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  1. Article ; Online: Roger Guillemin (1924-2024), neuroscientist who showed how the brain controls hormones.

    Lemke, Greg

    Nature

    2024  Volume 627, Issue 8003, Page(s) 266

    Language English
    Publishing date 2024-03-08
    Publishing country England
    Document type News
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/d41586-024-00714-4
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  2. Book: Developmental neurobiology

    Lemke, Greg

    2009  

    Author's details ed. Greg Lemke
    Language English
    Size XVII, 752 S. : Ill., 29 cm
    Publisher Elsevier Acad. Press
    Publishing place Amsterdam u.a.
    Publishing country Netherlands
    Document type Book
    HBZ-ID HT016122846
    ISBN 978-0-12-375081-5 ; 0-12-375081-4
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    2009 A 5285 order for loan Magazin

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  3. Article ; Online: How macrophages deal with death.

    Lemke, Greg

    Nature reviews. Immunology

    2019  Volume 19, Issue 9, Page(s) 539–549

    Abstract: Tissue macrophages rapidly recognize and engulf apoptotic cells. These events require the display of so-called eat-me signals on the apoptotic cell surface, the most fundamental of which is phosphatidylserine (PtdSer). Externalization of this ... ...

    Abstract Tissue macrophages rapidly recognize and engulf apoptotic cells. These events require the display of so-called eat-me signals on the apoptotic cell surface, the most fundamental of which is phosphatidylserine (PtdSer). Externalization of this phospholipid is catalysed by scramblase enzymes, several of which are activated by caspase cleavage. PtdSer is detected both by macrophage receptors that bind to this phospholipid directly and by receptors that bind to a soluble bridging protein that is independently bound to PtdSer. Prominent among the latter receptors are the MER and AXL receptor tyrosine kinases. Eat-me signals also trigger macrophages to engulf virus-infected or metabolically traumatized, but still living, cells, and this 'murder by phagocytosis' may be a common phenomenon. Finally, the localized presentation of PtdSer and other eat-me signals on delimited cell surface domains may enable the phagocytic pruning of these 'locally dead' domains by macrophages, most notably by microglia of the central nervous system.
    MeSH term(s) Animals ; Antigens, Surface/physiology ; Apoptosis ; Humans ; Macrophages/physiology ; Membrane Proteins/physiology ; Milk Proteins ; Phagocytosis ; Phosphatidylserines/physiology ; Receptor Protein-Tyrosine Kinases/physiology ; c-Mer Tyrosine Kinase/physiology
    Chemical Substances Antigens, Surface ; MFGE8 protein, human ; Membrane Proteins ; Milk Proteins ; Phosphatidylserines ; TIMD4 protein, human ; MERTK protein, human (EC 2.7.10.1) ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1) ; TYRO3 protein, human (EC 2.7.10.1) ; c-Mer Tyrosine Kinase (EC 2.7.10.1)
    Language English
    Publishing date 2019-04-24
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2062776-2
    ISSN 1474-1741 ; 1474-1733
    ISSN (online) 1474-1741
    ISSN 1474-1733
    DOI 10.1038/s41577-019-0167-y
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  4. Article ; Online: Adaptable toolbox to characterize Alzheimer's disease pathology in mouse models.

    Huang, Youtong / Lemke, Greg

    STAR protocols

    2022  Volume 3, Issue 4, Page(s) 101891

    Abstract: Here, we describe a highly adaptable toolbox for characterizing and analyzing molecular and histopathological changes in Alzheimer's disease (AD) mouse models. We detail optimized and streamlined approaches from sample preparation to image analysis to ... ...

    Abstract Here, we describe a highly adaptable toolbox for characterizing and analyzing molecular and histopathological changes in Alzheimer's disease (AD) mouse models. We detail optimized and streamlined approaches from sample preparation to image analysis to facilitate reproducible analyses. We also describe the extraction and measurement of the soluble Aβ level by sandwich ELISA in the cortex and hippocampus of AD mouse models before and after plaque deposition. Finally, we outline the steps for image quantification and analysis using Imaris and ImageJ. For complete details on the use and execution of this protocol, please refer to Huang et al. (2021).
    MeSH term(s) Mice ; Animals ; Alzheimer Disease/pathology ; Amyloid beta-Peptides/metabolism ; Mice, Transgenic ; Cerebral Cortex/metabolism ; Hippocampus/metabolism ; Disease Models, Animal
    Chemical Substances Amyloid beta-Peptides
    Language English
    Publishing date 2022-12-02
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 2666-1667
    ISSN (online) 2666-1667
    DOI 10.1016/j.xpro.2022.101891
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: The dense-core plaques of Alzheimer's disease are granulomas.

