Don W. Cleveland

Hindlimb gait defects due to motor axon loss and reduced distal muscles in a transgenic mouse model of Charcot-Marie-Tooth type 2A (2008)

Detmer, Scott A., Velde, Christine Vande, Cleveland, Don W., Chan, David C.

Charcot–Marie–Tooth (CMT) disease type 2A is a progressive, neurodegenerative disorder affecting long peripheral motor and sensory nerves. The most common clinical sign is weakness in the lower...

Neurodegeneration and neuroprotection in multiple sclerosis and other neurodegenerative diseases (2006)

Dhib-Jalbut, Suhayl, Arnold, Douglas L., Cleveland, Don W., Fisher, Marc, Friedlander, Robert M., Mouradian, M. Maral, ...

Multiple sclerosis is considered a disease of myelin destruction; Parkinson's disease (PD), one of dopaminergic neuron depletion; ALS, a disease of motor neuron death; and Alzheimer's, a disease of...

Motoneuron death triggered by a specific pathway downstream of Fas. potentiation by ALS-linked SOD1 mutations. (2002)

Raoul, Cédric, Estévez, Alvaro G, Nishimune, Hiroshi, Cleveland, Don W, DeLapeyrière, Odile, Henderson, Christopher E, ...

Death pathways restricted to specific neuronal classes could potentially allow for precise control of developmental neuronal death and also underlie the selectivity of neuronal loss in...

AU-A, an RNA-binding activity distinct from hnRNP A1, is selective for AUUUA repeats and shuttles between the nucleus and the cytoplasm (1994)

Katz, David A., Theodorakis, Nicholas G., Cleveland, Don W., Lindsten, Tullia

The 3′-untranslated regions of many labile transcripts contain AU-rich sequences that serve as cis determinants of mRNA stability and translatlonal efficiency. Using a photocrossllnklng technique,...

A Combination of RNase H and S1 nuclease Circumvents an artefact inherent to conventional S1 analysis of RNA splicing (1987)

Sisodia, Sangram S., Cleveland, Don W., Sollner-Webb, Barbara

SI nucleate napping it commonly used to analyze transcription and processing of unlabellod RNAs. However, the SI protoool that appears best suited to demonstrate splioing of a particular RNA (using...

High level transient expression of a chloramphenicol acetyl transferase gene by DEAE-dextran mediated DNA transfection coupled with a dimethyl sulfoxide or glycerol shock treatment (1984)

Lopata, Margaret A., Cleveland, Don W., Sollner-Webb, Barbara

Using a plasmid containing the bacterial chloramphenicol acetyl transferase gene, we have assayed for transient expression of DNA introduced into mouse L cells by a variety of transfection...

Glyceraldehyde 3-phosphate dehydrogenase protein and mRNA are both differentially expressed in adult chickens but not chick embryos (1983)

Millner, Robert J, Brow, MaryAnn D., Cleveland, Don W., Shinick, Thomas M., Sutclffe, J.Gregor

We have determined the 679 nucleotide sequence of a cDNA clone which, by hybridization-translation experiments, corresponds to a 36K chick brain protein. Our studies provide a partial amino add...

Tubulin requires tau for growth onto microtubule initiating sites (1976)

Witman, George B., Cleveland, Don W., Weingarten, Murray D., Kirschner, Marc W.

Tubulin purified by phosphocellulose chromatography and free of accessory proteins will not form microtubules in the absence or presence of microtubule initiating sites (flagellar microtubules). The...

Caspase-1 and -3 are sequentially activated in motor neuron death in Cu,Zn superoxide dismutase-mediated familial amyotrophic lateral sclerosis

Pasinelli, Piera, Houseweart, Megan K., Brown, Robert H., Cleveland, Don W.

Familial amyotrophic lateral sclerosis-linked mutations in copper-zinc superoxide dismutase cause motor neuron death through one or more acquired toxic properties. An early event in the mechanism of...

Protective effect of neurofilament heavy gene overexpression in motor neuron disease induced by mutant superoxide dismutase

Couillard-Després, Sébastien, Zhu, Qinzhang, Wong, Philip C., Price, Donald L., Cleveland, Don W., Julien, Jean-Pierre

To investigate the role of neurofilaments in motor neuron disease caused by superoxide dismutase (SOD1) mutations, transgenic mice expressing a amyotrophic lateral sclerosis-linked SOD1 mutant...

