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Cell Death and Differentiation

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https://www.readbyqxmd.com/read/29125604/the-oncolytic-compound-ltx-401-targets-the-golgi-apparatus
#1
Heng Zhou, Allan Sauvat, Lígia C Gomes-da-Silva, Sylvère Durand, Sabrina Forveille, Kristina Iribarren, Takahiro Yamazaki, Sylvie Souquere, Lucillia Bezu, Kevin Müller, Marion Leduc, Peng Liu, Liwei Zhao, Aurélien Marabelle, Laurence Zitvogel, Øystein Rekdal, Oliver Kepp, Guido Kroemer
This corrects the article DOI: 10.1038/cdd.2016.86.
November 10, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29125603/cell-cycle-arrest-through-indirect-transcriptional-repression-by-p53-i-have-a-dream
#2
REVIEW
Kurt Engeland
Activation of the p53 tumor suppressor can lead to cell cycle arrest. The key mechanism of p53-mediated arrest is transcriptional downregulation of many cell cycle genes. In recent years it has become evident that p53-dependent repression is controlled by the p53-p21-DREAM-E2F/CHR pathway (p53-DREAM pathway). DREAM is a transcriptional repressor that binds to E2F or CHR promoter sites. Gene regulation and deregulation by DREAM shares many mechanistic characteristics with the retinoblastoma pRB tumor suppressor that acts through E2F elements...
November 10, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29125602/mechanisms-of-transcriptional-regulation-by-p53
#3
REVIEW
Kelly D Sullivan, Matthew D Galbraith, Zdenek Andrysik, Joaquin M Espinosa
p53 is a transcription factor that suppresses tumor growth through regulation of dozens of target genes with diverse biological functions. The activity of this master transcription factor is inactivated in nearly all tumors, either by mutations in the TP53 locus or by oncogenic events that decrease the activity of the wild-type protein, such as overexpression of the p53 repressor MDM2. However, despite decades of intensive research, our collective understanding of the p53 signaling cascade remains incomplete...
November 10, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29125601/tm9sf4-is-a-novel-factor-promoting-autophagic-flux-under-amino-acid-starvation
#4
Lei Sun, Zhaoyue Meng, Yifei Zhu, Jun Lu, Zhichao Li, Qiannan Zhao, Yu Huang, Liwen Jiang, Xiaoqiang Yao
Autophagy is a highly complicated process with participation of large numbers of autophagy-related proteins. Under nutrient starvation, autophagy promotes cell survival by breaking down nonessential cellular components for recycling use. However, due to its high complexity, molecular mechanism of autophagy is still not fully understood. In the present study, we report a novel autophagy-related protein TM9SF4, which plays a functional role in the induction phase of autophagic process. TM9SF4 proteins were abundantly expressed in the kidney, especially in renal proximal tubular epithelial cells...
November 10, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29125600/bcl2-a-30-year-tale-of-life-death-and-much-more-to-come
#5
Francesca Pentimalli
No abstract text is available yet for this article.
November 10, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29125599/updates-from-the-tp53-universe
#6
Francesca Pentimalli
No abstract text is available yet for this article.
November 10, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29125598/a-mir-20a-mapk1-c-myc-regulatory-feedback-loop-regulates-breast-carcinogenesis-and-chemoresistance
#7
Wengong Si, Jiaying Shen, Chengyong Du, Danni Chen, Xidong Gu, Chenggong Li, Minya Yao, Jie Pan, Junchi Cheng, Donghai Jiang, Liang Xu, Chang Bao, Peifen Fu, Weimin Fan
Chemoresistance often leads to the failure of breast cancer treatment. MicroRNAs (miRNAs) play an important role in the progression and chemoresistance of cancer. However, because of the complexity of the mechanisms of chemoresistance and the specificity of miRNA regulation in different cell types, the function of miR-20a in breast cancer chemoresistance is still unclear. Here, by using miRNA microarray and high-content screening techniques, we found that miR-20a/b were significantly downregulated in breast cancer tissues compared with normal breast tissues, and low miR-20a/b expression was correlated with poor survival in breast cancer patients...
November 10, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29099489/deconstructing-networks-of-p53-mediated-tumor-suppression-in-vivo
#8
REVIEW
Alyssa M Kaiser, Laura D Attardi
The transcription factor p53 is a vital tumor suppressor. Upon activation by diverse stresses including oncogene activation, DNA damage, hypoxia and nutrient deprivation, p53 activates a panoply of target genes and orchestrates numerous downstream responses that suppress tumorigenesis. Although early studies of p53 suggested that its ability to induce cell cycle arrest, senescence and apoptosis programs accounted for its tumor-suppressor activity, more recent studies have challenged this notion. Moreover, p53 regulates a suite of additional processes, such as metabolism, stem cell function, invasion and metastasis...
