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Article ; Online: Inositol Polyphosphate-5-Phosphatase K (

Kauer, Sierra D / Fink, Kathryn L / Li, Elizabeth H F / Evans, Brian P / Golan, Noa / Cafferty, William B J

The Journal of neuroscience : the official journal of the Society for Neuroscience

2022 Volume 42, Issue 11, Page(s) 2190–2204

Abstract: Failure of CNS neurons to mount a significant growth response after trauma contributes to chronic functional deficits after spinal cord injury. Activator and repressor screening of embryonic cortical neurons and retinal ganglion ... ...

Abstract	Failure of CNS neurons to mount a significant growth response after trauma contributes to chronic functional deficits after spinal cord injury. Activator and repressor screening of embryonic cortical neurons and retinal ganglion cells
MeSH term(s)	Animals ; Axons/metabolism ; Female ; Inositol/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Nerve Regeneration/physiology ; Phosphoric Monoester Hydrolases/genetics ; Phosphoric Monoester Hydrolases/metabolism ; Polyphosphates/metabolism ; Pyramidal Tracts/physiology ; Spinal Cord Injuries
Chemical Substances	Polyphosphates ; Inositol (4L6452S749) ; Phosphoric Monoester Hydrolases (EC 3.1.3.2)
Language	English
Publishing date	2022-02-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	604637-x
ISSN	1529-2401 ; 0270-6474
ISSN (online)	1529-2401
ISSN	0270-6474
DOI	10.1523/JNEUROSCI.0897-21.2022
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Article ; Online: Plexina2 and CRMP2 Signaling Complex Is Activated by Nogo-A-Liganded Ngr1 to Restrict Corticospinal Axon Sprouting after Trauma.

Sekine, Yuichi / Algarate, Percy T / Cafferty, William B J / Strittmatter, Stephen M

The Journal of neuroscience : the official journal of the Society for Neuroscience

2019 Volume 39, Issue 17, Page(s) 3204–3216

Abstract: After brain or spinal cord trauma, interaction of Nogo-A with neuronal NgR1 limits regenerative axonal sprouting and functional recovery. Cellular signaling by lipid-anchored NgR1 requires a coreceptor but the relevant ... ...

Abstract	After brain or spinal cord trauma, interaction of Nogo-A with neuronal NgR1 limits regenerative axonal sprouting and functional recovery. Cellular signaling by lipid-anchored NgR1 requires a coreceptor but the relevant partner
MeSH term(s)	Animals ; Axons/metabolism ; COS Cells ; Chlorocebus aethiops ; Intercellular Signaling Peptides and Proteins/genetics ; Intercellular Signaling Peptides and Proteins/metabolism ; Mice ; Mice, Knockout ; Motor Activity/physiology ; Nerve Regeneration/physiology ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Neurons/metabolism ; Nogo Proteins/genetics ; Nogo Proteins/metabolism ; Nogo Receptor 1/metabolism ; Pyramidal Tracts/injuries ; Pyramidal Tracts/metabolism ; Receptors, Cell Surface/genetics ; Receptors, Cell Surface/metabolism ; Recovery of Function/physiology ; Spinal Cord Injuries/metabolism
Chemical Substances	Intercellular Signaling Peptides and Proteins ; Nerve Tissue Proteins ; Nogo Proteins ; Nogo Receptor 1 ; Plxna2 protein, mouse ; Receptors, Cell Surface ; collapsin response mediator protein-2
Language	English
Publishing date	2019-02-25
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	604637-x
ISSN	1529-2401 ; 0270-6474
ISSN (online)	1529-2401
ISSN	0270-6474
DOI	10.1523/JNEUROSCI.2996-18.2019
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Article ; Online: Reorganization of Intact Descending Motor Circuits to Replace Lost Connections After Injury.

Fink, Kathren L / Cafferty, William B J

Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics

2016 Volume 13, Issue 2, Page(s) 370–381

Abstract: Neurons have a limited capacity to regenerate in the adult central nervous system (CNS). The inability of damaged axons to re-establish original circuits results in permanent functional impairment after spinal cord injury (SCI). Despite abortive ... ...