Absence of neurofilaments reduces the selective vulnerability of motor neurons and slows disease caused by a familial amyotrophic lateral sclerosis-linked superoxide dismutase 1 mutant

Williamson, Toni L., Bruijn, Lucie I., Zhu, Qinzhang, Anderson, Karen L., Anderson, Scott D., Julien, Jean-Pierre, ...

Mutations in superoxide dismutase 1 (SOD1), the only proven cause of amyotrophic lateral sclerosis (ALS), provoke disease through an unidentified toxic property. Neurofilament aggregates are...

CENP-E is an essential kinetochore motor in maturing oocytes and is masked during Mos-dependent, cell cycle arrest at metaphase II

Duesbery, Nick S., Choi, Taesaeng, Brown, Kevin D., Wood, Kenneth W., Resau, James, Fukasawa, Kenji, ...

CENP-E, a kinesin-like protein that is known to associate with kinetochores during all phases of mitotic chromosome movement, is shown here to be a component of meiotic kinetochores as well. CENP-E...

Chaperone-facilitated copper binding is a property common to several classes of familial amyotrophic lateral sclerosis-linked superoxide dismutase mutants

Corson, Laura B., Strain, Jeffrey J., Culotta, Valeria C., Cleveland, Don W.

Mutations in Cu, Zn superoxide dismutase (SOD1) cause the neurodegenerative disease familial amyotrophic lateral sclerosis from an as-yet-unidentified toxic property(ies). Analysis in Saccharomyces...

Caspase-1 is activated in neural cells and tissue with amyotrophic lateral sclerosis-associated mutations in copper-zinc superoxide dismutase

Pasinelli, Piera, Borchelt, David R., Houseweart, Megan K., Cleveland, Don W., Brown, Robert H.

The mechanism by which mutations in the superoxide dismutase (SOD1) gene cause motor neuron degeneration in familial amyotrophic lateral sclerosis (ALS) is unknown. Recent reports that neuronal death...

Focal loss of the glutamate transporter EAAT2 in a transgenic rat model of SOD1 mutant-mediated amyotrophic lateral sclerosis (ALS)

Howland, David S., Liu, Jian, She, Yijin, Goad, Beth, Maragakis, Nicholas J., Kim, Benjamin, ...

Transgenic overexpression of Cu+2/Zn+2 superoxide dismutase 1 (SOD1) harboring an amyotrophic lateral sclerosis (ALS)-linked familial genetic mutation (SOD1G93A) in a Sprague–Dawley rat results in...

Unstable mutants in the peripheral endosomal membrane component ALS2 cause early-onset motor neuron disease

Yamanaka, Koji, Vande Velde, Christine, Eymard-Pierre, Eleonore, Bertini, Enrico, Boespflug-Tanguy, Odile, Cleveland, Don W.

Mutations in ALS2, carrying three putative guanine exchange factor (GEF) domains, are causative for a juvenile, autosomal recessive form of amyotrophic lateral sclerosis (ALS), primary lateral...

Lethality to human cancer cells through massive chromosome loss by inhibition of the mitotic checkpoint

Foltz, Daniel R., Cleveland, Don W.

A compromised mitotic checkpoint, the primary mechanism for ensuring that each new cell receives one copy of every chromosome, has been implicated as a contributor to carcinogenesis. However, a...

Altered axonal architecture by removal of the heavily phosphorylated neurofilament tail domains strongly slows superoxide dismutase 1 mutant-mediated ALS

Lobsiger, Christian S., Garcia, Michael L., Ward, Christopher M., Cleveland, Don W.

Eliminating assembled neurofilaments (NFs) from axons or misaccumulating NFs in motor neuron cell bodies strongly slows disease in mouse models of mutant superoxide dismutase 1 (SOD1)-induced...

Virus-Delivered Small RNA Silencing Sustains Strength in Amyotrophic Lateral Sclerosis

Miller, Timothy M., Kaspar, Brian K., Kops, Geert J., Yamanaka, Koji, Christian, Lindsey J., Gage, Fred H., ...

Mutations in superoxide dismutase cause a subset of familial amyotrophic lateral sclerosis and provoke progressive paralysis when expressed in mice. After retrograde transport to the spinal cord...

ZW10 links mitotic checkpoint signaling to the structural kinetochore

Kim, Yumi, Weaver, Beth A.A., Mao, Yinghui, McLeod, Ian, Yates, John R., ...

