovarian epithelial cells

Chang¹,

Liu²,

Yang³

et al. 2009

Cell Cycle

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REDD1 is a gene induced by hypoxia and stimuli from multiple DNA damage. Here we show that REDD1 expression was elevated in RAS-transformed ovarian epithelial cells lines and that this overexpression increased these cells' growth rate and anchorage-independent growth on soft agar. Injection of immortalized ovarian epithelial cells overexpressing REDD1 into nude mice resulted in tumor growth that developed into papillary serous carcinoma in the peritoneal cavity. Knockdown of REDD1 expression blocked the RAS-mediated transformation of these cell lines. REDD1 overexpression decreased apoptosis and associated with increased expression of Bcl-x L or Bcl-2 and decreased expression of FADD, caspase1, caspase8, caspase 9, caspase 10, BAX, Bad and Bcl-X S . Our data demonstrated that REDD1 is a key mediator in RAS-mediated transformation through an effect on anti-apoptosis.

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Identification of amyloid β-peptide responsive genes by cDNA microarray technology: Involvement of RTP801 in amyloid β-peptide toxicity

Cited by 76 publications

References 27 publications

Identification of Novel Genes That Modify Phenotypes Induced by Alzheimer's β-Amyloid Overexpression in Drosophila

Identification of Novel Genes That Modify Phenotypes Induced by Alzheimer's β-Amyloid Overexpression in Drosophila

Exploration of replicative senescence-associated genes in human dermal fibroblasts by cDNA microarray technology

REDD1 is required for RAS-mediated transformation of human ovarian epithelial cells

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