Abstract	Neurons have a limited capacity to regenerate in the adult central nervous system (CNS). The inability of damaged axons to re-establish original circuits results in permanent functional impairment after spinal cord injury (SCI). Despite abortive regeneration of axotomized CNS neurons, limited spontaneous recovery of motor function emerges after partial SCI in humans and experimental rodent models of SCI. It is hypothesized that this spontaneous functional recovery is the result of the reorganization of descending motor pathways spared by the injury, suggesting that plasticity of intact circuits is a potent alternative conduit to enhance functional recovery after SCI. In support of this hypothesis, several studies have shown that after unilateral corticospinal tract (CST) lesion (unilateral pyramidotomy), the intact CST functionally sprouts into the denervated side of the spinal cord. Furthermore, pharmacologic and genetic methods that enhance the intrinsic growth capacity of adult neurons or block extracellular growth inhibitors are effective at significantly enhancing intact CST reorganization and recovery of motor function. Owing to its importance in controlling fine motor behavior in primates, the CST is the most widely studied descending motor pathway; however, additional studies in rodents have shown that plasticity within other spared descending motor pathways, including the rubrospinal tract, raphespinal tract, and reticulospinal tract, can also result in restoration of function after incomplete SCI. Identifying the molecular mechanisms that drive plasticity within intact circuits is crucial in developing novel, potent, and specific therapeutics to restore function after SCI. In this review we discuss the evidence supporting a focus on exploring the capacity of intact motor circuits to functionally repair the damaged CNS after SCI.
MeSH term(s)	Animals ; Efferent Pathways/injuries ; Efferent Pathways/physiopathology ; Humans ; Motor Neurons/physiology ; Nerve Regeneration/physiology ; Neuronal Plasticity/physiology ; Spinal Cord/physiopathology ; Spinal Cord Injuries/physiopathology
Language	English
Publishing date	2016-02-02
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2316693-9
ISSN	1878-7479 ; 1933-7213
ISSN (online)	1878-7479
ISSN	1933-7213
DOI	10.1007/s13311-016-0422-x
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Zs.A 6156: Show issues

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Article ; Online: The nociceptin receptor inhibits axonal regeneration and recovery from spinal cord injury.

Sekine, Yuichi / Siegel, Chad S / Sekine-Konno, Tomoko / Cafferty, William B J / Strittmatter, Stephen M

Science signaling

2018 Volume 11, Issue 524

Abstract: Axonal growth after traumatic spinal cord injury is limited by endogenous inhibitors, selective blockade of which promotes partial neurological recovery. The partial repair phenotypes suggest that compensatory pathways limit improvement. Gene expression ... ...

Abstract	Axonal growth after traumatic spinal cord injury is limited by endogenous inhibitors, selective blockade of which promotes partial neurological recovery. The partial repair phenotypes suggest that compensatory pathways limit improvement. Gene expression profiles of mice deficient in
MeSH term(s)	Animals ; Axons/metabolism ; Axons/physiology ; COS Cells ; Cell Line, Tumor ; Cells, Cultured ; Chlorocebus aethiops ; HEK293 Cells ; Humans ; Mice, Inbred C57BL ; Mice, Knockout ; Nerve Regeneration/drug effects ; Nerve Regeneration/genetics ; Nerve Regeneration/physiology ; Neurons/cytology ; Neurons/metabolism ; Neurons/physiology ; Nogo Receptor 1/genetics ; Nogo Receptor 1/metabolism ; Opioid Peptides/pharmacology ; Receptors, Opioid/genetics ; Receptors, Opioid/metabolism ; Spinal Cord Injuries/genetics ; Spinal Cord Injuries/metabolism ; Spinal Cord Injuries/physiopathology ; Nociceptin Receptor ; Nociceptin
Chemical Substances	Nogo Receptor 1 ; Opioid Peptides ; Receptors, Opioid ; Nociceptin Receptor
Language	English
Publishing date	2018-04-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2417226-1
ISSN	1937-9145 ; 1945-0877
ISSN (online)	1937-9145
ISSN	1945-0877
DOI	10.1126/scisignal.aao4180
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Article ; Online: Comprehensive Corticospinal Labeling with mu-crystallin Transgene Reveals Axon Regeneration after Spinal Cord Trauma in ngr1-/- Mice.

