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Articles by Peter Baas
Microtubules in Spinal Cord Injury: From Cytoskeletal Dysregulation to Therapeutic Regeneration
+TIPs plus-end tracking proteins APC adenomatous polyposis coli CCK cholecystokinin CDK5 cyclin-dependent kinase 5 CNS central nervous system CRMP collapsin response mediator protein CSF cerebrospinal fluid CTE chronic traumatic encephalopathy DMAPT dimethylamino-parthenolide DRG dorsal root ganglion EB end-binding proteins EpoB epithilone B EpoD epithilone D FL2 fidgetin-like-2 GSK3β glycogen synthase kinase 3 beta HSP hereditary spastic paraplegia MAPs microtubule-associated proteins MTs...
SPG4 Hereditary Spastic Paraplegia: From Etiology to Therapy
Hereditary spastic paraplegias (HSPs) are rare diseases in which degeneration of the corticospinal nerve tracts leads to lower limb spasticity and gait deficiencies.1 Depending on the gene mutated and even within a family with the identical gene mutation, symptoms can vary a great deal in their severity, age of onset, and the degree to which other nerve tracts degenerate in addition to the corticospinal tracts.
Antagonistic Roles of Tau and MAP6 in Regulating Neuronal Development
Abstract Association of tau with microtubules causes them to be labile while association of MAP6 with microtubules causes them to be stable. As axons differentiate and grow long, tau and MAP6 segregate from one another on individual microtubules, resulting in the formation of stable and labile domains.
Reevaluating tau reduction as a therapeutic approach for tauopathies: Insights and perspectives
REFERENCES , , & (2016). Tau and tauopathies. Brain Research Bulletin, 126(Pt 3), 238–292. https://doi.org/10.1016/j.brainresbull.2016.08.018 , & (2019). Tau: It's not what you think. Trends in Cell Biology, 29(6), 452–461. https://doi.org/10.1016/j.tcb.2019.02.007 , , , & (2016). Stability properties of neuronal microtubules. Cytoskeleton (Hoboken), 73(9), 442–460. https://doi.org/10.1002/cm.21286 , , , , , , , , & (2019).
Is Gulf War Illness a prolonged early phase tauopathy?
REFERENCES , , , , , , , , & (2017). Screening for novel central nervous system biomarkers in veterans with Gulf War Illness. Neurotoxicology and Teratology, 61, 36–46. https://doi.org/10.1016/j.ntt.2017.03.002 , , , , , , , , , , , & (2020). Using plasma autoantibodies of central nervous system proteins to distinguish veterans with Gulf War Illness from healthy and symptomatic controls. Brain Sciences, 10(610), 1–15. https://doi.org/10.3390/brainsci10090610 , & (2013).
A half‐century of tau
From its original trademark as an esoteric factor that stimulates tubulin polymerization into microtubules (MTs; Weingarten et al., 1975), a nevertheless classic finding in the annals of cytoskeleton history, tau eventually gained notoriety as a protein whose malfunctioning contributes to a multitude of neurodegenerative diseases.
How neurons maintain their axons long-term: an integrated view of axon biology and pathology
The need for an integrated view of axonal cell biology Axons are the cellular processes of neurons which form the biological cables that wire nervous systems through processes of signal propagation and synaptic transmission. In humans, axons can be as short as tens of micrometres and as long as 2 m, with diameters ranging from ~0.3 to ~15 μm depending on axon type (Prokop, 2020).
KIFC1 Regulates the Trajectory of Neuronal Migration
KIFC1 is indispensable for directional rotation of the nucleus Given that both INM and neuronal migration require directional rotation of the nucleus, we wondered whether KIFC1 might also play a role in this process during neuronal migration. To explore this, we transfected the KIFC1-depleted neurons in vitro with fluorescently tagged HP1β, a nuclear histone protein classically used to trace nucleokinesis behavior.
KIFC1 regulates the trajectory of neuronal migration
Research Articles, Cellular/Molecular Hemalatha Muralidharan, Shrobona Guha, Kiran Madugula, Ankita Patil, Sarah A. Bennison, Xiaohuan Sun, Kazuhito Toyo-oka and Peter W.
Chronic neuronal activation increases dynamic microtubules to enhance functional axon regeneration after dorsal root crush injury
Abstract After a dorsal root crush injury, centrally-projecting sensory axons fail to regenerate across the dorsal root entry zone (DREZ) to extend into the spinal cord. We find that chemogenetic activation of adult dorsal root ganglion (DRG) neurons improves axon growth on an in vitro model of the inhibitory environment after injury.
Mitotic Motor KIFC1 Is an Organizer of Microtubules in the Axon
Research Articles, Cellular/Molecular Hemalatha Muralidharan and Peter W. Baas Journal of Neuroscience 15 May 2019, 39 (20) 3792-3811; DOI: https://doi.org/10.1523/JNEUROSCI.3099-18.2019 Abstract KIFC1 (also called HSET or kinesin-14a) is best known as a multifunctional motor protein essential for mitosis. The present studies are the first to explore KIFC1 in terminally postmitotic neurons.
Tau: It’s Not What You Think
Highlights Tau is concentrated on the labile domain of the axonal microtubule, not the stable domain, which is contrary to the expectation of tau dogma. Contrary to tau dogma, when tau is depleted from neurons, the stable domain is no less stable, but the labile domain becomes shorter and more stable.
Study shows how neurons reach their final destinations
As the human brain develops, neurons leave their birthplace and take a trip to distant locations. Once they reach their final destination, the neurons then send out axons and dendrites -- the branches that receive and send messages from other cells. Humans' most basic functions depend on this journey of neurons getting to where they need to go, and making correct connections once they arrive. This ensures that our eyes can see, our ears can hear, our fingers can touch and so on.
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