The mitotic checkpoint ensures that chromosomes are divided equally between daughter cells and is a primary mechanism preventing the chromosome instability often seen in aneuploid human tumors. ZW10...

Antisense oligonucleotide therapy for neurodegenerative disease

Smith, Richard A., Miller, Timothy M., Yamanaka, Koji, Monia, Brett P., Condon, Thomas P., Hung, Gene, ...

Neurotoxicity from accumulation of misfolded/mutant proteins is thought to drive pathogenesis in neurodegenerative diseases. Since decreasing levels of proteins responsible for such accumulations is...

Unstable microtubule capture at kinetochores depleted of the centromere-associated protein CENP-F

Bomont, Pascale, Maddox, Paul, Shah, Jagesh V, Desai, Arshad B, Cleveland, Don W

Centromere protein F (CENP-F) (or mitosin) accumulates to become an abundant nuclear protein in G2, assembles at kinetochores in late G2, remains kinetochore-bound until anaphase, and is degraded at...

Caspase-1 and -3 are sequentially activated in motor neuron death in Cu,Zn superoxide dismutase-mediated familial amyotrophic lateral sclerosis

Pasinelli, Piera, Houseweart, Megan K., Brown, Robert H., Cleveland, Don W.

Familial amyotrophic lateral sclerosis-linked mutations in copper-zinc superoxide dismutase cause motor neuron death through one or more acquired toxic properties. An early event in the mechanism of...

Protective effect of neurofilament heavy gene overexpression in motor neuron disease induced by mutant superoxide dismutase

Couillard-Després, Sébastien, Zhu, Qinzhang, Wong, Philip C., Price, Donald L., Cleveland, Don W., Julien, Jean-Pierre

To investigate the role of neurofilaments in motor neuron disease caused by superoxide dismutase (SOD1) mutations, transgenic mice expressing a amyotrophic lateral sclerosis-linked SOD1 mutant...

Absence of neurofilaments reduces the selective vulnerability of motor neurons and slows disease caused by a familial amyotrophic lateral sclerosis-linked superoxide dismutase 1 mutant

Williamson, Toni L., Bruijn, Lucie I., Zhu, Qinzhang, Anderson, Karen L., Anderson, Scott D., Julien, Jean-Pierre, ...

Mutations in superoxide dismutase 1 (SOD1), the only proven cause of amyotrophic lateral sclerosis (ALS), provoke disease through an unidentified toxic property. Neurofilament aggregates are...

CENP-E is an essential kinetochore motor in maturing oocytes and is masked during Mos-dependent, cell cycle arrest at metaphase II

Duesbery, Nick S., Choi, Taesaeng, Brown, Kevin D., Wood, Kenneth W., Resau, James, Fukasawa, Kenji, ...

CENP-E, a kinesin-like protein that is known to associate with kinetochores during all phases of mitotic chromosome movement, is shown here to be a component of meiotic kinetochores as well. CENP-E...

Chaperone-facilitated copper binding is a property common to several classes of familial amyotrophic lateral sclerosis-linked superoxide dismutase mutants

Corson, Laura B., Strain, Jeffrey J., Culotta, Valeria C., Cleveland, Don W.

Mutations in Cu, Zn superoxide dismutase (SOD1) cause the neurodegenerative disease familial amyotrophic lateral sclerosis from an as-yet-unidentified toxic property(ies). Analysis in Saccharomyces...

Caspase-1 is activated in neural cells and tissue with amyotrophic lateral sclerosis-associated mutations in copper-zinc superoxide dismutase

Pasinelli, Piera, Borchelt, David R., Houseweart, Megan K., Cleveland, Don W., Brown, Robert H.

The mechanism by which mutations in the superoxide dismutase (SOD1) gene cause motor neuron degeneration in familial amyotrophic lateral sclerosis (ALS) is unknown. Recent reports that neuronal death...

Focal loss of the glutamate transporter EAAT2 in a transgenic rat model of SOD1 mutant-mediated amyotrophic lateral sclerosis (ALS)

Howland, David S., Liu, Jian, She, Yijin, Goad, Beth, Maragakis, Nicholas J., Kim, Benjamin, ...

Transgenic overexpression of Cu+2/Zn+2 superoxide dismutase 1 (SOD1) harboring an amyotrophic lateral sclerosis (ALS)-linked familial genetic mutation (SOD1G93A) in a Sprague–Dawley rat results in...