Fink, Kathren L / Strittmatter, Stephen M / Cafferty, William B J

The Journal of neuroscience : the official journal of the Society for Neuroscience

2015 Volume 35, Issue 46, Page(s) 15403–15418

Abstract: Spinal cord injury interrupts descending motor tracts and creates persistent functional deficits due to the absence of spontaneous axon regeneration. Of descending pathways, the corticospinal tract (CST) is thought to be the most critical for voluntary ... ...

Abstract	Spinal cord injury interrupts descending motor tracts and creates persistent functional deficits due to the absence of spontaneous axon regeneration. Of descending pathways, the corticospinal tract (CST) is thought to be the most critical for voluntary function in primates. Even with multiple tracer injections and genetic tools, the CST is visualized to only a minor degree in experimental studies. Here, we identify and validate the mu-crystallin (crym) gene as a high-fidelity marker of the CST. In transgenic mice expressing green fluorescent protein (GFP) under crym regulatory elements (crym-GFP), comprehensive and near complete CST labeling is achieved throughout the spinal cord. Bilateral pyramidotomy eliminated the 17,000 GFP-positive CST axons that were reproducibly labeled in brainstem from the spinal cord. We show that CST tracing with crym-GFP is 10-fold more efficient than tracing with biotinylated dextran amine (BDA). Using crym-GFP, we reevaluated the CST in mice lacking nogo receptor 1 (NgR1), a protein implicated in limiting neural repair. The number and trajectory of CST axons in ngr1(-/-) mice without injury was indistinguishable from ngr1(+/+) mice. After dorsal hemisection in the midthoracic cord, CST axons did not significantly regenerate in ngr1(+/+) mice, but an average of 162 of the 6000 labeled thoracic CST axons (2.68%) regenerated >100 μm past the lesion site in crym-GFP ngr1(-/-) mice. Although traditional BDA tracing cannot reliably visualize regenerating ngr1(-/-) CST axons, their regenerative course is clear with crym-GFP. Therefore the crym-GFP transgenic mouse is a useful tool for studies of CST anatomy in experimental studies of motor pathways. Significance statement: Axon regeneration fails in the adult CNS, resulting in permanent functional deficits. Traditionally, inefficient extrinsic tracers such a biotinylated dextran amine (BDA) are used to label regenerating fibers after therapeutic intervention. We introduce crym-green fluorescent protein (GFP) transgenic mice as a comprehensive and specific tool with which to study the primary descending motor tract, the corticospinal tract (CST). CST labeling with crym-GFP is 10 times more efficient compared with BDA. The enhanced sensitivity afforded by crym-GFP revealed significant CST regeneration in NgR1 knock-out mice. Therefore, crym-GFP can be used as a standardized tool for future CST spinal cord injury studies.
MeSH term(s)	Amidines/metabolism ; Analysis of Variance ; Animals ; Axons/pathology ; Biotin/analogs & derivatives ; Biotin/metabolism ; Crystallins/biosynthesis ; Crystallins/genetics ; Crystallins/metabolism ; Dextrans/metabolism ; Disease Models, Animal ; Functional Laterality ; GPI-Linked Proteins/deficiency ; GPI-Linked Proteins/genetics ; Gene Expression Regulation/genetics ; Glial Fibrillary Acidic Protein/metabolism ; Luminescent Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Myelin Proteins/deficiency ; Myelin Proteins/genetics ; Nerve Regeneration/genetics ; Nogo Receptor 1 ; Pyramidal Tracts/metabolism ; Pyramidal Tracts/pathology ; Receptors, Cell Surface/deficiency ; Receptors, Cell Surface/genetics ; Recovery of Function/genetics ; Spinal Cord Injuries/complications ; Spinal Cord Injuries/pathology ; mu-Crystallins
Chemical Substances	Amidines ; Crym protein, mouse ; Crystallins ; Dextrans ; GPI-Linked Proteins ; Glial Fibrillary Acidic Protein ; Luminescent Proteins ; Myelin Proteins ; Nogo Receptor 1 ; Receptors, Cell Surface ; Rtn4r protein, mouse ; biotinylated dextran amine ; diamidino compound 253-50 ; Biotin (6SO6U10H04) ; mu-Crystallins (EC 1.5.1.25)
Language	English
Publishing date	2015-11-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	604637-x
ISSN	1529-2401 ; 0270-6474
ISSN (online)	1529-2401
ISSN	0270-6474
DOI	10.1523/JNEUROSCI.3165-15.2015
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Article ; Online: NRF2 Activation Reprograms Defects in Oxidative Metabolism to Restore Macrophage Function in Chronic Obstructive Pulmonary Disease.

