共 100 条
The engine driving the ship: metabolic steering of cell proliferation and death
被引:178
作者:

Buchakjian, Marisa R.
论文数: 0 引用数: 0
h-index: 0
机构:
Duke Univ, Med Ctr, Dept Pharmacol & Canc Biol, Durham, NC 27710 USA Duke Univ, Med Ctr, Dept Pharmacol & Canc Biol, Durham, NC 27710 USA

Kornbluth, Sally
论文数: 0 引用数: 0
h-index: 0
机构:
Duke Univ, Med Ctr, Dept Pharmacol & Canc Biol, Durham, NC 27710 USA Duke Univ, Med Ctr, Dept Pharmacol & Canc Biol, Durham, NC 27710 USA
机构:
[1] Duke Univ, Med Ctr, Dept Pharmacol & Canc Biol, Durham, NC 27710 USA
关键词:
OUTER-MEMBRANE PERMEABILIZATION;
LACKING MITOCHONDRIAL-DNA;
CYTOCHROME-C RELEASE;
GLUCOSE-METABOLISM;
P53-INDUCIBLE REGULATOR;
CASPASE-2;
ACTIVATION;
HISTONE ACETYLATION;
DEPENDENT MECHANISM;
INHIBITS APOPTOSIS;
BCL-2;
FAMILY;
D O I:
10.1038/nrm2972
中图分类号:
Q2 [细胞生物学];
学科分类号:
071009 ;
090102 ;
摘要:
Metabolic activity is a crucial determinant of a cell's decision to proliferate or die. Although it is not fully understood how metabolic pathways such as glycolysis and the pentose phosphate pathway communicate to cell cycle and apoptotic effectors, it is clear that a complex network of signalling molecules is required to integrate metabolic inputs. D-type cyclins, cyclin-dependent kinases, the anaphase-promoting complex, p53, caspase 2 and B cell lymphoma 2 proteins, among others, have been shown to be regulated by metabolic crosstalk. Elucidating these pathways is of great importance, as metabolic aberrations and their downstream effects are known to contribute to the aetiology of cancer and degenerative disorders.
引用
收藏
页码:715 / 727
页数:13
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