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  1. Book: Apoptosis

    Reed, John C. / Green, Douglas R.

    physiology and pathology

    2011  

    Author's details ed. by John C. Reed ; Douglas R. Green
    Keywords Apoptosis ; Apoptosis / physiology ; Cell Death
    Language English
    Size XIII, 421 S., [16] Bl. : zahlr. Ill., graph. Darst., 28 cm
    Publisher Cambridge Univ. Press
    Publishing place Cambridge
    Publishing country Great Britain
    Document type Book
    Note Includes bibliographical references
    HBZ-ID HT017042792
    ISBN 978-0-521-88656-7 ; 0-521-88656-2
    Database Catalogue ZB MED Medicine, Health

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  2. Article ; Online: Bcl-2 on the brink of breakthroughs in cancer treatment.

    Reed, John C

    Cell death and differentiation

    2017  Volume 25, Issue 1, Page(s) 3–6

    MeSH term(s) Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Humans ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Proto-Oncogene Proteins c-bcl-2/antagonists & inhibitors ; Proto-Oncogene Proteins c-bcl-2/genetics ; Proto-Oncogene Proteins c-bcl-2/metabolism
    Chemical Substances Antineoplastic Agents ; Proto-Oncogene Proteins c-bcl-2
    Language English
    Publishing date 2017-12-14
    Publishing country England
    Document type Editorial ; Introductory Journal Article
    ZDB-ID 1225672-9
    ISSN 1476-5403 ; 1350-9047
    ISSN (online) 1476-5403
    ISSN 1350-9047
    DOI 10.1038/cdd.2017.188
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: K63 ubiquitination in immune signaling.

    Madiraju, Charitha / Novack, Jeffrey P / Reed, John C / Matsuzawa, Shu-Ichi

    Trends in immunology

    2022  Volume 43, Issue 2, Page(s) 148–162

    Abstract: Ubc13-catalyzed K63 ubiquitination is a major control point for immune signaling. Recent evidence has shown that the control of multiple immune functions, including chronic inflammation, pathogen responses, lymphocyte activation, and regulatory signaling, ...

    Abstract Ubc13-catalyzed K63 ubiquitination is a major control point for immune signaling. Recent evidence has shown that the control of multiple immune functions, including chronic inflammation, pathogen responses, lymphocyte activation, and regulatory signaling, is altered by K63 ubiquitination. In this review, we detail the novel cellular sensors that are dependent on K63 ubiquitination for their function in the immune signaling network. Many pathogens, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), can target K63 ubiquitination to inhibit pathogen immune responses; we describe novel details of the pathways involved and summarize recent clinically relevant SARS-CoV-2-specific responses. We also discuss recent evidence that regulatory T cell (Treg) versus T helper (T
    MeSH term(s) COVID-19 ; Humans ; Lysine/metabolism ; SARS-CoV-2 ; Signal Transduction ; Ubiquitin-Protein Ligases/metabolism ; Ubiquitination
    Chemical Substances Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Lysine (K3Z4F929H6)
    Language English
    Publishing date 2022-01-13
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2036831-8
    ISSN 1471-4981 ; 1471-4906
    ISSN (online) 1471-4981
    ISSN 1471-4906
    DOI 10.1016/j.it.2021.12.005
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  4. Book: Psychiatric services in the community

    Reed, John C.

    developments and innovations

    1984  

    Author's details ed. by John Reed
    Keywords COMMUNITY MENTAL HEALTH SERVICES / ORGANIZATION & ADMINISTRATION / GREAT BRITAIN ; COMMUNITY MENTAL HEALTH SERVICES / TRENDS / GREAT BRITAIN
    Language English
    Size 252 S.
    Publisher Croom Helm
    Publishing place London u.a.
    Publishing country Great Britain
    Document type Book
    HBZ-ID HT002579018
    ISBN 0-7099-2264-7 ; 978-0-7099-2264-3
    Database Catalogue ZB MED Medicine, Health

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    1984 A 276 order for loan Magazin

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  5. Article ; Online: Peter C. Nowell (1928-2016).

    Reed, John C / Druker, Brian J

    Proceedings of the National Academy of Sciences of the United States of America

    2017  Volume 114, Issue 18, Page(s) 4569–4570

    MeSH term(s) Animals ; Cytogenetics/history ; History, 20th Century ; History, 21st Century ; Humans ; Neoplasms/genetics ; Neoplasms/history ; Portraits as Topic
    Language English
    Publishing date 2017-04-17
    Publishing country United States
    Document type Biography ; Historical Article ; Journal Article
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.1705526114
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  6. Article ; Online: Cancer. Priming cancer cells for death.

    Reed, John C

    Science (New York, N.Y.)