Ryan, Eilise M / Sadiku, Pranvera / Coelho, Patricia / Watts, Emily R / Zhang, Ailiang / Howden, Andrew J M / Sanchez-Garcia, Manuel A / Bewley, Martin / Cole, Joby / McHugh, Brian J / Vermaelen, Wesley / Ghesquiere, Bart / Carmeliet, Peter / Rodriguez Blanco, Giovanny / Von Kriegsheim, Alex / Sanchez, Yolanda / Rumsey, William / Callahan, James F / Cooper, George /

Parkinson, Nicholas / Baillie, Kenneth / Cantrell, Doreen A / McCafferty, John / Choudhury, Gourab / Singh, Dave / Dockrell, David H / Whyte, Moira K B / Walmsley, Sarah R

American journal of respiratory and critical care medicine

2023 Volume 207, Issue 8, Page(s) 998–1011

Abstract: Rationale: ...

Abstract	Rationale:
MeSH term(s)	Humans ; Macrophages/metabolism ; NF-E2-Related Factor 2/metabolism ; Oxidative Stress ; Pulmonary Disease, Chronic Obstructive/metabolism ; Pulmonary Disease, Chronic Obstructive/physiopathology ; Malate Dehydrogenase/metabolism
Chemical Substances	NF-E2-Related Factor 2 ; malate dehydrogenase (decarboxylating) (EC 1.1.1.39) ; Malate Dehydrogenase (EC 1.1.1.37)
Language	English
Publishing date	2023-02-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1180953-x
ISSN	1535-4970 ; 0003-0805 ; 1073-449X
ISSN (online)	1535-4970
ISSN	0003-0805 ; 1073-449X
DOI	10.1164/rccm.202203-0482OC
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Article ; Online: Anatomical Diversity of the Adult Corticospinal Tract Revealed by Single-Cell Transcriptional Profiling.

Golan, Noa / Ehrlich, Daniel / Bonanno, James / O'Brien, Rory F / Murillo, Matias / Kauer, Sierra D / Ravindra, Neal / Van Dijk, David / Cafferty, William B

The Journal of neuroscience : the official journal of the Society for Neuroscience

2023 Volume 43, Issue 47, Page(s) 7929–7945

Abstract: The corticospinal tract (CST) forms a central part of the voluntary motor apparatus in all mammals. Thus, injury, disease, and subsequent degeneration within this pathway result in chronic irreversible functional deficits. Current strategies to repair ... ...

Abstract	The corticospinal tract (CST) forms a central part of the voluntary motor apparatus in all mammals. Thus, injury, disease, and subsequent degeneration within this pathway result in chronic irreversible functional deficits. Current strategies to repair the damaged CST are suboptimal in part because of underexplored molecular heterogeneity within the adult tract. Here, we combine spinal retrograde CST tracing with single-cell RNA sequencing (scRNAseq) in adult male and female mice to index corticospinal neuron (CSN) subtypes that differentially innervate the forelimb and hindlimb. We exploit publicly available datasets to confer anatomic specialization among CSNs and show that CSNs segregate not only along the forelimb and hindlimb axis but also by supraspinal axon collateralization. These anatomically defined transcriptional data allow us to use machine learning tools to build classifiers that discriminate between CSNs and cortical layer 2/3 and nonspinally terminating layer 5 neurons in M1 and separately identify limb-specific CSNs. Using these tools, CSN subtypes can be differentially identified to study postnatal patterning of the CST
MeSH term(s)	Mice ; Female ; Male ; Animals ; Pyramidal Tracts/physiology ; Spinal Cord Injuries/genetics ; Neurons/physiology ; Axons/physiology ; Mammals
Language	English
Publishing date	2023-11-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	604637-x
ISSN	1529-2401 ; 0270-6474
ISSN (online)	1529-2401
ISSN	0270-6474
DOI	10.1523/JNEUROSCI.0811-22.2023
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Article ; Online: Identification of Intrinsic Axon Growth Modulators for Intact CNS Neurons after Injury.

