Epigenetic modifications associated to diabetic peripheral neuropathic pain (Review) DOI Creative Commons
Tianle Gao,

Jingya Luo,

Jie Fan

et al.

Molecular Medicine Reports, Journal Year: 2024, Volume and Issue: 31(1)

Published: Nov. 13, 2024

The present review aimed to provide an update on the scientific progress of role epigenetic modifications diabetic peripheral neuropathic pain (DPNP). DPNP is a devastating and troublesome complication diabetes mellitus (DM), which affects one third patients with DM causes severe hyperalgesia allodynia, leading challenges in treatment these patients. pathophysiology multifactorial not yet fully understood options for this disease are currently unsatisfactory. underlying mechanisms have largely been explored animal models mechanism‑derived approach might offer potential therapeutic‑target attenuating certain phenotypes DPNP. Altered gene expression levels within or central nervous systems (CNS) crucial mechanism DPNP, however, transcriptional genes elucidated. Epigenetic modifications, such as DNA methylation histone (methylation, acetylation, phosphorylation), can alter via chromatin remodeling. Moreover, it has reported that altering CNS, contributes changes both sensitivity pharmacological efficacy Therefore, summarized findings relevant literature alterations therapeutic targeting future disease.

Language: Английский

Understanding GEMIN5 Interactions: From Structural and Functional Insights to Selective Translation DOI Creative Commons
Encarnación Martı́nez-Salas, Salvador Abellan, Rosario Francisco‐Velilla

et al.

Wiley Interdisciplinary Reviews - RNA, Journal Year: 2025, Volume and Issue: 16(2)

Published: March 1, 2025

ABSTRACT GEMIN5 is a predominantly cytoplasmic protein, initially identified as member of the survival motor neurons (SMN) complex. In addition, this abundant protein modulates diverse aspects RNA‐dependent processes, executing its functions through formation multi‐component complexes. The modular organization structural domains present in enables to perform various interaction with distinct partners. responsible for recognition small nuclear (sn)RNAs N‐terminal region, and therefore snRNP assembly. Beyond role spliceosome assembly, regulates translation either RNAs or proteins. central robust dimerization domain acts hub protein–protein interaction, while non‐canonical RNA‐binding site located towards C‐terminus. Interestingly, partitioning mRNAs into polysomes, likely due capacity ability bind native ribosomes. Understanding functional has brought an increasing interest last years important implications human disease. Patients carrying biallelic variants suffer from neurodevelopmental delay, hypotonia, cerebellar ataxia. This review discusses recent relevant works aimed at understanding molecular mechanisms activity gene expression, also challenges discover new functions.

Language: Английский

Citations

0
Ribosome profiling reveals that post-transcriptional control of Nalf1 by heterogeneous nuclear ribonucleoprotein L is required for paclitaxel-induced neuropathic pain DOI
June Bryan de la Peña, Guadalupe García, Zachary T. Campbell

et al.

Pain, Journal Year: 2025, Volume and Issue: unknown

Published: April 2, 2025

Abstract Sensory neurons are integral to the genesis and maintenance of neuropathic pain. The molecular mechanisms that mediate long-lived changes in their excitability unclear. Here, we leverage functional genomics approaches survey RNA abundance translation dorsal root ganglion from a mouse model paclitaxel-induced We focus specifically on females as paclitaxel is first-line therapy for breast cancer. sequencing data indicate substantially more occur at level (n = 404) than transcription decay 109). discovered core subunit sodium leak channel (NALCN) channel, auxiliary factor 1 (NALF1), preferentially translated response paclitaxel. This effect mediated by RNA-binding protein heterogeneous nuclear ribonucleoprotein L (HNRNP L). Heterogeneous binds 14 base CA-rich element (CARE) Nalf1 3′ untranslated region (3′UTR). Genetic elimination either HNRNP L, CARE motif, or pore-forming nonselective NALCN diminishes pain amplification vivo. Collectively, these results illustrate an situated 3′UTR required female mice.

Language: Английский

Citations

0
The RNA-binding protein CELF4 is a negative regulator of sensory neuron excitability and mechanical and heat behavioral sensitivity DOI Creative Commons

Madison Mueth,

Peter Neufeld,

Merilla Michael

et al.

Neurobiology of Pain, Journal Year: 2025, Volume and Issue: unknown, P. 100184 - 100184

Published: May 1, 2025

Language: Английский

Citations

0
Epigenetic modifications associated to diabetic peripheral neuropathic pain (Review) DOI Creative Commons
Tianle Gao,

Jingya Luo,

Jie Fan

et al.

Molecular Medicine Reports, Journal Year: 2024, Volume and Issue: 31(1)

Published: Nov. 13, 2024

The present review aimed to provide an update on the scientific progress of role epigenetic modifications diabetic peripheral neuropathic pain (DPNP). DPNP is a devastating and troublesome complication diabetes mellitus (DM), which affects one third patients with DM causes severe hyperalgesia allodynia, leading challenges in treatment these patients. pathophysiology multifactorial not yet fully understood options for this disease are currently unsatisfactory. underlying mechanisms have largely been explored animal models mechanism‑derived approach might offer potential therapeutic‑target attenuating certain phenotypes DPNP. Altered gene expression levels within or central nervous systems (CNS) crucial mechanism DPNP, however, transcriptional genes elucidated. Epigenetic modifications, such as DNA methylation histone (methylation, acetylation, phosphorylation), can alter via chromatin remodeling. Moreover, it has reported that altering CNS, contributes changes both sensitivity pharmacological efficacy Therefore, summarized findings relevant literature alterations therapeutic targeting future disease.

Language: Английский

Citations

1