Guinea pig Nav1.7 ELISA kit
- Known as:
- Guinea pig Nav1.7 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- e05n0034
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Blue gene shanghai
- Gene target:
- Guinea pig Nav1.7 ELISA kit
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- Gain-of-function mutations in , encoding the voltage-dependent Nav1.7 sodium channel, cause three autosomal-dominant disorders associated with severe pain: primary erythromelalgia, paroxysmal extreme pain disorder (PEPD), and small fiber neuropathy. On the other hand, biallelic loss-of-function mutations have been linked to impaired pain perception. Notably, the coexistence of both hyperalgesia and hypoalgesia within the same patient harboring the I234T variant has been reported in three independent patients to date. We report a 7-year-old girl harboring co-occurring (I234T) and variants who presented with paroxysmal extreme pain disorder, contradictory analgesia, sensitivity to heat, and intractable head-drop attacks. Based on the genetic and clinical analyses, she was diagnosed as having PEPD and -related paroxysmal dyskinesia. The intractable head-drop attacks were considered as paroxysmal non-kinesigenic dyskinesia. In addition, she exhibited easy fatigability and hypotonia. Taken together with her cold, cyanotic feet, these findings suggest that she may have also had small fiber neuropathy. - Source: PubMed
Publication date: 2026/06/22
Ikeda MikiKawashima AritomoKodama KaoriSato RyoUneoka SakiKatata YuOkubo YukimuneEndo WakabaInui TakehikoTogashi NorikoMizuno ChikaYaoita HisaoSaijo NaoyaTakayama JunTamiya GenKikuchi AtsuoKure ShigeoHaginoya Kazuhiro - Hypertension has been associated with altered nociceptive thresholds in humans and animal models, but the relationship between blood pressure (BP) and pain sensitivity remains inconsistent. Here, we investigated trigeminal nociception in male spontaneously hypertensive rats (SHRs) compared with normotensive Wistar-Kyoto (WKY) rats using operant facial pain assays, trigeminal ganglion (TG) electrophysiology, and bulk RNA sequencing with cell-type deconvolution. SHRs exhibited reduced thermal and mechanical facial pain sensitivity relative to WKY controls; however, measured systolic BP did not robustly explain the strain difference in thermal pain behavior. Whole-cell recordings of TG neurons revealed increased hyperpolarization-activated cyclic nucleotide-gated (HCN)-mediated currents and voltage-gated potassium currents in SHRs, while voltage-gated sodium currents were unchanged despite reduced expression of Scn8a, Scn9a, and Scn10a. Transcriptomic analysis further demonstrated broad downregulation of ion channel and sensory transduction genes in SHRs, including Hcn1, Hcn4, Kcnq3, Kcnq4, Piezo2, and Trpm8. Cell-type deconvolution revealed strain-dependent shifts in TG composition, including alterations in sensory neurons and non-neuronal populations such as immune cells, satellite glia, endothelial cells, pericytes, and Schwann cells. Together, these findings show that reduced trigeminal nociception in SHRs is associated with changes in TG ion channel function, sensory gene programs, and cell-type composition, while not being robustly explained by measured systolic BP. PERSPECTIVE: This study shows that reduced trigeminal pain in SHRs is associated with changes in ion channel function, gene expression, and TG cell-type composition, while not being robustly explained by measured systolic BP. - Source: PubMed
Publication date: 2026/06/20
Donertas-Ayaz BasakMurphy Niall PVivanco-Estela Airam NSapio Matthew RDe Paula Bruna BalbinoGuo SenMalphurs WendiSong QianqianNeubert John KCaudle Robert M - Polymorphisms in voltage-gated sodium channel (SCN) genes have been implicated in oxaliplatin-induced peripheral neuropathy (OXAIPN). However, their association with chronic OXAIPN in Japanese patients remains unclear. This study investigated the association between SCN gene polymorphisms and patient-reported chronic OXAIPN outcomes in Japanese patients with colorectal cancer. - Source: PubMed
Publication date: 2026/06/19
Matsuura MasatoNagamine AyumuMasuno TakashiTabei AkiraNasaka TerukoNishiba HiromiKoike MahoTakahashi YutaObayashi Kyoko - Antiepileptic drugs (AEDs) were frequently employed in glioma patients, especially those with low-grade glioma (LGG), in which epilepsy manifested in roughly 70-90% of cases. It has been reported that some AEDs can improve the survival of glioma patients. However, the molecular mechanisms of AEDs through which affect LGG prognosis remained unclear. Therefore, this study integrated 105 targets of 10 AEDs, by using machine learning, molecular docking, a retrospective clinical cohort, and in vitro experiments to clarify the biological mechanisms through which AEDs affect LGG prognosis. Our study established a reliable 13-gene AEDs-related LGG prognostic model. Carbamazepine, Oxcarbazepine and Lacosamide were supposed to improve the OS by inhibiting the hazard factor SCN9A. Phenobarbital was supposed to restrict the OS by inhibiting the identified protectors GRIN2C and GRIN3A. Molecular docking visualized the strong affinities between the above drugs and targets. Retrospective cohort further verified our speculation about the effect of the above drugs on the prognosis of LGG. In vitro experiments demonstrated that inhibiting SCN9A, a common targets for most AEDs, could suppress LGG cells malignant behaviors; while the suppression of GRIN2C and GRIN3A enhanced the malignant behaviors of LGG cells. This study provided guidance for individualized AEDs selection for LGG patients, and provide new insights into the potential biological functions and molecular mechanisms of AEDs affecting LGG. - Source: PubMed
Publication date: 2026/06/15
Zhou MingHuang QinhongLiang HuiYang HanjieLi Min - Mutations in the SCN9A gene, which encodes the sodium voltage-gated channel alpha subunit 9 on chromosome 2 (Nav1.7), are extremely rare and play a crucial role in pain signaling. Depending on the type of mutation, the clinical presentation of these mutations can vary widely from hyperactive pain phenotypes such as primary erythromelalgia to hypoactive pain phenotypes manifesting as congenital insensitivity to pain. Despite multiple descriptions in the literature of pain-associated behaviors in sodium voltage-gated channelopathies, there are no perioperative guidelines in this patient population that can be used to manage pain-associated procedures. Incorporating reported insights from pain literature into an anesthetic plan may improve perioperative patient satisfaction and outcomes. We present a case of a patient with a novel SCN9A mutation (c.3019C>T) who underwent a common surgical procedure and suffered atypical complications. We propose that her SCN9A mutation may have contributed to these sequelae and recommend a greater familiarity with sodium channelopathies-especially those attributed to the SCN9A gene-to improve perioperative management. - Source: PubMed
Publication date: 2026/06/12
Wadle MichaelSzafarowicz BiancaNykiel-Bailey SydneyTan BrandonAuBuchon JacobNjoku Dolores