    2011  Volume 334, Issue 6059, Page(s) 1075–1076

    MeSH term(s) Animals ; Antineoplastic Agents/therapeutic use ; Apoptosis ; Female ; Humans ; Male ; Mitochondria/physiology ; Neoplasms/drug therapy ; Neoplasms/physiopathology
    Chemical Substances Antineoplastic Agents
    Language English
    Publishing date 2011-11-25
    Publishing country United States
    Document type Comment ; Journal Article
    ZDB-ID 128410-1
    ISSN 1095-9203 ; 0036-8075
    ISSN (online) 1095-9203
    ISSN 0036-8075
    DOI 10.1126/science.1215568
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  7. Article ; Online: Finally, An Apoptosis-Targeting Therapeutic for Cancer.

    Croce, Carlo M / Reed, John C

    Cancer research

    2016  Volume 76, Issue 20, Page(s) 5914–5920

    Abstract: Resistance to cell death represents one of the hallmarks of cancer. Various genetic and epigenetic changes in malignant cells afford cytoprotection in the face of genomic instability, oncogene activation, microenvironment stress, chemotherapy, targeted ... ...

    Abstract Resistance to cell death represents one of the hallmarks of cancer. Various genetic and epigenetic changes in malignant cells afford cytoprotection in the face of genomic instability, oncogene activation, microenvironment stress, chemotherapy, targeted anticancer drugs, and even immunotherapy. Central among the regulators of cell life and death are Bcl-2 family proteins, with the founding member of the family (B-cell lymphoma/leukemia-2) discovered via its involvement in chromosomal translocations in lymphomas. The quest for therapeutics that target cell survival protein Bcl-2 represents a long road traveled, with many dead-ends, disappointments, and delays. Finally, a Bcl-2-targeting medicine has gained approval as a new class of anticancer agent. Cancer Res; 76(20); 5914-20. ©2016 AACR.
    MeSH term(s) Animals ; Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Drug Design ; Humans ; Leukemia, Lymphocytic, Chronic, B-Cell/drug therapy ; Neoplasms/drug therapy ; Proto-Oncogene Proteins c-bcl-2/antagonists & inhibitors ; Proto-Oncogene Proteins c-bcl-2/physiology ; bcl-X Protein/antagonists & inhibitors ; bcl-X Protein/physiology
    Chemical Substances Antineoplastic Agents ; Proto-Oncogene Proteins c-bcl-2 ; bcl-X Protein
    Language English
    Publishing date 2016-10-15
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-16-1248
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Therapeutics targeting Bcl-2 in hematological malignancies.

    Ruefli-Brasse, Astrid / Reed, John C

    The Biochemical journal

    2017  Volume 474, Issue 21, Page(s) 3643–3657

    Abstract: Members of ... ...

    Abstract Members of the
    MeSH term(s) Animals ; Bridged Bicyclo Compounds, Heterocyclic/therapeutic use ; Drug Delivery Systems/methods ; Hematologic Neoplasms/drug therapy ; Hematologic Neoplasms/genetics ; Hematologic Neoplasms/metabolism ; Hematologic Neoplasms/pathology ; Humans ; Leukemia, Lymphocytic, Chronic, B-Cell/drug therapy ; Leukemia, Lymphocytic, Chronic, B-Cell/genetics ; Leukemia, Lymphocytic, Chronic, B-Cell/metabolism ; Leukemia, Lymphocytic, Chronic, B-Cell/pathology ; Myeloid Cell Leukemia Sequence 1 Protein/antagonists & inhibitors ; Myeloid Cell Leukemia Sequence 1 Protein/genetics ; Myeloid Cell Leukemia Sequence 1 Protein/metabolism ; Proto-Oncogene Proteins c-bcl-2/antagonists & inhibitors ; Proto-Oncogene Proteins c-bcl-2/genetics ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Sulfonamides/therapeutic use ; bcl-X Protein/antagonists & inhibitors ; bcl-X Protein/genetics ; bcl-X Protein/metabolism
    Chemical Substances BCL2 protein, human ; BCL2L1 protein, human ; Bridged Bicyclo Compounds, Heterocyclic ; MCL1 protein, human ; Myeloid Cell Leukemia Sequence 1 Protein ; Proto-Oncogene Proteins c-bcl-2 ; Sulfonamides ; bcl-X Protein ; venetoclax (N54AIC43PW)
    Language English
    Publishing date 2017-10-23
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2969-5
    ISSN 1470-8728 ; 0006-2936 ; 0306-3275 ; 0264-6021
    ISSN (online) 1470-8728
    ISSN 0006-2936 ; 0306-3275 ; 0264-6021
    DOI 10.1042/BCJ20170080
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  9. Article: Bcl-2-family proteins and hematologic malignancies: history and future prospects.

    Reed, John C

    Blood

    2008  Volume 111, Issue 7, Page(s) 3322–3330

    Abstract: BCL-2 was the first antideath gene discovered, a milestone that effectively launched a new era in cell death research. Since its discovery more than 2 decades ago, multiple members of the human Bcl-2 family of apoptosis-regulating proteins have been ... ...

