Davidson T

References (2)

Title : Generation and annotation of the DNA sequences of human chromosomes 2 and 4 - Hillier_2005_Nature_434_724
Author(s) : Hillier LW , Graves TA , Fulton RS , Fulton LA , Pepin KH , Minx P , Wagner-McPherson C , Layman D , Wylie K , Sekhon M , Becker MC , Fewell GA , Delehaunty KD , Miner TL , Nash WE , Kremitzki C , Oddy L , Du H , Sun H , Bradshaw-Cordum H , Ali J , Carter J , Cordes M , Harris A , Isak A , Van Brunt A , Nguyen C , Du F , Courtney L , Kalicki J , Ozersky P , Abbott S , Armstrong J , Belter EA , Caruso L , Cedroni M , Cotton M , Davidson T , Desai A , Elliott G , Erb T , Fronick C , Gaige T , Haakenson W , Haglund K , Holmes A , Harkins R , Kim K , Kruchowski SS , Strong CM , Grewal N , Goyea E , Hou S , Levy A , Martinka S , Mead K , McLellan MD , Meyer R , Randall-Maher J , Tomlinson C , Dauphin-Kohlberg S , Kozlowicz-Reilly A , Shah N , Swearengen-Shahid S , Snider J , Strong JT , Thompson J , Yoakum M , Leonard S , Pearman C , Trani L , Radionenko M , Waligorski JE , Wang C , Rock SM , Tin-Wollam AM , Maupin R , Latreille P , Wendl MC , Yang SP , Pohl C , Wallis JW , Spieth J , Bieri TA , Berkowicz N , Nelson JO , Osborne J , Ding L , Sabo A , Shotland Y , Sinha P , Wohldmann PE , Cook LL , Hickenbotham MT , Eldred J , Williams D , Jones TA , She X , Ciccarelli FD , Izaurralde E , Taylor J , Schmutz J , Myers RM , Cox DR , Huang X , McPherson JD , Mardis ER , Clifton SW , Warren WC , Chinwalla AT , Eddy SR , Marra MA , Ovcharenko I , Furey TS , Miller W , Eichler EE , Bork P , Suyama M , Torrents D , Waterston RH , Wilson RK
Ref : Nature , 434 :724 , 2005
Abstract : Human chromosome 2 is unique to the human lineage in being the product of a head-to-head fusion of two intermediate-sized ancestral chromosomes. Chromosome 4 has received attention primarily related to the search for the Huntington's disease gene, but also for genes associated with Wolf-Hirschhorn syndrome, polycystic kidney disease and a form of muscular dystrophy. Here we present approximately 237 million base pairs of sequence for chromosome 2, and 186 million base pairs for chromosome 4, representing more than 99.6% of their euchromatic sequences. Our initial analyses have identified 1,346 protein-coding genes and 1,239 pseudogenes on chromosome 2, and 796 protein-coding genes and 778 pseudogenes on chromosome 4. Extensive analyses confirm the underlying construction of the sequence, and expand our understanding of the structure and evolution of mammalian chromosomes, including gene deserts, segmental duplications and highly variant regions.
ESTHER : Hillier_2005_Nature_434_724
PubMedSearch : Hillier_2005_Nature_434_724
PubMedID: 15815621
Gene_locus related to this paper: human-ABHD1 , human-LDAH , human-ABHD18 , human-KANSL3 , human-PGAP1 , human-PREPL

Title : The involvement of hypoxia-inducible transcription factor-1-dependent pathway in nickel carcinogenesis - Salnikow_2003_Cancer.Res_63_3524
Author(s) : Salnikow K , Davidson T , Zhang Q , Chen LC , Su W , Costa M
Ref : Cancer Research , 63 :3524 , 2003
Abstract : Nickel is a potent environmental pollutant in industrial countries. Because nickel compounds are carcinogenic, exposure to nickel represents a serious hazard to human health. The understanding of how nickel exerts its toxic and carcinogenic effects at a molecular level may be important in risk assessment, as well as in the treatment and prevention of occupational diseases. Previously, using human and rodent cells in vitro, we showed that hypoxia-inducible signaling pathway was activated by carcinogenic nickel compounds. Acute exposure to nickel resulted in the accumulation of hypoxia-inducible transcription factor (HIF)-1, which strongly activated hypoxia-inducible genes, including the recently discovered tumor marker NDRG1 (Cap43). To further identify HIF-1-dependent nickel-inducible genes and to understand the role of the HIF-dependent signaling pathway in nickel-induced transformation, we used the Affymetrix GeneChip to compare the gene expression profiles in wild-type cells or in cells from HIF-1 alpha knockout mouse embryos exposed to nickel chloride. As expected, when we examined 12,000 genes for expression changes, we found that genes coding for glycolytic enzymes and glucose transporters, known to be regulated by HIF-1 transcription factor, were induced by nickel only in HIF-1 alpha-proficient cells. In addition, we found a number of other hypoxia-inducible genes up-regulated by nickel in a HIF-dependent manner including BCL-2-binding protein Nip3, EGLN1, hypoxia-inducible gene 1 (HIG1), and prolyl 4-hydroxylase. Additionally, we found a number of genes induced by nickel in a HIF-independent manner, suggesting that Ni activated other signaling pathways besides HIF-1. Finally, we found that in HIF-1 alpha knockout cells, nickel strongly induced the expression of the whole group of genes that were not expressed in the presence of HIF-1. Because the majority of modulated genes were induced or suppressed by nickel in a HIF-1-dependent manner, we elucidated the role of HIF-1 transcription factor in cell transformation. In HIF-1 alpha-proficient cells, nickel exposure increased soft agar growth, whereas it decreased soft agar growth in HIF-1 alpha-deficient cells. We hypothesize that the induction of HIF-1 transcription factor by nickel may be important during the nickel-induced carcinogenic process.
ESTHER : Salnikow_2003_Cancer.Res_63_3524
PubMedSearch : Salnikow_2003_Cancer.Res_63_3524
PubMedID: 12839937