Wendy Bruening

TL;DR: Evidence is presented that mutations in the Cu/Zn‐superoxidedismutase (SOD‐1) gene underlie some familial cases of amytotrophic lateral sclerosis, a neurodegenerative disorder charactreized by loss of cortical, brainstem, and spinal motor nrurons, and that insufficiency of molecular chaperones may be directly involved in loss of motor neurons in this disease.

TL;DR: Examination of a panel of breast and ovarian carcinomas for expression of α, β, and γ synucleins found that α synuclein has attracted considerable attention due to its involvement in neurodegenerative diseases.

TL;DR: Oncogenic activation of γ-synuclein contributes to the development of breast and ovarian cancer by promoting tumor cell survival under adverse conditions and by providing resistance to certain chemotherapeutic drugs.

TL;DR: It is found that the same conditions that lead to activation of SAPK/JNKs and p38 kinases can also dramatically increase expression from the CMV promoter, which may complicate, if not invalidate, the interpretation of a wide range of experiments.

TL;DR: Results suggest that slight alterations in the level of OVCA1, such as would occur after reduction of chromosome 17p13.13 to hemizygosity, may result in cell cycle deregulation and promote tumorigenesis.