Nikiben Patel

ORCID: 0000-0002-0129-7622
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About
Contact & Profiles
Research Areas
  • Nerve injury and regeneration
  • Histone Deacetylase Inhibitors Research
  • Neurogenesis and neuroplasticity mechanisms
  • Signaling Pathways in Disease
  • Peripheral Neuropathies and Disorders
  • Neurogenetic and Muscular Disorders Research
  • Autism Spectrum Disorder Research
  • Amyotrophic Lateral Sclerosis Research
  • Conducting polymers and applications
  • Hereditary Neurological Disorders
  • Toxin Mechanisms and Immunotoxins

Instituto de Neurociencias
2020-2024

Instituto de investigación sanitaria y biomédica de Alicante
2021-2022

Consejo Superior de Investigaciones Científicas
2022

Hospital General Universitario de Alicante Doctor Balmis
2020

Fundación para el Fomento de la Investigación Sanitaria y Biomédica de la Comunitat Valenciana
2020

Hospital Marina Baixa
2020

Hospital Clínica Benidorm
2020

The class IIa histone deacetylases (HDACs) have pivotal roles in the development of different tissues. Of this family, Schwann cells express Hdac4, 5, and 7 but not Hdac9. Here, we show that a transcription factor regulated genetic compensatory mechanism within family proteins, blocks negative regulators myelination ensuring peripheral nerve developmental remyelination after injury. Thus, when Hdac4 5 are knocked-out from mice, JUN-dependent induces overexpression Hdac7 permitting, although...

10.7554/elife.72917 article EN cc-by eLife 2022-01-25

Abstract Amyotrophic lateral sclerosis is a devastating neurodegenerative disease characterized by motor neuron death and distal axonopathy. Despite its clinical severity profound impact in the patients their families, many questions about pathogenesis remain still unclear, including role of Schwann cells axon‐glial signaling progression. Upon axonal injury, upregulation JUN transcription factor promotes cell reprogramming into repair phenotype that favors axon regrowth neuronal survival. To...

10.1002/glia.24604 article EN cc-by-nc-nd Glia 2024-08-16

To identify novel genetic mechanisms causing Charcot-Marie-Tooth (CMT) disease.We performed a next-generation sequencing study of 34 genes associated with CMT in patient peripheral neuropathy.We found non-previously described mutation EGR2 (p.P397H). P397H is located within the loop that connects zinc fingers 2 and 3, pivotal domain for activity this transcription factor. Using promoter luciferase assays, we promotes decreased transcriptional EGR2. In patient, also previously nonpathogenic...

10.1212/nxg.0000000000000407 article EN cc-by-nc-nd Neurology Genetics 2020-03-04

ABSTRACT The class IIa histone-deacetylases (HDACs) have pivotal roles in the development of different tissues. Of this family, Schwann cells express HDAC4, 5 and 7 but not HDCA9. Here we show that a transcription factor regulated genetic compensatory mechanism within family proteins, blocks negative regulators myelination ensuring peripheral nerve developmental remyelination after injury. Thus, when HDAC4 are knocked-out from cells, c-Jun dependent induces overexpression HDAC7 permitting,...

10.1101/2021.09.20.461026 preprint EN cc-by bioRxiv (Cold Spring Harbor Laboratory) 2021-09-21
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