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  1. Book: The LINC complex

    Gundersen, Gregg G. / Worman, Howard J.

    methods and protocols

    (Methods in molecular biology ; 1840 ; Springer protocols)

    2018  

    Author's details edited by Gregg G. Gundersen (Department of Pathology and Cell Biology, Columbia University, New York, NY, USA), Howard J. Worman (Department of Medicine and Department of Pathology and Cell Biology, Columbia University, New York, NY, USA)
    Series title Methods in molecular biology ; 1840
    Springer protocols
    Collection
    Language English
    Size xiv, 338 Seiten, Illustrationen
    Publisher Humana Press
    Publishing place New York, NY
    Publishing country United States
    Document type Book
    HBZ-ID HT019861562
    ISBN 978-1-4939-8690-3 ; 9781493986910 ; 1-4939-8690-2 ; 1493986910
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    Zs A 7042 -1840- verfügbar in Königswinter Königswinter

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  2. Article ; Online: Long live lamins.

    Jin, Qi / Worman, Howard J

    The Journal of cell biology

    2023  Volume 223, Issue 1

    Abstract: Mutations in genes encoding nuclear lamins cause diseases called laminopathies. In this issue, Hasper et al. (https://doi.org/10.1083/jcb.202307049) show that lamin A/C and the prelamin A variant in Hutchinson-Gilford progeria syndrome have relatively ... ...

    Abstract Mutations in genes encoding nuclear lamins cause diseases called laminopathies. In this issue, Hasper et al. (https://doi.org/10.1083/jcb.202307049) show that lamin A/C and the prelamin A variant in Hutchinson-Gilford progeria syndrome have relatively long lifetimes in affected tissues.
    MeSH term(s) Humans ; Lamins/genetics ; Lamin Type A/genetics ; Nuclear Lamina ; Progeria/genetics
    Chemical Substances Lamins ; Lamin Type A
    Language English
    Publishing date 2023-12-11
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 218154-x
    ISSN 1540-8140 ; 0021-9525
    ISSN (online) 1540-8140
    ISSN 0021-9525
    DOI 10.1083/jcb.202311193
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Prelamin A and ZMPSTE24 in premature and physiological aging.

    Worman, Howard J / Michaelis, Susan

    Nucleus (Austin, Tex.)

    2023  Volume 14, Issue 1, Page(s) 2270345

    Abstract: As human longevity increases, understanding the molecular mechanisms that drive aging becomes ever more critical to promote health and prevent age-related disorders. Premature aging disorders or progeroid syndromes can provide critical insights into ... ...

    Abstract As human longevity increases, understanding the molecular mechanisms that drive aging becomes ever more critical to promote health and prevent age-related disorders. Premature aging disorders or progeroid syndromes can provide critical insights into aspects of physiological aging. A major cause of progeroid syndromes which result from mutations in the genes
    MeSH term(s) Humans ; Animals ; Mice ; Lamin Type A/genetics ; Lamin Type A/metabolism ; Metalloendopeptidases/genetics ; Metalloendopeptidases/metabolism ; Health Promotion ; Progeria/genetics ; Progeria/metabolism ; Aging/genetics ; Membrane Proteins/metabolism
    Chemical Substances prelamin A ; Lamin Type A ; Metalloendopeptidases (EC 3.4.24.-) ; ZMPSTE24 protein, human (EC 3.4.24.84) ; Membrane Proteins
    Language English
    Publishing date 2023-10-26
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural
    ZDB-ID 2619626-8
    ISSN 1949-1042 ; 1949-1042
    ISSN (online) 1949-1042
    ISSN 1949-1042
    DOI 10.1080/19491034.2023.2270345
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: LINC complex protein nesprin-2 has pro-apoptotic activity via Bcl-2 family proteins.

