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Book: Necrotic cell death

Shen, Han-Ming / Vandenabeele, Peter

(Cell death in biology and diseases)

2014

Author's details	Han-Ming Shen ; Peter Vandenabeele ed
Series title	Cell death in biology and diseases
Keywords	Cell death ; Necrosis
Subject code	571.936
Language	English
Size	XIV, 397 S. : Ill., 24 cm
Publisher	Humana Press
Publishing place	New York u.a.
Publishing country	United States
Document type	Book
HBZ-ID	HT018239760
ISBN	978-1-4614-8219-2 ; 9781461482208 ; 1-4614-8219-4 ; 1461482208
Database	Catalogue ZB MED Medicine, Health

In stock of ZB MED Cologne/Königswinter

Shelf mark	Loan status	Location
2014 A 1575	available for loan (reading room)	Lesesaal EG

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Article ; Online: The emerging mechanisms and functions of microautophagy.

Wang, Liming / Klionsky, Daniel J / Shen, Han-Ming

Nature reviews. Molecular cell biology

2022 Volume 24, Issue 3, Page(s) 186–203

Abstract: Autophagy' refers to an evolutionarily conserved process through which cellular contents, such as damaged organelles and protein aggregates, are delivered to lysosomes for degradation. Different forms of autophagy have been described on the basis of the ...

Abstract	'Autophagy' refers to an evolutionarily conserved process through which cellular contents, such as damaged organelles and protein aggregates, are delivered to lysosomes for degradation. Different forms of autophagy have been described on the basis of the nature of the cargoes and the means used to deliver them to lysosomes. At present, the prevailing categories of autophagy in mammalian cells are macroautophagy, microautophagy and chaperone-mediated autophagy. The molecular mechanisms and biological functions of macroautophagy and chaperone-mediated autophagy have been extensively studied, but microautophagy has received much less attention. In recent years, there has been a growth in research on microautophagy, first in yeast and then in mammalian cells. Here we review this form of autophagy, focusing on selective forms of microautophagy. We also discuss the upstream regulatory mechanisms, the crosstalk between macroautophagy and microautophagy, and the functional implications of microautophagy in diseases such as cancer and neurodegenerative disorders in humans. Future research into microautophagy will provide opportunities to develop novel interventional strategies for autophagy- and lysosome-related diseases.
MeSH term(s)	Animals ; Humans ; Microautophagy ; Autophagy ; Lysosomes/metabolism ; Cell Communication ; Macroautophagy ; Mammals
Language	English
Publishing date	2022-09-12
Publishing country	England
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2031313-5
ISSN	1471-0080 ; 1471-0072
ISSN (online)	1471-0080
ISSN	1471-0072
DOI	10.1038/s41580-022-00529-z
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Zs.A 5446: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Autophagic secretion of mitochondria (ASM): an alternative way for getting rid of damaged mitochondria.

Tan, Hayden Weng Siong / Lu, Guang / Shen, Han-Ming

Autophagy

2022 Volume 19, Issue 2, Page(s) 739–741

Abstract: PINK1-PRKN/Parkin-mediated mitophagy represents an important mitochondrial quality control (MQC) pathway that clears damaged/dysfunctional mitochondria. Although the conjugation of mammalian Atg8-family proteins (mATG8s) to phosphatidylethanolamine (PE) ... ...

Abstract	PINK1-PRKN/Parkin-mediated mitophagy represents an important mitochondrial quality control (MQC) pathway that clears damaged/dysfunctional mitochondria. Although the conjugation of mammalian Atg8-family proteins (mATG8s) to phosphatidylethanolamine (PE) is a defining step in autophagy, its role in mitophagy remains unclear. In our recent study, we found that the mATG8 conjugation system is not required for PINK1-PRKN-mediated mitochondria clearance. Instead, mATG8 conjugation system-independent mitochondria clearance relies on secretory autophagy, a process we term as the autophagic secretion of mitochondria (ASM). As ASM results in the spurious activation of the CGAS-STING1 pathway, we propose that defects in mATG8 lipidation may promote inflammation through ASM.
MeSH term(s)	Animals ; Mitophagy ; Autophagy ; Protein Kinases/metabolism ; Ubiquitin-Protein Ligases/metabolism ; Mitochondria/metabolism ; Biological Transport ; Mammals/metabolism
Chemical Substances	Protein Kinases (EC 2.7.-) ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
Language	English
Publishing date	2022-08-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2022.2107310
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Zs.A 6741: Show issues

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Article ; Online: Targeting the Endocytic Pathway and Autophagy Process as a Novel Therapeutic Strategy in COVID-19.

