A5065624513- Nerve injury and regeneration
- Neurogenesis and neuroplasticity mechanisms
- Axon Guidance and Neuronal Signaling
- Retinal Development and Disorders
- Spinal Cord Injury Research
- Neuroinflammation and Neurodegeneration Mechanisms
- Signaling Pathways in Disease
- Neuroscience and Neuropharmacology Research
- Zebrafish Biomedical Research Applications
- DNA Repair Mechanisms
- Neural dynamics and brain function
- CRISPR and Genetic Engineering
- Neuroscience and Neural Engineering
- Photoreceptor and optogenetics research
- Neuroscience of respiration and sleep
- Receptor Mechanisms and Signaling
- PI3K/AKT/mTOR signaling in cancer
- Virus-based gene therapy research
- Sirtuins and Resveratrol in Medicine
- Mitochondrial Function and Pathology
- Autophagy in Disease and Therapy
- Neuropeptides and Animal Physiology
- Hippo pathway signaling and YAP/TAZ
- RNA Interference and Gene Delivery
- Pain Mechanisms and Treatments
Boston Children's Hospital
2016-2025
Harvard University
2016-2025
Boston Children's Museum
2010-2024
University of Massachusetts Amherst
2024
Binghamton University
2024
Zhejiang University
2023
Boston University
2006-2022
Harvard University Press
2005-2019
National Institute of Neurological Disorders and Stroke
2014
Imaging Center
2012
The failure of axons to regenerate is a major obstacle for functional recovery after central nervous system (CNS) injury. Removing extracellular inhibitory molecules results in limited axon regeneration vivo. To test the role intrinsic impediments regrowth, we analyzed cell growth control genes using virus-assisted vivo conditional knockout approach. Deletion PTEN (phosphatase and tensin homolog), negative regulator mammalian target rapamycin (mTOR) pathway, adult retinal ganglion cells...
Nerve growth is regulated by attractive and repulsive factors in the nervous system. Microscopic gradients of Collapsin-1/Semaphorin III/D (Sema III) myelin-associated glycoprotein trigger turning responses cones cultured Xenopus spinal neurons; repulsion can be converted to attraction pharmacological activation guanosine 3′,5′-monophosphate (cGMP) adenosine signaling pathways, respectively. Sema III also causes collapse rat sensory cones, which inhibited cGMP pathway. Thus cyclic...
Chondroitin sulfate proteoglycans (CSPGs) present a barrier to axon regeneration. However, no specific receptor for the inhibitory effect of CSPGs has been identified. We showed that transmembrane protein tyrosine phosphatase, PTPsigma, binds with high affinity neural CSPGs. Binding involves chondroitin chains and site on first immunoglobulin-like domain PTPsigma. In culture, PTPsigma(-/-) neurons show reduced inhibition by CSPG. A PTPsigma fusion probe can detect cognate ligands are...
Inhibitory molecules associated with myelin and the glial scar limit axon regeneration in adult central nervous system (CNS), but underlying signaling mechanisms of inhibition are not fully understood. Here, we show that suppressing kinase function epidermal growth factor receptor (EGFR) blocks activities both inhibitors chondroitin sulfate proteoglycans inhibiting neurite outgrowth. In addition, trigger phosphorylation EGFR a calcium-dependent manner. Local administration promotes...