mProX™ Human FOLR1 Stable Cell Line

Bariş, Savaş, Serkan Kırık, and Özgür Balasar. "Importance of targeted next-generation sequencing in pediatric patients with developmental epileptic encephalopathy." Revista da Associação Médica Brasileira 69 (2023): e20230547.
Childhood epilepsy is a frequently seen neurological condition, affecting approximately 300-600 individuals per 100,000. It has been linked to difficult-to-treat manifestations of epilepsy, as well as global developmental delay and epileptic encephalopathies. These factors contribute to the development of epileptic syndromes that exhibit cognitive and behavioral impairments.
Bariş, Savaş, Serkan Kırık, and Özgür Balasar. "Importance of targeted next-generation sequencing in pediatric patients with developmental epileptic encephalopathy." Revista da Associação Médica Brasileira 69 (2023): e20230547.
Pubmed: 37820178   DOI: 10.1590/1806-9282.20230547

N Westlund, Karin. et al. "Epigenetic HDAC5 Inhibitor Reverses Craniofacial Neuropathic Pain in Mice." The journal of pain, 2023.
The identification and resolution of molecular complexities involved in chronic neuropathic pain is a significant challenge. The best studied classes of histone deacetylases (HDAC), specifically Class I (HDAC 1-3) and Class III (sirtuins), have been found to play a role in experimental pain models. Inhibition of these classes before pain model induction has been shown to prevent the development of pain-related behaviors. In this study, the less well-studied Class IIa HDAC4/5 selective inhibitor LMK235 was used post-treatment in week 3 to decrease the levels of HDAC5 RNA and protein in the trigeminal ganglia (TG) in two chronic orofacial neuropathic pain models. This resulted in levels similar to those found in naïve mice at week 10 post-model induction. Unlike in lower limb inflammatory pain models, HDAC4 RNA was not found in the trigeminal models. Treatment with LMK235 also restored many other gene alterations in the TG to naïve levels at week 10. Key pain-related upregulated genes, such as Hoxc8,b9,d8; Slc6a4, P2rx4, Cckbr, growth hormone (Gh), and schlafen (Slfn4), were significantly reduced with LMK235 treatment. Additionally, LMK235 doubled the fold increase in axon regeneration/repair genes, Sostdc1, TTr, and Folr1, after injury. Furthermore, LMK235 reduced the excitability of TG neurons in culture isolated from nerve-injured mice, while having no effect on neurons from naïve mice. Electrophysiological experiments showed that under LMK235-treated conditions, around 20% of recorded small neurons were high threshold, whereas none under control conditions had high thresholds. Treatment with LMK235 also reversed long-standing mechanical and cold hypersensitivity in both male and female models of chronic trigeminal neuropathic pain at a dosage of 5-10 mg/kg, and prevented the development of anxiety- and depression-like behaviors. These findings suggest that HDAC5 is a crucial epigenetic factor in the persistence of chronic trigeminal neuropathic pain, and are supported by the study of RNA alterations, TG neuronal excitability, and pain-related behaviors. Treatment with HDAC5 inhibitor in week 3 restored RNA balance at 10 weeks, while upregulation of response to wound healing
N Westlund, Karin. et al. "Epigenetic HDAC5 Inhibitor Reverses Craniofacial Neuropathic Pain in Mice." The journal of pain, 2023.
Pubmed: 37777035   DOI: 10.1016/j.jpain.2023.09.015