Yang, Naidi / Shen, Han-Ming

International journal of biological sciences

2020 Volume 16, Issue 10, Page(s) 1724–1731

Abstract: Coronaviruses (CoVs) are a group of enveloped, single-stranded positive genomic RNA viruses and some of them are known to cause severe respiratory diseases in human, including Severe Acute Respiratory Syndrome (SARS), Middle East Respiratory Syndrome ( ... ...

Abstract	Coronaviruses (CoVs) are a group of enveloped, single-stranded positive genomic RNA viruses and some of them are known to cause severe respiratory diseases in human, including Severe Acute Respiratory Syndrome (SARS), Middle East Respiratory Syndrome (MERS) and the ongoing coronavirus disease-19 (COVID-19). One key element in viral infection is the process of viral entry into the host cells. In the last two decades, there is increasing understanding on the importance of the endocytic pathway and the autophagy process in viral entry and replication. As a result, the endocytic pathway including endosome and lysosome has become important targets for development of therapeutic strategies in combating diseases caused by CoVs. In this mini-review, we will focus on the importance of the endocytic pathway as well as the autophagy process in viral infection of several pathogenic CoVs inclusive of SARS-CoV, MERS-CoV and the new CoV named as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and discuss the development of therapeutic agents by targeting these processes. Such knowledge will provide important clues for control of the ongoing epidemic of SARS-CoV-2 infection and treatment of COVID-19.
MeSH term(s)	Animals ; Autophagy ; Betacoronavirus/physiology ; Cell Line ; Coronavirus ; Coronavirus Infections/drug therapy ; Coronavirus Infections/virology ; Endocytosis ; Humans ; Molecular Targeted Therapy ; Pandemics ; Pneumonia, Viral/drug therapy ; Pneumonia, Viral/virology ; SARS Virus ; Virus Internalization
Keywords	covid19
Language	English
Publishing date	2020-03-15
Publishing country	Australia
Document type	Journal Article ; Review
ZDB-ID	2179208-2
ISSN	1449-2288 ; 1449-2288
ISSN (online)	1449-2288
ISSN	1449-2288
DOI	10.7150/ijbs.45498
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Article ; Online: Seeing is believing: a novel tool for quantitating mitophagy.

Wang, Liming / Shen, Han-Ming

Cell research

2020 Volume 30, Issue 9, Page(s) 715–716

MeSH term(s)	Mitophagy
Keywords	covid19
Language	English
Publishing date	2020-06-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	1319303-x
ISSN	1748-7838 ; 1001-0602
ISSN (online)	1748-7838
ISSN	1001-0602
DOI	10.1038/s41422-020-0360-3
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Zs.A 5283: Show issues

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Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

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Article ; Online: The resurrection of RIP kinase 1 as an early cell death checkpoint regulator-a potential target for therapy in the necroptosis era.

Ju, Eunjin / Park, Kyeong Ah / Shen, Han-Ming / Hur, Gang Min

Experimental & molecular medicine

2022 Volume 54, Issue 9, Page(s) 1401–1411

Abstract: Receptor-interacting serine threonine protein kinase 1 (RIPK1) has emerged as a central molecular switch in controlling the balance between cell survival and cell death. The pro-survival role of RIPK1 in maintaining cell survival is achieved via its ... ...

Abstract	Receptor-interacting serine threonine protein kinase 1 (RIPK1) has emerged as a central molecular switch in controlling the balance between cell survival and cell death. The pro-survival role of RIPK1 in maintaining cell survival is achieved via its ability to induce NF-κB-dependent expression of anti-apoptotic genes. However, recent advances have identified the pro-death function of RIPK1: posttranslational modifications of RIPK1 in the tumor necrosis factor receptor 1 (TNFR1)-associated complex-I, in the cytosolic complex-IIb or in necrosomes regulate the cytotoxic potential of RIPK1, forming an early cell death checkpoint. Since the kinase activity of RIPK1 is indispensable in RIPK3- and MLKL-mediated necroptosis induction, while it is dispensable in apoptosis, a better understanding of this early cell death checkpoint via RIPK1 might lead to new insights into the molecular mechanisms controlling both apoptotic and necroptotic modes of cell death and help develop novel therapeutic approaches for cancer. Here, we present an emerging view of the regulatory mechanisms for RIPK1 activity, especially with respect to the early cell death checkpoint. We also discuss the impact of dysregulated RIPK1 activity in pathophysiological settings and highlight its therapeutic potential in treating human diseases.
MeSH term(s)	Apoptosis/physiology ; Cell Death ; Humans ; NF-kappa B/metabolism ; Necroptosis ; Necrosis ; Protein Kinases/genetics ; Protein Kinases/metabolism ; Receptor-Interacting Protein Serine-Threonine Kinases/genetics ; Receptor-Interacting Protein Serine-Threonine Kinases/metabolism ; Receptors, Tumor Necrosis Factor, Type I/metabolism
Chemical Substances	NF-kappa B ; Receptors, Tumor Necrosis Factor, Type I ; Protein Kinases (EC 2.7.-) ; Receptor-Interacting Protein Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2022-09-28
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1328915-9
ISSN	2092-6413 ; 1226-3613 ; 0378-8512
ISSN (online)	2092-6413
ISSN	1226-3613 ; 0378-8512
DOI	10.1038/s12276-022-00847-4
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Zs.A 4775: Show issues

