Abnormal reaction to central nervous system injury in mice lacking glial fibrillary acidic protein and vimentin. - Wikidata - awgldk - TriplyDB

Abnormal reaction to central nervous system injury in mice lacking glial fibrillary acidic protein and vimentin.

Abnormal reaction to central nervous system injury in mice lacking glial fibrillary acidic protein and vimentin.

http://www.wikidata.org/entity/Q41782223

about

Neuroprotection for traumatic brain injury Structural remodeling of astrocytes in the injured CNS Role of the lesion scar in the response to damage and repair of the central nervous system Glial cells in (patho)physiology Astroglial excitability and gliotransmission: an appraisal of Ca2+ as a signalling route New aspects of the pathogenesis of canine distemper leukoencephalitis Clonal astrocytic response to cortical injury Localization of West Nile Virus in monkey brain: double staining antigens immunohistochemically of neurons, neuroglia cells and West Nile Virus Axonal plasticity and functional recovery after spinal cord injury in mice deficient in both glial fibrillary acidic protein and vimentin genes.Reactive astrocytes and therapeutic potential in focal ischemic stroke Role of gap junction protein connexin43 in astrogliosis induced by brain injury A role for intermediate filaments in determining and maintaining the shape of nerve cells Attenuating astrocyte activation accelerates plaque pathogenesis in APP/PS1 mice.Ependymal ciliary dysfunction and reactive astrocytosis in a reorganized subventricular zone after stroke Intermediate filaments: a historical perspective A novel and efficient gene transfer strategy reduces glial reactivity and improves neuronal survival and axonal growth in vitro.Modulation of inflammatory responses after global ischemia by transplanted umbilical cord matrix stem cells Mechanically induced reactive gliosis causes ATP-mediated alterations in astrocyte stiffness.Withaferin A targets intermediate filaments glial fibrillary acidic protein and vimentin in a model of retinal gliosis Modulating astrogliosis after neurotrauma.Activation of the TRPV1 cation channel contributes to stress-induced astrocyte migration Increased levels of keratin 16 alter epithelialization potential of mouse skin keratinocytes in vivo and ex vivo.Re-establishing the regenerative potential of central nervous system axons in postnatal mice.Multiple implants do not aggravate the tissue reaction in rat brain.Stem cells for spinal cord regeneration: Current status Reactive astrocytes promote axonal remodeling and neurological recovery after stroke Plasticity response in the contralesional hemisphere after subtle neurotrauma: gene expression profiling after partial deafferentation of the hippocampus.Beneficial effects of gfap/vimentin reactive astrocytes for axonal remodeling and motor behavioral recovery in mice after stroke.Axonal regeneration after sciatic nerve lesion is delayed but complete in GFAP- and vimentin-deficient mice The 14-3-3 protein epsilon isoform expressed in reactive astrocytes in demyelinating lesions of multiple sclerosis binds to vimentin and glial fibrillary acidic protein in cultured human astrocytes Transforming growth factor α transforms astrocytes to a growth-supportive phenotype after spinal cord injury The role of attenuated astrocyte activation in infantile neuronal ceroid lipofuscinosis.Corneal antifibrotic switch identified in genetic and pharmacological deficiency of vimentin Transient changes in spinal cord glial cells following transection of preganglionic sympathetic axons.Induction of glial fibrillary acidic protein expression in astrocytes by nitric oxide Astrocyte roles in traumatic brain injury.Loss of keratin 6 (K6) proteins reveals a function for intermediate filaments during wound repair Worms reveal essential functions for intermediate filaments Blockade of Astrocytic Calcineurin/NFAT Signaling Helps to Normalize Hippocampal Synaptic Function and Plasticity in a Rat Model of Traumatic Brain Injury.A genetic approach to dissect sexually dimorphic behaviors.

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P2860

Abnormal reaction to central nervous system injury in mice lacking glial fibrillary acidic protein and vimentin.

http://www.wikidata.org/entity/Q41782223

description

1999 nî lūn-bûn

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1999年の論文

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1999年論文

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1999年論文

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1999年论文

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1999年论文

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Abnormal reaction to central n ...... y acidic protein and vimentin.

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Abnormal reaction to central n ...... y acidic protein and vimentin.

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Abnormal reaction to central n ...... y acidic protein and vimentin.

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A Wallén

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C B Johansson

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C Eliasson

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C H Berthold

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T Perlmann

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P2860

Onset of re-epithelialization after skin injury correlates with a reorganization of keratin filaments in wound edge keratinocytes: defining a potential role for keratin 16

Desmin is essential for the tensile strength and integrity of myofibrils but not for myogenic commitment, differentiation, and fusion of skeletal muscle

Intermediate-sized filaments of human endothelial cells

Targeted deletion in astrocyte intermediate filament (Gfap) alters neuronal physiology

CNS stem cells express a new class of intermediate filament protein

A single protocol to detect transcripts of various types and expression levels in neural tissue and cultured cells: in situ hybridization using digoxigenin-labelled cRNA probes

Mice lacking vimentin develop and reproduce without an obvious phenotype.

Molecular profile of reactive astrocytes--implications for their role in neurologic disease.

GFAP is necessary for the integrity of CNS white matter architecture and long-term maintenance of myelination.

A structural scaffolding of intermediate filaments in health and disease.

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3

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Christer Betsholtz

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236238609

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