نتایج جستجو برای: ژن bad الکترومغناطیس

تعداد نتایج: 47276  

2013
Lawrence Martis Anne Westhues

Objectives: This study was done to explore the experiences of physicians in India about being the messengers of bad news and management of psychosocial burdens associated with such consultations. Methods: Narrative data was collected from 27 physicians working in four teaching hospitals, using a semi-structured interview schedule. Constant comparison analytic procedures were used to examine phy...

Journal: :Cell 1997
Sandeep Robert Datta Henryk Dudek Xu Tao Shane Masters Haian Fu Yukiko Gotoh Michael E Greenberg

Growth factors can promote cell survival by activating the phosphatidylinositide-3'-OH kinase and its downstream target, the serine-threonine kinase Akt. However, the mechanism by which Akt functions to promote survival is not understood. We show that growth factor activation of the PI3'K/Akt signaling pathway culminates in the phosphorylation of the BCL-2 family member BAD, thereby suppressing...

Journal: :Lancet 2004
Lesley Fallowfield Valerie Jenkins

In every medical specialty bad, sad, and difficult information must be given to patients and their families. An insensitive approach increases the distress of recipients of bad news, may exert a lasting impact on their ability to adapt and adjust, and can lead to anger and an increased risk of litigation. Many doctors also find these interactions stressful, and in the absence of much effective ...

Journal: :Molecular and cellular biology 2003
Chi-Wu Chiang Cindy Kanies Kwang Woon Kim Wei Bin Fang Christina Parkhurst Minhui Xie Travis Henry Elizabeth Yang

BAD, a proapoptotic molecule of the BCL2 family, is regulated by reversible phosphorylation. During survival, BAD is sequestered by 14-3-3 through serine 136 phosphorylation and is dissociated from BCL-X(L) through serine 155 phosphorylation. We report that phosphoserine 112 (pSer112) dephosphorylation functions as a gatekeeper for BAD-mediated apoptosis. During apoptosis, dephosphorylation of ...

2017
Alix Rexford Diego A R Zorio Brian G Miller

The glycolytic enzyme glucokinase (GCK) and the pro-apoptotic protein BAD reportedly reside within a five-membered complex that localizes to the mitochondria of mammalian hepatocytes and pancreatic β-cells. Photochemical crosslinking studies using a synthetic analog of BAD's BH3 domain and in vitro transcription/translation experiments support a direct interaction between BAD and GCK. To invest...

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