Although E<sub>2</sub> and E<sub>3</sub> were equally efficacious and potent on the endogenous ERE-containing pS2 promoter in the MCF-7 BUS breast cancer cell line co-expressing ERα and ERβ, E<sub>1</sub> was less efficacious and potent than E<sub>2</sub>.
Although E<sub>2</sub> and E<sub>3</sub> were equally efficacious and potent on the endogenous ERE-containing pS2 promoter in the MCF-7 BUS breast cancer cell line co-expressing ERα and ERβ, E<sub>1</sub> was less efficacious and potent than E<sub>2</sub>.
Mutations in APP and PS-1 and PS-2 genes that are associated with early-onset, autosomal, dominantly inherited AD, in addition to the at-risk gene polymorphisms responsible for late-onset AD, all indicate a direct and early role of Aβ in the pathogenesis of AD.
While genetic mutations in amyloid precursor protein and presenilin-1 and -2 (PS1 and PS2) genes cause early-onset familial AD, the etiology of sporadic AD is not fully understood.
The session took place in three stages: 1) a round of individual contributions from participants addressing areas that they considered of interest; 2) a general recommendation whereby studies about prevention and early diagnosis and treatment were to be initiated targeting persons bearing the dominant mutations in AbetaPP, PS-1 and PS-2 genes that result in development of AD; and 3) a proposal was made to the effect that a network be set up to facilitate interaction among those participating in the meeting.
Recent studies have revealed that forebrain specific conditional knockouts of PS1 and PS2 genes (cPSKO) cause both neuronal degeneration and memory loss without evidence of formation of amyloid plaques.
Recent studies have revealed that forebrain specific conditional knockouts of PS1 and PS2 genes (cPSKO) cause both neuronal degeneration and memory loss without evidence of formation of amyloid plaques.
Early onset familial Alzheimer's disease (FAD) is linked to autosomal dominant mutations in the amyloid precursor protein (APP) and presenilin 1 and 2 (PS1 and PS2) genes.
Early onset familial Alzheimer's disease (FAD) is linked to autosomal dominant mutations in the amyloid precursor protein (APP) and presenilin 1 and 2 (PS1 and PS2) genes.
An increased production of Abeta-42 by mutation of PS2 genes promotes caspase expression and is associated with the Cox-2 found in the brain of AD patients.
To investigate the expression and possible role of pS2 protein as a predictor of tumor recurrence in superficial transitional cell carcinoma of the bladder and to determine its relation with tumor stage, grade, size, number, recurrence and proliferative activity.
At completion of the study, half of the animals per treatment group were killed and tumors collected for evaluation of cellular proliferation and estrogen-responsive pS2 gene expression.
Otherwise, no overlapping of pS2 protein values was obtained between ER-positive and ER-negative carcinomas within defined unfavorable menopausal - and histologic grade-related expression of pS2 protein subgroups.
To investigate the expression and possible role of pS2 protein as a predictor of tumor recurrence in superficial transitional cell carcinoma of the bladder and to determine its relation with tumor stage, grade, size, number, recurrence and proliferative activity.
The pS2 gene product was firstly identified as an oestrogen-induced molecule in a breast cancer cell line, while recent studies demonstrate a close association with mucus-secreting epithelia.