Unstable mutants in the peripheral endosomal membrane component ALS2 cause early-onset motor neuron disease

Yamanaka, Koji, Vande Velde, Christine, Eymard-Pierre, Eleonore, Bertini, Enrico, Boespflug-Tanguy, Odile, Cleveland, Don W.

Mutations in ALS2, carrying three putative guanine exchange factor (GEF) domains, are causative for a juvenile, autosomal recessive form of amyotrophic lateral sclerosis (ALS), primary lateral...

Lethality to human cancer cells through massive chromosome loss by inhibition of the mitotic checkpoint

Foltz, Daniel R., Cleveland, Don W.

A compromised mitotic checkpoint, the primary mechanism for ensuring that each new cell receives one copy of every chromosome, has been implicated as a contributor to carcinogenesis. However, a...

Altered axonal architecture by removal of the heavily phosphorylated neurofilament tail domains strongly slows superoxide dismutase 1 mutant-mediated ALS

Lobsiger, Christian S., Garcia, Michael L., Ward, Christopher M., Cleveland, Don W.

Eliminating assembled neurofilaments (NFs) from axons or misaccumulating NFs in motor neuron cell bodies strongly slows disease in mouse models of mutant superoxide dismutase 1 (SOD1)-induced...

Unstable microtubule capture at kinetochores depleted of the centromere-associated protein CENP-F

Bomont, Pascale, Maddox, Paul, Shah, Jagesh V, Desai, Arshad B, Cleveland, Don W

Centromere protein F (CENP-F) (or mitosin) accumulates to become an abundant nuclear protein in G2, assembles at kinetochores in late G2, remains kinetochore-bound until anaphase, and is degraded at...

Antisense oligonucleotide therapy for neurodegenerative disease

Smith, Richard A., Miller, Timothy M., Yamanaka, Koji, Monia, Brett P., Condon, Thomas P., Hung, Gene, ...

Neurotoxicity from accumulation of misfolded/mutant proteins is thought to drive pathogenesis in neurodegenerative diseases. Since decreasing levels of proteins responsible for such accumulations is...

Gene transfer demonstrates that muscle is not a primary target for non-cell-autonomous toxicity in familial amyotrophic lateral sclerosis

Miller, Timothy M., Kim, Soo H., Yamanaka, Koji, Hester, Mark, Umapathi, Priya, Arnson, Hannah, ...

Amyotrophic lateral sclerosis (ALS) is a fatal, progressive paralysis arising from the premature death of motor neurons. An inherited form is caused by a dominant mutation in the ubiquitously...

In Vivo Quantitative Studies of Dynamic Intracellular Processes Using Fluorescence Correlation Spectroscopy

Wang, Zifu, Shah, Jagesh V., Berns, Michael W., Cleveland, Don W.

It has been a significant challenge to quantitatively study the dynamic intracellular processes in live cells. These studies are essential for a thorough understanding of the underlying mechanisms...

An epigenetic mark generated by the incorporation of CENP-A into centromeric nucleosomes

Black, Ben E., Brock, Melissa A., Bédard, Sabrina, Woods, Virgil L., Cleveland, Don W.

Mammalian centromeres are defined epigenetically. Although the physical nature of the epigenetic mark is unknown, nucleosomes in which CENP-A replaces histone H3 are at the foundation of centromeric...

Toxicity from different SOD1 mutants dysregulates the complement system and the neuronal regenerative response in ALS motor neurons

Lobsiger, Christian S., Boillée, Séverine, Cleveland, Don W.

Global, age-dependent changes in gene expression from rodent models of inherited ALS caused by dominant mutations in superoxide-dismutase 1 (SOD1) were identified by using gene arrays and RNAs...

Propagation of centromeric chromatin requires exit from mitosis

Jansen, Lars E.T., Black, Ben E., Foltz, Daniel R., Cleveland, Don W.

Centromeres direct chromosomal inheritance by nucleating assembly of the kinetochore, a large multiprotein complex required for microtubule attachment during mitosis. Centromere identity in humans is...

Common molecular signature in SOD1 for both sporadic and familial amyotrophic lateral sclerosis

Gruzman, Arie, Wood, William L., Alpert, Evgenia, Prasad, M. Dharma, Miller, Robert G., Rothstein, Jeffery D., ...

Amyotrophic lateral sclerosis (ALS) is a devastating motor neuron degenerative disease whose etiology and pathogenesis remain poorly understood. Most cases of ALS (≈90%) are sporadic (SALS),...

