Zobrazeno 1 - 10
of 27
pro vyhledávání: '"J A, Tischfield"'
Publikováno v:
Cancer research. 60(13)
Heritable gene silencing is an important mechanism of tumor suppressor gene inactivation in a variety of human cancers. In the present study, we show that methylation-associated silencing of the autosomal adenine phosphoribosyltransferase (Aprt) locu
Autor:
M S, Turker, B M, Gage, J A, Rose, O N, Ponomareva, J A, Tischfield, P J, Stambrook, C, Barlow, A, Wynshaw-Boris
Publikováno v:
Cancer research. 59(19)
The presence of increased frequencies of blood-derived and solid tumors in ataxia-telangiectasia (A-T) patients, coupled with a role for the ATM (A-T mutation) protein in detecting specific forms of DNA damage, has led to the assumption of a mutator
Autor:
M S, Turker, B M, Gage, J A, Rose, D, Elroy, O N, Ponomareva, P J, Stambrook, J A, Tischfield
Publikováno v:
Cancer research. 59(8)
To determine the types of mutations induced by oxidative damage, a kidney cell line with a heterozygous deficiency for the autosomal Aprt (adenine phosphoribosyltransferase) gene was tested for its mutagenic response to hydrogen peroxide. Aprt-defici
Autor:
H J, Edenberg, J, Reynolds, D L, Koller, H, Begleiter, K K, Bucholz, P M, Conneally, R, Crowe, A, Goate, V, Hesselbrock, T K, Li, J I, Nurnberger, B, Porjesz, T, Reich, J P, Rice, M, Schuckit, J A, Tischfield, T, Foroud
Publikováno v:
Alcoholism, clinical and experimental research. 22(5)
A population association between a regulatory variation in the promoter of the serotonin transporter gene (HTT) and severe alcohol dependence was recently reported. We analyzed this potential association in a large number of systematically ascertaine
Autor:
C R, Cloninger, P, Van Eerdewegh, A, Goate, H J, Edenberg, J, Blangero, V, Hesselbrock, T, Reich, J, Nurnberger, M, Schuckit, B, Porjesz, R, Crowe, J P, Rice, T, Foroud, T R, Przybeck, L, Almasy, K, Bucholz, W, Wu, S, Shears, K, Carr, C, Crose, C, Willig, J, Zhao, J A, Tischfield, T K, Li, P M, Conneally
Publikováno v:
American journal of medical genetics. 81(4)
A genome-wide scan between normal human personality traits and a set of genetic markers at an average interval of 13 centimorgans was carried out in 758 pairs of siblings in 177 nuclear families of alcoholics. Personality traits were measured by the
Publikováno v:
The Journal of biological chemistry. 273(23)
We examined the relative contributions of five distinct mammalian phospholipase A2 (PLA2) enzymes (cytosolic PLA2 (cPLA2; type IV), secretory PLA2s (sPLA2s; types IIA, V, and IIC), and Ca2+-independent PLA2 (iPLA2; type VI)) to arachidonic acid (AA)
Autor:
P K, Gupta, A, Sahota, S A, Boyadjiev, S, Bye, C, Shao, J P, O'Neill, T C, Hunter, R J, Albertini, P J, Stambrook, J A, Tischfield
Publikováno v:
Cancer research. 57(6)
We have used the adenine phosphoribosyltransferase gene (APRT; 16q24) to investigate the mechanisms of loss of heterozygosity (LOH) in normal human somatic cells in vivo. APRT-deficient (APRT-/-, APRT-/0) T lymphocytes from the peripheral blood of fo
Publikováno v:
Journal of cellular biochemistry. 64(3)
We use in situ hybridization to demonstrate that the testicular expression of a novel, mouse, low molecular weight phospholipase A2 (PLA2 Group IIc) mRNA is specific to cells undergoing meiosis. A complete cDNA (1421 bp) encoding the mouse Pla2g2c ge
Autor:
L N, Spirio, W, Kutchera, M V, Winstead, B, Pearson, C, Kaplan, M, Robertson, E, Lawrence, R W, Burt, J A, Tischfield, M F, Leppert, S M, Prescott, R, White
Publikováno v:
Cancer research. 56(5)
Mutation of Pla2g2a, a secretory phospholipase A(2) gene, dramatically increases the number of intestinal polyps that develop in the multiple intestinal neoplasia (Min) mouse, a murine model for adenomatous polyposis coli in humans. We tested the hyp
Publikováno v:
Environmental and molecular mutagenesis. 28(4)
We describe an in vivo mutagenesis model that utilizes reverse mutation and forward mutation at the endogenous Aprt locus. Reverse mutation provides an in situ method for detecting environments or agents that cause point mutations. Forward mutation d