    Abstract BCL-2 was the first antideath gene discovered, a milestone that effectively launched a new era in cell death research. Since its discovery more than 2 decades ago, multiple members of the human Bcl-2 family of apoptosis-regulating proteins have been identified, including 6 antiapoptotic proteins, 3 structurally similar proapoptotic proteins, and several structurally diverse proapoptotic interacting proteins that operate as upstream agonists or antagonists. Bcl-2-family proteins regulate all major types of cell death, including apoptosis, necrosis, and autophagy. As such, they operate as nodal points at the convergence of multiple pathways with broad relevance to biology and medicine. Bcl-2 derives its name from its original discovery in the context of B-cell lymphomas, where chromosomal translocations commonly activate the BCL-2 protooncogene, endowing B cells with a selective survival advantage that promotes their neoplastic expansion. The concept that defective programmed cell death contributes to malignancy was established by studies of Bcl-2, representing a major step forward in current understanding of tumorigenesis. Experimental therapies targeting Bcl-2 family mRNAs or proteins are currently in clinical testing, raising hopes that a new class of anticancer drugs may be near.
    MeSH term(s) Animals ; Antineoplastic Agents/therapeutic use ; Cell Death ; Cell Transformation, Neoplastic/drug effects ; Cell Transformation, Neoplastic/metabolism ; Drug Delivery Systems/methods ; History, 20th Century ; History, 21st Century ; Humans ; Inhibitor of Apoptosis Proteins/antagonists & inhibitors ; Inhibitor of Apoptosis Proteins/history ; Inhibitor of Apoptosis Proteins/metabolism ; Lymphoma, B-Cell/drug therapy ; Lymphoma, B-Cell/history ; Lymphoma, B-Cell/metabolism ; Proto-Oncogene Proteins c-bcl-2/antagonists & inhibitors ; Proto-Oncogene Proteins c-bcl-2/history ; Proto-Oncogene Proteins c-bcl-2/metabolism ; RNA, Messenger/antagonists & inhibitors ; RNA, Messenger/metabolism ; RNA, Neoplasm/antagonists & inhibitors ; RNA, Neoplasm/metabolism
    Chemical Substances Antineoplastic Agents ; Inhibitor of Apoptosis Proteins ; Proto-Oncogene Proteins c-bcl-2 ; RNA, Messenger ; RNA, Neoplasm
    Language English
    Publishing date 2008-03-24
    Publishing country United States
    Document type Historical Article ; Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2007-09-078162
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Reconstituting the NLRP1 inflammasome in vitro.

    Faustin, Benjamin / Reed, John C

    Methods in molecular biology (Clifton, N.J.)

    2013  Volume 1040, Page(s) 137–152

    Abstract: Nucleotide-binding domain leucine-rich-repeat containing receptors; NOD-Like Receptors (NLRs) were originally described as microbial sensors involved in host defense against pathogens that comprise an important component of the innate immune system. ... ...

    Abstract Nucleotide-binding domain leucine-rich-repeat containing receptors; NOD-Like Receptors (NLRs) were originally described as microbial sensors involved in host defense against pathogens that comprise an important component of the innate immune system. Recently, their cellular functions have expanded beyond classical pathogen detection, to danger sensors that may contribute to the pathophysiology of a wide range of inflammation-driven human illnesses such as metabolic diseases (atherosclerosis, obesity, type 2 diabetes, gout, age-related macular degeneration) and neurological disorders (Alzheimer's disease). Pathogen-stimulated NLRs such as NLR family Pyrin domain-containing protein 1 (NLRP1) assemble into molecular platforms called "inflammasomes" to activate inflammatory protease caspase-1, which processes pro-IL-1β and pro-IL-18 into active cytokines. We describe methods for reconstituting the human NLRP1 inflammasome in vitro. Protocols are provided for: (a) expression and purification of inflammasome core components (NLRP1 and pro-caspase-1 proteins) using the baculovirus/insect cell expression system, and (b) functional monitoring of NLRP1-mediated caspase-1 activation in response to NLRP1 ligand muramyl dipeptide (MDP) and ATP.
    MeSH term(s) Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/isolation & purification ; Adaptor Proteins, Signal Transducing/metabolism ; Adenosine Triphosphate/metabolism ; Apoptosis Regulatory Proteins/genetics ; Apoptosis Regulatory Proteins/isolation & purification ; Apoptosis Regulatory Proteins/metabolism ; Caspase 1/metabolism ; Enzyme Activation ; Gene Expression ; Humans ; Inflammasomes/metabolism ; Protein Binding ; Recombinant Proteins/genetics ; Recombinant Proteins/isolation & purification ; Recombinant Proteins/metabolism
    Chemical Substances Adaptor Proteins, Signal Transducing ; Apoptosis Regulatory Proteins ; Inflammasomes ; NLRP1 protein, human ; Recombinant Proteins ; Adenosine Triphosphate (8L70Q75FXE) ; Caspase 1 (EC 3.4.22.36)
    Language English
    Publishing date 2013
    Publishing country United States
    Document type Journal Article
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-62703-523-1_11
    Database MEDical Literature Analysis and Retrieval System OnLINE

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