Revisiting oxidative damage in ALS: microglia, Nox, and mutant SOD1

Boillée, Séverine, Cleveland, Don W.

Mutation in superoxide dismutase–1 (SOD1) causes the inherited degenerative neurological disease familial amyotrophic lateral sclerosis (ALS), a non–cell-autonomous disease: mutant SOD1 synthesis...

ZW10 links mitotic checkpoint signaling to the structural kinetochore

Kim, Yumi, Weaver, Beth A.A., Mao, Yinghui, McLeod, Ian, Yates, John R., ...

The mitotic checkpoint ensures that chromosomes are divided equally between daughter cells and is a primary mechanism preventing the chromosome instability often seen in aneuploid human tumors. ZW10...

A standardized kinesin nomenclature

Lawrence, Carolyn J., Dawe, R. Kelly, Christie, Karen R., Cleveland, Don W., Dawson, Scott C., Endow, Sharyn A., ...

In recent years the kinesin superfamily has become so large that several different naming schemes have emerged, leading to confusion and miscommunication. Here, we set forth a standardized kinesin...

Microtubule capture by CENP-E silences BubR1-dependent mitotic checkpoint signaling

Mao, Yinghui, Desai, Arshad, Cleveland, Don W.

The mitotic checkpoint is the major cell cycle control mechanism for maintaining chromosome content in multicellular organisms. Prevention of premature onset of anaphase requires activation at...

Neurofilament-dependent Radial Growth of Motor Axons and Axonal Organization of Neurofilaments Does Not Require the Neurofilament Heavy Subunit (NF-H) or Its Phosphorylation

Rao, Mala V., Houseweart, Megan K., Williamson, Toni L., Crawford, Thomas O., Folmer, Janet, Cleveland, Don W.

Neurofilaments are essential for establishment and maintenance of axonal diameter of large myelinated axons, a property that determines the velocity of electrical signal conduction. One prominent...

The Microtubule-dependent Motor Centromere–associated Protein E (CENP-E) Is an Integral Component of Kinetochore Corona Fibers That Link Centromeres to Spindle Microtubules

Yao, Xuebiao, Anderson, Karen L., Cleveland, Don W.

Centromere-associated protein E (CENP-E) is a kinesin-related microtubule motor protein that is essential for chromosome congression during mitosis. Using immunoelectron microscopy, CENP-E is shown...

Abnormal neurofilament transport caused by targeted disruption of neuronal kinesin heavy chain KIF5A

Xia, Chun-Hong, Roberts, Elizabeth A., Her, Lu-Shiun, Liu, Xinran, Williams, David S., Cleveland, Don W., ...

To test the hypothesis that fast anterograde molecular motor proteins power the slow axonal transport of neurofilaments (NFs), we used homologous recombination to generate mice lacking the...

NF-M is an essential target for the myelin-directed “outside-in” signaling cascade that mediates radial axonal growth

Garcia, Michael L., Lobsiger, Christian S., Shah, Sameer B., Deerinck, Tom J., Crum, John, Young, Darren, ...

Neurofilaments are essential for acquisition of normal axonal calibers. Several lines of evidence have suggested that neurofilament-dependent structuring of axoplasm arises through an...

Centromere-associated protein-E is essential for the mammalian mitotic checkpoint to prevent aneuploidy due to single chromosome loss

Weaver, Beth A.A., Bonday, Zahid Q., Putkey, Frances R., Silk, Alain D., Cleveland, Don W.

Centromere-associated protein-E (CENP-E) is an essential mitotic kinesin that is required for efficient, stable microtubule capture at kinetochores. It also directly binds to BubR1, a...

Gene replacement in mice reveals that the heavily phosphorylated tail of neurofilament heavy subunit does not affect axonal caliber or the transit of cargoes in slow axonal transport

Rao, Mala V., Garcia, Michael L., Miyazaki, Yukio, Gotow, Takahiro, Yuan, Aidong, Mattina, Salvatore, ...

The COOH-terminal tail of mammalian neurofilament heavy subunit (NF-H), the largest neurofilament subunit, contains 44-51 lysine–serine–proline repeats that are nearly stoichiometrically...

Local Control of Neurofilament Accumulation during Radial Growth of Myelinating Axons in Vivo: Selective Role of Site-Specific Phosphorylation

Sánchez, Ivelisse, Hassinger, Linda, Sihag, Ram K., Cleveland, Don W., Mohan, Panaiyur, Nixon, Ralph A.