    Lindenboim, Liora / Zohar, Hila / Gundersen, Gregg G / Worman, Howard J / Stein, Reuven

    Cell death discovery

    2024  Volume 10, Issue 1, Page(s) 29

    Abstract: The apoptotic intrinsic pathway is initiated by perforation of the mitochondrial outer membrane by the effector pro-apoptotic proteins of the Bcl-2 family, Bax and Bak. Bax and Bak need to be activated, a process facilitated by the action of BH3-only pro- ...

    Abstract The apoptotic intrinsic pathway is initiated by perforation of the mitochondrial outer membrane by the effector pro-apoptotic proteins of the Bcl-2 family, Bax and Bak. Bax and Bak need to be activated, a process facilitated by the action of BH3-only pro-apoptotic members of the Bcl-2 family. The latter either directly activates the effector proteins or antagonizes the action of pro-survival Bcl-2 family members such as Bcl-x
    Language English
    Publishing date 2024-01-15
    Publishing country United States
    Document type Journal Article
    ISSN 2058-7716
    ISSN 2058-7716
    DOI 10.1038/s41420-023-01763-w
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Molecular Pathology of Laminopathies.

    Shin, Ji-Yeon / Worman, Howard J

    Annual review of pathology

    2021  Volume 17, Page(s) 159–180

    Abstract: The nuclear envelope is composed of the nuclear membranes, nuclear lamina, and nuclear pore complexes. Laminopathies are diseases caused by mutations in genes encoding protein components of the lamina and these other nuclear envelope substructures. ... ...

    Abstract The nuclear envelope is composed of the nuclear membranes, nuclear lamina, and nuclear pore complexes. Laminopathies are diseases caused by mutations in genes encoding protein components of the lamina and these other nuclear envelope substructures. Mutations in the single gene encoding lamin A and C, which are expressed in most differentiated somatic cells, cause diseases affecting striated muscle, adipose tissue, peripheral nerve, and multiple systems with features of accelerated aging. Mutations in genes encoding other nuclear envelope proteins also cause an array of diseases that selectively affect different tissues or organs. In some instances, the molecular and cellular consequences of laminopathy-causing mutations are known. However, even when these are understood, mechanisms explaining specific tissue or organ pathology remain enigmatic. Current mechanistic hypotheses focus on how alterations in the nuclear envelope may affect gene expression, including via the regulation of signaling pathways, or cellular mechanics, including responses to mechanical stress.
    MeSH term(s) Humans ; Lamin Type A/genetics ; Lamin Type A/metabolism ; Laminopathies/genetics ; Mutation ; Signal Transduction/genetics
    Chemical Substances Lamin Type A
    Language English
    Publishing date 2021-10-21
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 2227429-7
    ISSN 1553-4014 ; 1553-4006
    ISSN (online) 1553-4014
    ISSN 1553-4006
    DOI 10.1146/annurev-pathol-042220-034240
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Coronavirus Disease 2019 and Liver Injury: A Retrospective Analysis of Hospitalized Patients in New York City.

    Bender, Joshua M / Worman, Howard J

    Journal of clinical and translational hepatology

    2021  Volume 9, Issue 4, Page(s) 551–558

    Abstract: Background and aims: Coronavirus disease 2019 (COVID-19) is a global threat, affecting more than 100 million people and causing over 2 million deaths. Liver laboratory test abnormalities are an extrapulmonary manifestation of COVID-19, yet ... ...