November 3, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29099488/mutant-p53-partners-in-crime
#9
REVIEW
Michael P Kim, Guillermina Lozano
Mutant p53 proteins impart changes in cellular behavior and function through interactions with proteins that alter gene expression. The milieu of intracellular proteins available to interact with mutant p53 is context specific and changes with disease, cell type, and environmental conditions. Varying conformations of mutant p53 largely dictate protein-protein interactions as different point mutations within protein-coding regions greatly alter the extent and array of gain-of-function (GOF) activities. Given such variables, how can knowledge regarding p53 missense mutations be translated into predicting or altering biologic activity for therapy? How may knowledge regarding mutant p53 functions within certain disease contexts be harnessed to blunt or ablate mutant p53 GOF for therapy? In this article, we review known proteins that interact with mutant p53 and result in the activation of genes that contribute to p53 GOF with particular emphasis on context dependency and an evolving appreciation of GOF mechanisms...
November 3, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29099487/why-are-there-hotspot-mutations-in-the-tp53-gene-in-human-cancers
#10
REVIEW
Evan H Baugh, Hua Ke, Arnold J Levine, Richard A Bonneau, Chang S Chan
The p53 gene contains homozygous mutations in ~50-60% of human cancers. About 90% of these mutations encode missense mutant proteins that span ~190 different codons localized in the DNA-binding domain of the gene and protein. These mutations produce a protein with a reduced capacity to bind to a specific DNA sequence that regulates the p53 transcriptional pathway. Eight of these mutations are localized in codons that account for ~28% of the total p53 mutations and these alleles appear to be selected for preferentially in human cancers of many tissue types...
November 3, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29099486/a-large-shrna-library-approach-identifies-lncrna-ntep-as-an-essential-regulator-of-cell-proliferation
#11
Julia Beermann, Dominique Kirste, Katharina Iwanov, Dongchao Lu, Felix Kleemiß, Regalla Kumarswamy, Katharina Schimmel, Christian Bär, Thomas Thum
The mammalian cell cycle is a complex and tightly controlled event. Myriads of different control mechanisms are involved in its regulation. Long non-coding RNAs (lncRNA) have emerged as important regulators of many cellular processes including cellular proliferation. However, a more global and unbiased approach to identify lncRNAs with importance for cell proliferation is missing. Here, we present a lentiviral shRNA library-based approach for functional lncRNA profiling. We validated our library approach in NIH3T3 (3T3) fibroblasts by identifying lncRNAs critically involved in cell proliferation...
November 3, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29099485/caspase-10-a-molecular-switch-from-cell-autonomous-apoptosis-to-communal-cell-death-in-response-to-chemotherapeutic-drug-treatment
#12
Andrea Mohr, Laura Deedigan, Sylwia Jencz, Yasamin Mehrabadi, Lily Houlden, Stella-Maris Albarenque, Ralf M Zwacka
The mechanisms of how chemotherapeutic drugs lead to cell cycle checkpoint regulation and DNA damage repair are well understood, but how such signals are transmitted to the cellular apoptosis machinery is less clear. We identified a novel apoptosis-inducing complex, we termed FADDosome, which is driven by ATR-dependent caspase-10 upregulation. During FADDosome-induced apoptosis, cFLIPL is ubiquitinated by TRAF2, leading to its degradation and subsequent FADD-dependent caspase-8 activation. Cancer cells lacking caspase-10, TRAF2 or ATR switch from this cell-autonomous suicide to a more effective, autocrine/paracrine mode of apoptosis initiated by a different complex, the FLIPosome...
November 3, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29099484/lin28b-and-mir-142-3p-regulate-neuronal-differentiation-by-modulating-staufen1-expression
#13
Younseo Oh, Jungyun Park, Jin-Il Kim, Mi-Yoon Chang, Sang-Hun Lee, Youl-Hee Cho, Jungwook Hwang
Staufen1 (STAU1) and Lin28B are RNA-binding proteins that are involved in neuronal differentiation as a function of post-transcriptional regulation. STAU1 triggers post-transcriptional regulation, including mRNA export, mRNA relocation, translation and mRNA decay. Lin28B also has multiple functions in miRNA biogenesis and the regulation of translation. Here, we examined the connection between STAU1 and Lin28B and found that Lin28B regulates the abundance of STAU1 mRNA via miRNA maturation. Decreases in the expression of both STAU1 and Lin28B were observed during neuronal differentiation...
November 3, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29099483/the-bcl-2-arbiters-of-apoptosis-and-their-growing-role-as-cancer-targets
#14
REVIEW
Jerry M Adams, Suzanne Cory
Impaired apoptosis plays a central role in cancer development and limits the efficacy of conventional cytotoxic therapies. Deepening understanding of how opposing factions of the BCL-2 protein family switch on apoptosis and of their structures has driven development of a new class of cancer drugs that targets various pro-survival members by mimicking their natural inhibitors, the BH3-only proteins. These 'BH3 mimetic' drugs seem destined to become powerful new weapons in the arsenal against cancer. Successful clinical trials of venetoclax/ABT-199, a specific inhibitor of BCL-2, have led to its approval for a refractory form of chronic lymphocytic leukaemia and to scores of on-going trials for other malignancies...
