EMBO Journal
0261-4189
1460-2075
Đức
Cơ quản chủ quản: Wiley-Blackwell , WILEY
Phân tích ảnh hưởng
Thông tin về tạp chí
Lĩnh vực:
Neuroscience (miscellaneous)Immunology and Microbiology (miscellaneous)Molecular BiologyMedicine (miscellaneous)Biochemistry, Genetics and Molecular Biology (miscellaneous)
The EMBO Journal publishes papers describing original research of broad general interest in molecular and cell biology - a particular emphasis is placed on molecular mechanism and physiological relevance. The journal encourages and publishes articles that report novel findings of wide biological significance in the areas of: Ageing; Autophagy; Cancer; Cell Adhesion, Polarity & Cytoskeleton; Cell Cycle; Cell Death; Developmental Biology; DNA Replication, Repair & Recombination; Chromatin, Epigenetics & Genomics; Immunology; Membrane & Intracellular Transport; Metabolism; Microbiology, Virology & Host Pathogen Interaction; Molecular Biology of Disease; Neuroscience; Plant Biology; Post-translational Modifications, Proteolysis & Proteomics; RNA Biology; Signal Transduction; Stem Cells; Structural Biology; Systems, Chemical & Computational Biology; Transcription; Protein Biosynthesis & Quality Control; Vascular Biology
Activation of sarcoplasmic reticular Ca2+ transport ATPase by phosphorylation of an associated phosphatidylinositol.
Tập 2 Số 9 - Trang 1543-1548 - 1983
p21 maintains senescent cell viability under persistent <scp>DNA</scp> damage response by restraining <scp>JNK</scp> and caspase signaling Abstract Cellular senescence is a permanent state of cell cycle arrest that protects the organism from tumorigenesis and regulates tissue integrity upon damage and during tissue remodeling. However, accumulation of senescent cells in tissues during aging contributes to age‐related pathologies. A deeper understanding of the mechanisms regulating the viability of senescent cells is therefore required. Here, we show that the CDK inhibitor p21 (CDKN 1A) maintains the viability of DNA damage‐induced senescent cells. Upon p21 knockdown, senescent cells acquired multiple DNA lesions that activated ataxia telangiectasia mutated (ATM ) and nuclear factor (NF )‐κB kinase, leading to decreased cell survival. NF ‐κB activation induced TNF ‐α secretion and JNK activation to mediate death of senescent cells in a caspase‐ and JNK ‐dependent manner. Notably, p21 knockout in mice eliminated liver senescent stellate cells and alleviated liver fibrosis and collagen production. These findings define a novel pathway that regulates senescent cell viability and fibrosis.
Tập 36 Số 15 - Trang 2280-2295 - 2017
T4 polynucleotide kinase; cloning of the gene (pseT) and amplification of its product.
Tập 4 Số 10 - Trang 2695-2703 - 1985
The effect of tyrosine-specific protein phosphorylation on the assembly of adherens-type junctions.
Tập 11 Số 5 - Trang 1733-1742 - 1992
Dysregulated mi <scp>RNA</scp> biogenesis downstream of cellular stress and <scp>ALS</scp> ‐causing mutations: a new mechanism for <scp>ALS</scp>
Tập 34 Số 21 - Trang 2633-2651 - 2015
FUS stimulates microRNA biogenesis by facilitating co-transcriptional Drosha recruitment
Tập 31 Số 24 - Trang 4502-4510 - 2012
Destruction of the CDC28/CLB mitotic kinase is not required for the metaphase to anaphase transition in budding yeast.
Tập 12 Số 5 - Trang 1969-1978 - 1993
The role of proteolysis in cell cycle progression in Schizosaccharomyces pombe.
Tập 15 Số 19 - Trang 5268-5279 - 1996