Fink, Kathren L / López-Giráldez, Francesc / Kim, In-Jung / Strittmatter, Stephen M / Cafferty, William B J

Cell reports

2017 Volume 18, Issue 11, Page(s) 2687–2701

Abstract: Functional deficits persist after spinal cord injury (SCI) because axons in the adult mammalian central nervous system (CNS) fail to regenerate. However, modest levels of spontaneous functional recovery are typically observed after trauma and are thought ...

Abstract	Functional deficits persist after spinal cord injury (SCI) because axons in the adult mammalian central nervous system (CNS) fail to regenerate. However, modest levels of spontaneous functional recovery are typically observed after trauma and are thought to be mediated by the plasticity of intact circuitry. The mechanisms underlying intact circuit plasticity are not delineated. Here, we characterize the in vivo transcriptome of sprouting intact neurons from Ngr1 null mice after partial SCI. We identify the lysophosphatidic acid signaling modulators LPPR1 and LPAR1 as intrinsic axon growth modulators for intact corticospinal motor neurons after adjacent injury. Furthermore, in vivo LPAR1 inhibition or LPPR1 overexpression enhances sprouting of intact corticospinal tract axons and yields greater functional recovery after unilateral brainstem lesion in wild-type mice. Thus, the transcriptional profile of injury-induced sprouting of intact neurons reveals targets for therapeutic enhancement of axon growth initiation and new synapse formation.
MeSH term(s)	Animals ; Axons/pathology ; Central Nervous System/injuries ; Central Nervous System/pathology ; Gene Expression Profiling ; Mice, Inbred C57BL ; Mice, Transgenic ; Motor Neurons/pathology ; Neurites/metabolism ; Neurogenesis ; Protein Binding ; Signal Transduction ; Spinal Cord/pathology ; Transcription, Genetic
Language	English
Publishing date	2017-04-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2017.02.058
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Article ; Online: Inhibition of Poly-ADP-Ribosylation Fails to Increase Axonal Regeneration or Improve Functional Recovery after Adult Mammalian CNS Injury.

Wang, Xingxing / Sekine, Yuichi / Byrne, Alexandra B / Cafferty, William B J / Hammarlund, Marc / Strittmatter, Stephen M

eNeuro

2016 Volume 3, Issue 6

Abstract: After traumatic damage of the brain or spinal cord, many surviving neurons are disconnected, and recovery of function is limited by poor axon regeneration. Recent data have suggested that poly ADP-ribosylation plays a role in limiting axonal regrowth ... ...