    Lemke, Greg / Huang, Youtong

    The Journal of experimental medicine

    2022  Volume 219, Issue 8

    Abstract: Dense-core plaques, whose centers contain highly polymerized and compacted aggregates of amyloid β peptides, are one of the two defining histopathological features of Alzheimer's disease. Recent findings indicate that these plaques do not form ... ...

    Abstract Dense-core plaques, whose centers contain highly polymerized and compacted aggregates of amyloid β peptides, are one of the two defining histopathological features of Alzheimer's disease. Recent findings indicate that these plaques do not form spontaneously but are instead constructed by microglia, the tissue macrophages of the central nervous system. We discuss cellular, structural, functional, and gene expression criteria by which the microglial assembly of dense-core plaques in the Alzheimer's brain parallels the construction of granulomas by macrophages in other settings. We compare the genesis of these plaques to the macrophage assembly of mycobacterial granulomas, the defining histopathological features of tuberculosis. We suggest that if dense-core plaques are indeed granulomas, their simple disassembly may be contraindicated as an Alzheimer's therapy.
    MeSH term(s) Alzheimer Disease/pathology ; Amyloid beta-Peptides/metabolism ; Granuloma/metabolism ; Granuloma/pathology ; Humans ; Microglia/metabolism ; Plaque, Amyloid/metabolism
    Chemical Substances Amyloid beta-Peptides
    Language English
    Publishing date 2022-06-22
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 218343-2
    ISSN 1540-9538 ; 0022-1007
    ISSN (online) 1540-9538
    ISSN 0022-1007
    DOI 10.1084/jem.20212477
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  6. Article ; Online: Early death in a mouse model of Alzheimer's disease exacerbated by microglial loss of TAM receptor signaling.

    Huang, Youtong / Lemke, Greg

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

    2022  Volume 119, Issue 41, Page(s) e2204306119

    Abstract: Recurrent seizure is a common comorbidity in early-stage Alzheimer's disease (AD) and may contribute to AD pathogenesis and cognitive decline. Similarly, many mouse models of Alzheimer's disease that overproduce amyloid beta are prone to epileptiform ... ...

    Abstract Recurrent seizure is a common comorbidity in early-stage Alzheimer's disease (AD) and may contribute to AD pathogenesis and cognitive decline. Similarly, many mouse models of Alzheimer's disease that overproduce amyloid beta are prone to epileptiform seizures that may result in early sudden death. We studied one such model, designated
    MeSH term(s) Alzheimer Disease/genetics ; Alzheimer Disease/pathology ; Amyloid beta-Peptides ; Amyloid beta-Protein Precursor/genetics ; Animals ; Dentate Gyrus ; Disease Models, Animal ; Hippocampus/metabolism ; Ligands ; Mice ; Mice, Transgenic ; Microglia/metabolism ; Neurogenesis ; Phagocytosis ; Plaque, Amyloid/pathology ; Polymers ; Protein-Tyrosine Kinases ; Seizures/genetics ; Seizures/pathology
    Chemical Substances Amyloid beta-Peptides ; Amyloid beta-Protein Precursor ; Ligands ; Polymers ; Protein-Tyrosine Kinases (EC 2.7.10.1)
    Language English
    Publishing date 2022-10-03
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.2204306119
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  7. Article ; Online: Regulation of brain endothelial cell physiology by the TAM receptor tyrosine kinase Mer.

    Happonen, Kaisa E / Burrola, Patrick G / Lemke, Greg

    Communications biology

    2023  Volume 6, Issue 1, Page(s) 916

    Abstract: The receptor tyrosine kinase Mer (gene name Mertk) acts in vascular endothelial cells (ECs) to tighten the blood-brain barrier (BBB) subsequent to viral infection, but how this is achieved is poorly understood. We find that Mer controls the expression ... ...

    Abstract The receptor tyrosine kinase Mer (gene name Mertk) acts in vascular endothelial cells (ECs) to tighten the blood-brain barrier (BBB) subsequent to viral infection, but how this is achieved is poorly understood. We find that Mer controls the expression and activity of a large cohort of BBB regulators, along with endothelial nitric oxide synthase. It also controls, via an Akt-Foxo1 pathway, the expression of multiple angiogenic genes. Correspondingly, EC-specific Mertk gene inactivation resulted in perturbed vascular sprouting and a compromised BBB after induced photothrombotic stroke. Unexpectedly, stroke lesions in the brain were also reduced in the absence of EC Mer, which was linked to reduced plasma expression of fibrinogen, prothrombin, and other effectors of blood coagulation. Together, these results demonstrate that Mer is a central regulator of angiogenesis, BBB integrity, and blood coagulation in the mature vasculature. They may also account for disease severity following infection with the coronavirus SARS-CoV-2.
    MeSH term(s) Humans ; c-Mer Tyrosine Kinase/genetics ; COVID-19/genetics ; Endothelial Cells ; SARS-CoV-2 ; Receptor Protein-Tyrosine Kinases ; Brain
    Chemical Substances c-Mer Tyrosine Kinase (EC 2.7.10.1) ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1)
    Language English
    Publishing date 2023-09-07
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ISSN 2399-3642
    ISSN (online) 2399-3642
    DOI 10.1038/s42003-023-05287-y
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  8. Article ; Online: Adaptable toolbox to characterize Alzheimer’s disease pathology in mouse models