    Abstract Background and aims: Coronavirus disease 2019 (COVID-19) is a global threat, affecting more than 100 million people and causing over 2 million deaths. Liver laboratory test abnormalities are an extrapulmonary manifestation of COVID-19, yet characterization of hepatic injury is incomplete. Our objective was to further characterize and identify causes of liver injury in patients with COVID-19.
    Methods: We conducted a retrospective cohort study of 551 patients hospitalized with COVID-19 at NewYork-Presbyterian Hospital/Columbia University Irving Medical Center between March 1, 2020 and May 31, 2020. We analyzed patient demographics, liver laboratory test results, vital signs, other relevant test results, and clinical outcomes (mortality and intensive care unit admission).
    Results: Abnormal liver laboratory tests were common on hospital admission for COVID-19 and the incidence increased during hospitalization. Of those with elevated serum alanine aminotransferase and/or alkaline phosphatase activities on admission, 58.2% had a cholestatic injury pattern, 35.2% mixed, and 6.6% hepatocellular. Comorbid liver disease was not associated with outcome; however, abnormal direct bilirubin or albumin on admission were associated with intensive care unit stay and mortality. On average, patients who died had greater magnitudes of abnormalities in all liver laboratory tests than those who survived. Ischemic hepatitis was a mechanism of severe hepatocellular injury in some patients.
    Conclusions: Liver laboratory test abnormalities are common in hospitalized patients with COVID-19, and some are associated with increased odds of intensive care unit stay or death. Severe hepatocellular injury is likely attributable to secondary effects such as systemic inflammatory response syndrome, sepsis, and ischemic hepatitis.
    Language English
    Publishing date 2021-04-30
    Publishing country China
    Document type Journal Article
    ZDB-ID 3019822-7
    ISSN 2310-8819 ; 2225-0719
    ISSN (online) 2310-8819
    ISSN 2225-0719
    DOI 10.14218/JCTH.2020.00171
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Jaundice in patients with COVID-19.

    Bender, Joshua M / Worman, Howard J

    JGH open : an open access journal of gastroenterology and hepatology

    2021  Volume 5, Issue 10, Page(s) 1166–1171

    Abstract: Background and aim: While many studies have reported on liver injury in patients with coronavirus disease 2019 (COVID-19), none have specifically addressed the significance of hepatic jaundice. We aimed to determine the clinical consequences and ... ...

    Abstract Background and aim: While many studies have reported on liver injury in patients with coronavirus disease 2019 (COVID-19), none have specifically addressed the significance of hepatic jaundice. We aimed to determine the clinical consequences and etiologies of jaundice in patients with COVID-19.
    Methods: We retrospectively analyzed clinical features, laboratory abnormalities, and rates of survival and intensive care unit admission in 551 patients with COVID-19, hospitalized between 1 March 2020, and 31 May 2020 at a tertiary care academic medical center. Hepatic jaundice was defined as a serum total bilirubin concentration >2.5 mg/dL and a direct bilirubin concentration >0.3 mg/dL that was >25% of the total. Liver injury was characterized as cholestatic, mixed, or hepatocellular at the time of peak serum total bilirubin concentration by calculating the R factor.
    Results: Hepatic jaundice was present in 49 (8.9%) patients and associated with a mortality rate of 40.8% and intensive care unit admission rate of 69.4%, both significantly higher than for patients without jaundice. Jaundiced patients had an increased frequency of fever, leukopenia, leukocytosis, thrombocytopenia, hypotension, hypoxemia, elevated serum creatinine concentration, elevated serum procalcitonin concentration, and sepsis. Nine jaundiced patients had isolated hyperbilirubinemia. Of the 40 patients with abnormally elevated serum alanine aminotransferase or alkaline phosphatase activities, 62.5% had a cholestatic, 20.0% mixed, and 17.5% hepatocellular pattern of liver injury.
    Conclusion: Hepatic jaundice in patients with COVID-19 is associated with high mortality. The main etiologies of liver dysfunction leading to jaundice appear to be sepsis, severe systemic inflammation, and hypoxic/ischemic hepatitis.
    Language English
    Publishing date 2021-08-24
    Publishing country Australia
    Document type Journal Article
    ISSN 2397-9070
    ISSN (online) 2397-9070
    DOI 10.1002/jgh3.12645
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Cell signaling abnormalities in cardiomyopathy caused by lamin A/C gene mutations.