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Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Critical role of AMPK in redox regulation under glucose starvation.

Ren, Yi / Shen, Han-Ming

Redox biology

2019 Volume 25, Page(s) 101154

Abstract: Glucose starvation is one of the major forms of metabolic stress in cancer cells. Deprivation of glucose impairs glycolysis and the pentose phosphate pathway, which elicits oxidative stress due to enhanced production of reactive oxygen species (ROS) and ... ...

Abstract	Glucose starvation is one of the major forms of metabolic stress in cancer cells. Deprivation of glucose impairs glycolysis and the pentose phosphate pathway, which elicits oxidative stress due to enhanced production of reactive oxygen species (ROS) and impaired antioxidant system, leading to redox imbalance and cell death. Under glucose starvation, the 5' AMP-activated protein kinase (AMPK) plays a critical role in maintaining redox homeostasis and cell survival via multiple pathways, such as regulation of fatty acid metabolism and antioxidant response. Convergence of ROS and the glucose metabolic pathway reveals novel molecular targets for the development of effective cancer therapeutic strategies. Interestingly, AMPK, along with its upstream kinase liver kinase B1 (LKB1), has been regarded to play a tumor suppressor role. However, emerging studies have provided novel insights into the pro-tumor survival function of the LKB1-AMPK pathway. Therefore, targeting metabolic and oxidative stress in cancer cells, with manipulation of AMPK activity, is a promising strategy in developing novel cancer therapeutic agents.
MeSH term(s)	AMP-Activated Protein Kinases/metabolism ; Animals ; Glucose/deficiency ; Humans ; Neoplasms/enzymology ; Neoplasms/pathology ; Oxidation-Reduction ; Oxidative Stress ; Reactive Oxygen Species/metabolism
Chemical Substances	Reactive Oxygen Species ; AMP-Activated Protein Kinases (EC 2.7.11.31) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2019-03-02
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2701011-9
ISSN	2213-2317 ; 2213-2317
ISSN (online)	2213-2317
ISSN	2213-2317
DOI	10.1016/j.redox.2019.101154
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: FBP1 inhibits NSCLC stemness by promoting ubiquitination of Notch1 intracellular domain and accelerating degradation.

He, Tianyu / Wang, Yanye / Lv, Wang / Wang, Yiqing / Li, Xinye / Zhang, Qingyi / Shen, Han-Ming / Hu, Jian

Cellular and molecular life sciences : CMLS

2024 Volume 81, Issue 1, Page(s) 87

Abstract: The existence of cancer stem cells is widely acknowledged as the underlying cause for the challenging curability and high relapse rates observed in various tumor types, including non-small cell lung cancer (NSCLC). Despite extensive research on numerous ... ...