The accumulation of neurofilaments required for postnatal radial growth of myelinated axons is controlled regionally along axons by oligodendroglia. Developmentally regulated processes previously...

Formation of Spindle Poles by Dynein/Dynactin-Dependent Transport of Numa

Merdes, Andreas, Heald, Rebecca, Samejima, Kumiko, Earnshaw, William C., Cleveland, Don W.

NuMA is a large nuclear protein whose relocation to the spindle poles is required for bipolar mitotic spindle assembly. We show here that this process depends on directed NuMA transport toward...

CENP-meta, an Essential Kinetochore Kinesin Required for the Maintenance of Metaphase Chromosome Alignment in Drosophila

Yucel, Jennifer K., Marszalek, Janet D., McIntosh, J. Richard, Goldstein, Lawrence S.B., Cleveland, Don W., Philp, Alastair Valentine

CENP-meta has been identified as an essential, kinesin-like motor protein in Drosophila. The 257-kD CENP-meta protein is most similar to the vertebrate kinetochore-associated kinesin-like protein...

Selective association of misfolded ALS-linked mutant SOD1 with the cytoplasmic face of mitochondria

Vande Velde, Christine, Miller, Timothy M., Cashman, Neil R., Cleveland, Don W.

Mutations in copper/zinc superoxide dismutase (SOD1) are causative for dominantly inherited amyotrophic lateral sclerosis (ALS). Despite high variability in biochemical properties among the...

CENP-E combines a slow, processive motor and a flexible coiled coil to produce an essential motile kinetochore tether

Kim, Yumi, Heuser, John E., Waterman, Clare M., Cleveland, Don W.

The mitotic kinesin centromere protein E (CENP-E) is an essential kinetochore component that directly contributes to the capture and stabilization of spindle microtubules by kinetochores. Although...

Mutant SOD1 in cell types other than motor neurons and oligodendrocytes accelerates onset of disease in ALS mice

Yamanaka, Koji, Boillee, Severine, Roberts, Elizabeth A., Garcia, Michael L., McAlonis-Downes, Melissa, Mikse, Oliver R., ...

Dominant mutations in ubiquitously expressed superoxide dismutase (SOD1) cause familial ALS by provoking premature death of adult motor neurons. To test whether mutant damage to cell types beyond...

Mutant dynein (Loa) triggers proprioceptive axon loss that extends survival only in the SOD1 ALS model with highest motor neuron death

Ilieva, Hristelina S., Yamanaka, Koji, Malkmus, Shelle, Kakinohana, Osamu, Yaksh, Tony, Marsala, Martin, ...

Dominant mutations in cytoplasmic dynein (Loa or Cra) have been reported to provoke selective, age-dependent killing of motor neurons, while paradoxically slowing degeneration and death of motor...

Human Condensin Function Is Essential for Centromeric Chromatin Assembly and Proper Sister Kinetochore Orientation

Samoshkin, Alexander, Arnaoutov, Alexei, Jansen, Lars E. T., Ouspenski, Ilia, Dye, Louis, Karpova, Tatiana, ...

Condensins I and II in vertebrates are essential ATP-dependent complexes necessary for chromosome condensation in mitosis. Condensins depletion is known to perturb structure and function of...

Requirements for NuMA in maintenance and establishment of mammalian spindle poles

Silk, Alain D., Holland, Andrew J., Cleveland, Don W.

Microtubules of the mitotic spindle in mammalian somatic cells are focused at spindle poles, a process thought to include direct capture by astral microtubules of kinetochores and/or noncentrosomally...

Schwann cells expressing dismutase active mutant SOD1 unexpectedly slow disease progression in ALS mice

Lobsiger, Christian S., Boillee, Severine, McAlonis-Downes, Melissa, Khan, Amir M., Feltri, M. Laura, Yamanaka, Koji, ...

Neurodegeneration in an inherited form of ALS is non-cell-autonomous, with ALS-causing mutant SOD1 damage developed within multiple cell types. Selective inactivation within motor neurons of an...

Activated protein C therapy slows ALS-like disease in mice by transcriptionally inhibiting SOD1 in motor neurons and microglia cells

Zhong, Zhihui, Ilieva, Hristelina, Hallagan, Lee, Bell, Robert, Singh, Itender, Paquette, Nicole, ...

Activated protein C (APC) is a signaling protease with anticoagulant activity. Here, we have used mice expressing a mutation in superoxide dismutase-1 (SOD1) that is linked to amyotrophic lateral...