    Youtong Huang / Greg Lemke

    STAR Protocols, Vol 3, Iss 4, Pp 101891- (2022)

    2022  

    Abstract: Summary: Here, we describe a highly adaptable toolbox for characterizing and analyzing molecular and histopathological changes in Alzheimer’s disease (AD) mouse models. We detail optimized and streamlined approaches from sample preparation to image ... ...

    Abstract Summary: Here, we describe a highly adaptable toolbox for characterizing and analyzing molecular and histopathological changes in Alzheimer’s disease (AD) mouse models. We detail optimized and streamlined approaches from sample preparation to image analysis to facilitate reproducible analyses. We also describe the extraction and measurement of the soluble Aβ level by sandwich ELISA in the cortex and hippocampus of AD mouse models before and after plaque deposition. Finally, we outline the steps for image quantification and analysis using Imaris and ImageJ.For complete details on the use and execution of this protocol, please refer to Huang et al. (2021).1 : Publisher’s note: Undertaking any experimental protocol requires adherence to local institutional guidelines for laboratory safety and ethics.
    Keywords Health Sciences ; Microscopy ; Model Organisms ; Neuroscience ; Science (General) ; Q1-390
    Language English
    Publishing date 2022-12-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article: Phosphatidylserine Is the Signal for TAM Receptors and Their Ligands.

    Lemke, Greg

    Trends in biochemical sciences

    2017  Volume 42, Issue 9, Page(s) 738–748

    Abstract: Nature repeatedly repurposes, in that molecules that serve as metabolites, energy depots, or polymer subunits are at the same time used to deliver signals within and between cells. The preeminent example of this repurposing is ATP, which functions as a ... ...

    Abstract Nature repeatedly repurposes, in that molecules that serve as metabolites, energy depots, or polymer subunits are at the same time used to deliver signals within and between cells. The preeminent example of this repurposing is ATP, which functions as a building block for nucleic acids, an energy source for enzymatic reactions, a phosphate donor to regulate intracellular signaling, and a neurotransmitter to control the activity of neurons. A series of recent studies now consolidates the view that phosphatidylserine (PtdSer), a common phospholipid constituent of membrane bilayers, is similarly repurposed for use as a signal between cells and that the ligands and receptors of the Tyro3/Axl/Mer (TAM) family of receptor tyrosine kinases (RTKs) are prominent transducers of this signal.
    MeSH term(s) Animals ; Humans ; Ligands ; Phosphatidylserines/chemistry ; Phosphatidylserines/pharmacology ; Receptor Protein-Tyrosine Kinases/deficiency ; Receptor Protein-Tyrosine Kinases/metabolism ; Signal Transduction/drug effects
    Chemical Substances Ligands ; Phosphatidylserines ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1)
    Language English
    Publishing date 2017-07-19
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 194216-5
    ISSN 1362-4326 ; 0968-0004 ; 0376-5067
    ISSN (online) 1362-4326
    ISSN 0968-0004 ; 0376-5067
    DOI 10.1016/j.tibs.2017.06.004
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  10. Article: Tyro3 promotes the maturation of glutamatergic synapses.

    Miao, Sheng / Fourgeaud, Lawrence / Burrola, Patrick G / Stern, Shani / Zhang, Yuhan / Happonen, Kaisa E / Novak, Sammy Weiser / Gage, Fred H / Lemke, Greg

    Frontiers in neuroscience

    2024  Volume 18, Page(s) 1327423

    Abstract: The receptor tyrosine kinase Tyro3 is abundantly expressed in neurons of the neocortex, hippocampus, and striatum, but its role in these cells is unknown. We found that neuronal expression of this receptor was markedly up-regulated in the postnatal mouse ...

    Abstract The receptor tyrosine kinase Tyro3 is abundantly expressed in neurons of the neocortex, hippocampus, and striatum, but its role in these cells is unknown. We found that neuronal expression of this receptor was markedly up-regulated in the postnatal mouse neocortex immediately prior to the final development of glutamatergic synapses. In the absence of Tyro3, cortical and hippocampal synapses never completed end-stage differentiation and remained electrophysiologically and ultrastructurally immature.
    Language English
    Publishing date 2024-02-12
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2411902-7
    ISSN 1662-453X ; 1662-4548
    ISSN (online) 1662-453X
    ISSN 1662-4548
    DOI 10.3389/fnins.2024.1327423
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