November 3, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29099482/anti-apoptotic-bcl-2-family-members-in-development
#15
REVIEW
Joseph T Opferman, Anisha Kothari
Almost 30 years ago it was first appreciated that anti-apoptotic B-cell lymphoma-2 (BCL-2) prevents the induction of apoptosis not only in malignant cells, but also in normal cellular lineages. This critical observation has rapidly evolved from merely identifying new BCL-2 family members to understanding how their biochemical interactions trigger the cell death process, and, more recently, to pharmacological inhibition of anti-apoptotic BCL-2 function in disease. Indeed, the proper regulation of apoptosis is important in many aspects of life including development, homeostasis, and disease biology...
November 3, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29099481/viewing-bcl2-and-cell-death-control-from-an-evolutionary-perspective
#16
REVIEW
Andreas Strasser, David L Vaux
The last 30 years of studying BCL2 have brought cell death research into the molecular era, and revealed its relevance to human pathophysiology. Most, if not all metazoans use an evolutionarily conserved process for cellular self destruction that is controlled and implemented by proteins related to BCL2. We propose the anti-apoptotic BCL2-like and pro-apoptotic BH3-only members of the family arose through duplication and modification of genes for the pro-apoptotic multi-BH domain family members, such as BAX and BAK1...
November 3, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29077095/caspase-4-activation-by-a-bacterial-surface-protein-is-mediated-by-cathepsin-g-in-human-gingival-fibroblasts
#17
Hye-Kyoung Jun, Young-Jung Jung, Suk Ji, Sun-Jin An, Bong-Kyu Choi
Caspase-4 is an inflammatory caspase; however, its mechanism of activation is poorly understood. In this study, we demonstrate that Td92, a surface protein of the periodontal pathogen Treponema denticola and a homolog of the Treponema pallidum surface protein Tp92, activates caspase-4 and induces pyroptosis in primary cultured human gingival fibroblasts (HGFs) via cathepsin G activation. Cathepsin G inhibition or siRNA knockdown of cathepsin G inhibited Td92-induced caspase-4 activation and cell death. Td92-induced cell death was significantly inhibited by siRNA knockdown of gasdermin D...
October 27, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29077094/non-oncogenic-roles-of-tap73-from-multiciliogenesis-to-metabolism
#18
REVIEW
Alice Nemajerova, Ivano Amelio, Jakob Gebel, Volker Dötsch, Gerry Melino, Ute M Moll
The p53 family of transcription factors (p53, p63 and p73) covers a wide range of functions critical for development, homeostasis and health of mammals across their lifespan. Beside the well-established tumor suppressor role, recent evidence has highlighted novel non-oncogenic functions exerted by p73. In particular, p73 is required for multiciliated cell (MCC) differentiation; MCCs have critical roles in brain and airways to move fluids across epithelial surfaces and to transport germ cells in the reproductive tract...
October 27, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29077093/why-do-bcl-2-inhibitors-work-and-where-should-we-use-them-in-the-clinic
#19
REVIEW
Joan Montero, Antony Letai
Intrinsic apoptosis is controlled by the BCL-2 family of proteins but the complexity of intra-family interactions makes it challenging to predict cell fate via standard molecular biology techniques. We discuss BCL-2 family regulation and how to determine cells' readiness for apoptosis and anti-apoptotic dependence. Cancer cells often adopt anti-apoptotic defense mechanisms in response to oncogenic stress or anti-cancer therapy. However, by determining their anti-apoptotic addiction, we can use novel BH3 mimetics to overwhelm this apoptotic blockade...
October 27, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29077092/paxx-and-xlf-interplay-revealed-by-impaired-cns-development-and-immunodeficiency-of-double-ko-mice
#20
Vincent Abramowski, Olivier Etienne, Ramy Elsaid, Junjie Yang, Aurélie Berland, Laetitia Kermasson, Benoit Roch, Stefania Musilli, Jean-Paul Moussu, Karelia Lipson-Ruffert, Patrick Revy, Ana Cumano, François D Boussin, Jean-Pierre de Villartay
The repair of DNA double-stranded breaks (DNAdsb) through non-homologous end joining (NHEJ) is a prerequisite for the proper development of the central nervous system and the adaptive immune system. Yet, mice with Xlf or PAXX loss of function are viable and present with very mild immune phenotypes, although their lymphoid cells are sensitive to ionizing radiation attesting for the role of these factors in NHEJ. In contrast, we show here that mice defective for both Xlf and PAXX are embryonically lethal owing to a massive apoptosis of post-mitotic neurons, a situation reminiscent to XRCC4 or DNA Ligase IV KO conditions...
October 27, 2017: Cell Death and Differentiation
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