Abstract	The existence of cancer stem cells is widely acknowledged as the underlying cause for the challenging curability and high relapse rates observed in various tumor types, including non-small cell lung cancer (NSCLC). Despite extensive research on numerous therapeutic targets for NSCLC treatment, the strategies to effectively combat NSCLC stemness and achieve a definitive cure are still not well defined. The primary objective of this study was to examine the underlying mechanism through which Fructose-1,6-bisphosphatase 1 (FBP1), a gluconeogenic enzyme, functions as a tumor suppressor to regulate the stemness of NSCLC. Herein, we showed that overexpression of FBP1 led to a decrease in the proportion of CD133-positive cells, weakened tumorigenicity, and decreased expression of stemness factors. FBP1 inhibited the activation of Notch signaling, while it had no impact on the transcription level of Notch 1 intracellular domain (NICD1). Instead, FBP1 interacted with NICD1 and the E3 ubiquitin ligase FBXW7 to facilitate the degradation of NICD1 through the ubiquitin-proteasome pathway, which is independent of the metabolic enzymatic activity of FBP1. The aforementioned studies suggest that targeting the FBP1-FBXW7-NICD1 axis holds promise as a therapeutic approach for addressing the challenges of NSCLC recurrence and drug resistance.
MeSH term(s)	Humans ; Carcinoma, Non-Small-Cell Lung/genetics ; F-Box-WD Repeat-Containing Protein 7/genetics ; Fructose ; Lung Neoplasms/genetics ; Ubiquitin-Protein Ligases/genetics ; Ubiquitination
Chemical Substances	F-Box-WD Repeat-Containing Protein 7 ; Fructose (30237-26-4) ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; NOTCH1 protein, human ; FBP1 protein, human (EC 3.1.3.11)
Language	English
Publishing date	2024-02-13
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-024-05138-x
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Zs.A 195: Show issues

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Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

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Article: The Role of Autophagy in Liver Cancer: Crosstalk in Signaling Pathways and Potential Therapeutic Targets.

Cui, Jianzhou / Shen, Han-Ming / Lim, Lina Hsiu Kim

Pharmaceuticals (Basel, Switzerland)

2020 Volume 13, Issue 12

Abstract: Autophagy is an evolutionarily conserved lysosomal-dependent pathway for degrading cytoplasmic proteins, macromolecules, and organelles. Autophagy-related genes (Atgs) are the core molecular machinery in the control of autophagy, and several major ... ...

Abstract	Autophagy is an evolutionarily conserved lysosomal-dependent pathway for degrading cytoplasmic proteins, macromolecules, and organelles. Autophagy-related genes (Atgs) are the core molecular machinery in the control of autophagy, and several major functional groups of Atgs coordinate the entire autophagic process. Autophagy plays a dual role in liver cancer development via several critical signaling pathways, including the PI3K-AKT-mTOR, AMPK-mTOR, EGF, MAPK, Wnt/β-catenin, p53, and NF-κB pathways. Here, we review the signaling pathways involved in the cross-talk between autophagy and hepatocellular carcinoma (HCC) and analyze the status of the development of novel HCC therapy by targeting the core molecular machinery of autophagy as well as the key signaling pathways. The induction or the inhibition of autophagy by the modulation of signaling pathways can confer therapeutic benefits to patients. Understanding the molecular mechanisms underlying the cross-link of autophagy and HCC may extend to translational studies that may ultimately lead to novel therapy and regimen formation in HCC treatment.
Language	English
Publishing date	2020-11-28
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2193542-7
ISSN	1424-8247
ISSN	1424-8247
DOI	10.3390/ph13120432
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Article: The Long and the Short of PTEN in the Regulation of Mitophagy.

Wang, Liming / Lu, Guang / Shen, Han-Ming

Frontiers in cell and developmental biology

2020 Volume 8, Page(s) 299

Abstract: Mitophagy is a key mitochondrial quality control mechanism for effective and selective elimination of damaged mitochondria through the autophagy-lysosome machinery. Defective mitophagy is associated with pathogenesis of important human diseases including ...

Abstract	Mitophagy is a key mitochondrial quality control mechanism for effective and selective elimination of damaged mitochondria through the autophagy-lysosome machinery. Defective mitophagy is associated with pathogenesis of important human diseases including neurodegenerative diseases, heart failure, innate immunity, and cancer. In the past two decades, the mechanistic studies of mitophagy have made many breakthroughs with the discoveries of phosphatase and tensin homolog (PTEN)-induced kinase protein 1 (PINK1)-parkin-mediated ubiquitin (Ub)-driven pathway and BCL2/adenovirus E1B 19 kDa protein-interacting proteins 3 (BNIP3)/NIX or FUN14 domain containing 1 (FUNDC1) mitochondrial receptor-mediated pathways. Recently, several isoforms of dual phosphatase PTEN, such as PTEN-long (PTEN-L), have been identified, and some of them are implicated in the mitophagy process via their protein phosphatase activity. In this review, we aim to discuss the regulatory roles of PTEN isoforms in mitophagy. These discoveries may provide new opportunities for development of novel therapeutic strategies for mitophagy-related diseases such as neurodegenerative disorders via targeting PTEN isoforms and mitophagy.
Language	English
Publishing date	2020-05-13
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2020.00299
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