Abstract	After traumatic damage of the brain or spinal cord, many surviving neurons are disconnected, and recovery of function is limited by poor axon regeneration. Recent data have suggested that poly ADP-ribosylation plays a role in limiting axonal regrowth such that inhibition of poly (ADP-ribose) polymerase (PARP) may have therapeutic efficacy for neurological recovery after trauma. Here, we tested systemic administration of the PARP inhibitor, veliparib, and showed effective suppression of PARylation in the mouse CNS. After optic nerve crush injury or dorsal hemisection of the thoracic spinal cord in mice, treatment with veliparib at doses with pharmacodynamic action had no benefit for axonal regeneration or functional recovery. We considered whether PARP gene family specificity might play a role.
MeSH term(s)	Animals ; Axons/drug effects ; Axons/enzymology ; Benzimidazoles/pharmacology ; Cells, Cultured ; Cerebral Cortex/drug effects ; Cerebral Cortex/enzymology ; Cerebral Cortex/pathology ; Disease Models, Animal ; Female ; Isoenzymes/antagonists & inhibitors ; Isoenzymes/metabolism ; Male ; Mice, 129 Strain ; Mice, Inbred C57BL ; Mice, Transgenic ; Motor Activity/drug effects ; Motor Activity/physiology ; Nerve Regeneration/drug effects ; Nerve Regeneration/physiology ; Optic Nerve Injuries/drug therapy ; Optic Nerve Injuries/enzymology ; Optic Nerve Injuries/pathology ; Poly (ADP-Ribose) Polymerase-1/antagonists & inhibitors ; Poly (ADP-Ribose) Polymerase-1/genetics ; Poly (ADP-Ribose) Polymerase-1/metabolism ; Poly(ADP-ribose) Polymerase Inhibitors/pharmacology ; Recovery of Function/drug effects ; Recovery of Function/physiology ; Spinal Cord Injuries/drug therapy ; Spinal Cord Injuries/enzymology ; Spinal Cord Injuries/pathology ; Thoracic Vertebrae
Chemical Substances	Benzimidazoles ; Isoenzymes ; Poly(ADP-ribose) Polymerase Inhibitors ; veliparib (01O4K0631N) ; Parp1 protein, mouse (EC 2.4.2.30) ; Poly (ADP-Ribose) Polymerase-1 (EC 2.4.2.30)
Language	English
Publishing date	2016-12-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2800598-3
ISSN	2373-2822 ; 2373-2822
ISSN (online)	2373-2822
ISSN	2373-2822
DOI	10.1523/ENEURO.0270-16.2016
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Article ; Online: Myelin associated inhibitors: a link between injury-induced and experience-dependent plasticity.

Akbik, Feras / Cafferty, William B J / Strittmatter, Stephen M

Experimental neurology

2011 Volume 235, Issue 1, Page(s) 43–52

Abstract: ... Immunoglobulin-like-Receptor-B (PirB), to regulate cytoskeletal dynamics and inhibit growth. Initially described ...

Abstract	In the adult, both neurologic recovery and anatomical growth after a CNS injury are limited. Two classes of growth inhibitors, myelin associated inhibitors (MAIs) and extracellular matrix associated inhibitors, limit both functional recovery and anatomical rearrangements in animal models of spinal cord injury. Here we focus on how MAIs limit a wide spectrum of growth that includes regeneration, sprouting, and plasticity in both the intact and lesioned CNS. Three classic myelin associated inhibitors, Nogo-A, MAG, and OMgp, signal through their common receptors, Nogo-66 Receptor-1 (NgR1) and Paired-Immunoglobulin-like-Receptor-B (PirB), to regulate cytoskeletal dynamics and inhibit growth. Initially described as inhibitors of axonal regeneration, subsequent work has demonstrated that MAIs also limit activity and experience-dependent plasticity in the intact, adult CNS. MAIs therefore represent a point of convergence for plasticity that limits anatomical rearrangements regardless of the inciting stimulus, blurring the distinction between injury studies and more "basic" plasticity studies.
MeSH term(s)	Animals ; Axons/metabolism ; Brain/metabolism ; GPI-Linked Proteins/metabolism ; Myelin Proteins/metabolism ; Myelin-Associated Glycoprotein/metabolism ; Neuronal Plasticity/physiology ; Nogo Proteins ; Recovery of Function/physiology ; Spinal Cord Injuries/metabolism ; Spinal Cord Injuries/physiopathology
Chemical Substances	GPI-Linked Proteins ; Myelin Proteins ; Myelin-Associated Glycoprotein ; Nogo Proteins ; Omg protein, mouse ; Rtn4 protein, mouse
Language	English
Publishing date	2011-06-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	207148-4
ISSN	1090-2430 ; 0014-4886
ISSN (online)	1090-2430
ISSN	0014-4886
DOI	10.1016/j.expneurol.2011.06.006
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