Your competent? doctor created dendritic branching and axon pathfinding and regeneration protocols years ago, right? Oh, your incompetent doctor hasn't even started creating protocols! WOW!
axon pathfinding (42 posts to March 2012)
dendritic branching (42 posts to February 2012)
Send me hate mail on this: oc1dean@gmail.com. I'll print your complete statement with your name and my response in my blog. Or are you afraid to engage with my stroke-addled mind? No excuses are allowed! You're medically trained; it should be simple to precisely state EXACTLY WHY you haven't created those protocols in the last decade with NO EXCUSES! Your definition of competence in stroke is obviously much lower than stroke survivors' definition of your competence! Swearing at me is allowed, I'll return the favor. Don't even attempt to use the excuse that brain research is hard.
Axonal Regeneration, Growth Cone, and the FIGN Gene Family: A Comprehensive Review
- PMID: 41220267
- DOI: 10.2174/011570159X437847251023113715
Abstract
Mature mammalian central nervous system (CNS) neurons exhibit limited regenerative capacity, resulting in severe and often irreversible functional deficits following injuries such as spinal cord injury or stroke. Both inhibitory extrinsic environments and intrinsic neuronal constraints govern this regenerative failure. Growth cones-cytoskeleton-rich structures at axonal tips-are critical for axon extension and pathfinding during neural repair, with their structural integrity and motility heavily dependent on microtubule (MT) stability and dynamics. Pharmacological stabilization of MTs has been shown to prevent growth cone collapse and support regeneration, highlighting MTs as a promising therapeutic target. The FIGN gene family-FIGN, FIGNL1, and FIGNL2-encodes microtubule-severing enzymes (MSEs) that regulate MT remodeling, thereby directing axonal growth and regeneration. FIGN and FIGNL2 act as key negative regulators: FIGN destabilizes dynamic tyrosinated MTs, whereas FIGNL2 selectively severs stable acetylated MTs, both leading to excessive microtubule fragmentation, growth cone collapse, and impaired regeneration. Inhibition of FIGN or FIGNL2, particularly via siRNA-mediated knockdown, enhances MT integrity, promotes robust axonal regrowth, and improves functional recovery in preclinical models. In contrast, FIGNL1 modulates MT dynamics in a context-dependent manner, primarily contributing to developmental neurite outgrowth. These proteins intersect with critical signaling pathways, including RhoA/ROCK and PI3K/Akt, linking cytoskeletal regulation to regenerative signaling. Targeting FIGN or FIGNL2 represents a promising neuropharmacological strategy to overcome intrinsic barriers to CNS repair. This review elucidates the regulatory mechanisms and functional roles of the FIGN gene family in neural regeneration and proposes novel therapeutic approaches for CNS injury and neurodegenerative diseases.
Keywords: Axonal regeneration; FIGN gene family; cytoskeleton.; gene therapy; microtubule stability.
Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.
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