    Worman, Howard J

    Biochemical Society transactions

    2017  Volume 46, Issue 1, Page(s) 37–42

    Abstract: Mutations in the lamin A/C gene ( ...

    Abstract Mutations in the lamin A/C gene (
    MeSH term(s) Animals ; Cardiomyopathies/genetics ; Cardiomyopathies/metabolism ; Cardiomyopathies/pathology ; Disease Models, Animal ; Humans ; Lamin Type A/genetics ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Mice ; Mutation ; Myocardium/metabolism ; Myocardium/pathology ; Protein Kinases/metabolism ; Signal Transduction/genetics ; Transforming Growth Factor beta/metabolism
    Chemical Substances Lamin Type A ; Transforming Growth Factor beta ; Protein Kinases (EC 2.7.-) ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1)
    Language English
    Publishing date 2017-12-01
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 184237-7
    ISSN 1470-8752 ; 0300-5127
    ISSN (online) 1470-8752
    ISSN 0300-5127
    DOI 10.1042/BST20170236
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 944: Show issues Location:
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  9. Article ; Online: mTOR Inhibition Prolongs Survival and Has Beneficial Effects on Heart Function After Onset of Lamin A/C Gene Mutation Cardiomyopathy in Mice.

    Wu, Wei / Jin, Qi / Östlund, Cecilia / Tanji, Kurenai / Shin, Ji-Yeon / Han, Jiying / Leu, Cheng-Shiun / Kushner, Jared / Worman, Howard J

    Circulation. Heart failure

    2024  Volume 17, Issue 4, Page(s) e011110

    Abstract: Background: Mutations in : Methods: We treated male : Results: Everolimus treatment (n=17) significantly reduced left ventricular dilatation and increased contractility on echocardiography, with a 7% (: Conclusions: These results suggest that ... ...

    Abstract Background: Mutations in
    Methods: We treated male
    Results: Everolimus treatment (n=17) significantly reduced left ventricular dilatation and increased contractility on echocardiography, with a 7% (
    Conclusions: These results suggest that mTOR inhibitors may be beneficial in patients with cardiomyopathy caused by
    MeSH term(s) Mice ; Humans ; Male ; Animals ; Everolimus/pharmacology ; Everolimus/therapeutic use ; Lamin Type A/genetics ; Lamin Type A/metabolism ; MTOR Inhibitors ; Heart Failure ; Cardiomyopathies/drug therapy ; Cardiomyopathies/genetics ; Cardiomyopathies/pathology ; Mutation ; TOR Serine-Threonine Kinases ; Mechanistic Target of Rapamycin Complex 1/genetics ; Drug-Related Side Effects and Adverse Reactions ; Mammals/metabolism
    Chemical Substances Everolimus (9HW64Q8G6G) ; Lamin Type A ; MTOR Inhibitors ; TOR Serine-Threonine Kinases (EC 2.7.11.1) ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1)
    Language English
    Publishing date 2024-04-03
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2429459-7
    ISSN 1941-3297 ; 1941-3289
    ISSN (online) 1941-3297
    ISSN 1941-3289
    DOI 10.1161/CIRCHEARTFAILURE.123.011110
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 6745: Show issues Location:
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  10. Article ; Online: Permanently Farnesylated Prelamin A, Progeria, and Atherosclerosis.

    Worman, Howard J / Michaelis, Susan

    Circulation

    2018  Volume 138, Issue 3, Page(s) 283–286

    MeSH term(s) Animals ; Atherosclerosis ; Lamin Type A ; Mice ; Muscle, Smooth, Vascular ; Progeria
    Chemical Substances Lamin Type A ; prelamin A
    Language English
    Publishing date 2018-07-16
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 80099-5
    ISSN 1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
    ISSN (online) 1524-4539
    ISSN 0009-7322 ; 0069-4193 ; 0065-8499
    DOI 10.1161/CIRCULATIONAHA.118.034480
    Database MEDical Literature Analysis and Retrieval System OnLINE

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