HDL2 + HDL3 Precipitation Reagent
- Known as:
- HDL2 + HDL3 Precipitation Reagent
- Catalog number:
- 85R-106
- Product Quantity:
- 50 ml
- Category:
- -
- Supplier:
- Fitzgerald
- Gene target:
- HDL2 + HDL3 Precipitation Reagent
Related genes to: HDL2 + HDL3 Precipitation Reagent
- Gene:
- JPH3 NIH gene
- Name:
- junctophilin 3
- Previous symbol:
- TNRC22
- Synonyms:
- JP-3, CAGL237, HDL2, JP3
- Chromosome:
- 16q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 2000-12-08
- Date modifiied:
- 2016-10-05
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- Therapeutic resistance is a major cause of treatment failure in glioblastoma (GBM), highlighting the need for physiologically relevant models to identify actionable resistance mechanisms. While two-dimensional (2D) cultures are widely used for target discovery, they poorly represent the tumor microenvironment. In contrast, three-dimensional (3D) spheroid cultures better recapitulate spatial heterogeneity, hypoxic gradients, and stress-adaptive signaling observed in tumors. - Source: PubMed
Khotchawan WannawatRuengket PakornKheolamai PakpoomSathornsumetee SithSinthuvanich ChomdaoLorthongpanich ChanchaoIssaragrisil Surapol - Chorea can arise from genetic, metabolic, pharmacologic, and autoimmune causes. In clinical practice, however, non-genetic causes are rare. The most common genetic cause is a CAG repeat expansion in HTT, leading to Huntington's disease (HD). Beyond HD, systematic studies have been lacking and many individuals with non-HD chorea remain without a molecular diagnosis. We conducted whole-exome and genome sequencing analysis on 190 non-HD chorea cases, leveraging data from the All of Us Research Program (n = 134), UK Biobank (n = 26), and a clinically ascertained multicenter Spanish cohort recruited by the Spanish Study Group for Genetics of Chorea (SSGGC) (n = 30). Variant calling was performed without pre-filtering based on a disease or gene list, and variants were clinically contextualized using OMIM, ClinVar, and in silico predictions. We identified thirteen protein-altering variants, including six previously described as pathogenic or likely pathogenic. Notably, we identified a pathogenic JPH3 expansion in a patient of Black race and c9orf72 expansions in individuals of European and South Asian ancestry. These findings explained 23% of cases in the SSGGC, 12% in UK Biobank, and 4% in All of Us. Our results broaden the genetic architecture of non-HD chorea and highlight the value of multi-ancestry genomic approaches for rare movement disorders. - Source: PubMed
Publication date: 2026/04/09
Akçimen FulyaDiez-Fairen MonicaAlvarez IgnacioPuente VictorGrant SpencerHernandez-Vara JorgeKhani MarziehBuongiorno MariateresaJiménez-Jiménez Félix JavierAgúndez José A GAguilar MiquelCubo EstherPerez JesusPagonabarraga JavierCaballol NúriaAvila AsuncionDing JinhuiGarcía-Martín ElenaAlonso-Navarro HortensiaCompta YaroslauCruchaga CarlosBeyer KatrinGibbs J RaphaelSingleton AndrewBandres-Ciga SaraPastor Pau - Junctophilin 3 (JPH3) acts as a tumor suppressor in several cancers; however, the role of JPH3 in anaplastic thyroid cancer (ATC) is still unknown. - Source: PubMed
Wang XiuyanLuan ShaSun LeiLian LixinQi Ming - - Source: PubMed
Publication date: 2026/01/23
Boone Dayany LeonelSoares Maria CarolinaSilva Carolina Candeias daVeiga Beatriz Azevedo Dos Anjos GodkeTumas VitorSilva Thiago Yoshinaga TonholoPedroso José LuizPinto Roberta Arb Saba RodriguesBorges VanderciFerraz Henrique Ballalai - We previously identified a set of genes with hypermethylated promoter regions that expressed reduced levels of mRNAs by next-generation sequencing in the hippocampal dentate gyrus (DG) of weaned rats [postnatal day (PND) 21] after maternal exposure to valproic acid, propylthiouracil (PTU), or glycidol, compounds that induce persistent disruption of hippocampal neurogenesis until adulthood at PND 77. The current study was performed to identify immunohistochemically available epigenetic markers of developmental neurotoxicity, focusing on neurite outgrowth and synaptic plasticity-related genes from those identified previously. After maternal PTU exposure, hypermethylation of Jph3, Kcnj6, and Scn1b at weaning and their persistent reduced expression until adulthood were confirmed by methylation-sensitive high-resolution melting and real-time reverse transcription PCR, respectively. Among the translated products of candidate genes, immunohistochemistry revealed decreased numbers of sodium voltage-gated channel β subunit 1 (SCN1B)+ DG granule cells both at weaning and in adulthood after maternal PTU exposure. Maternal or postpubertal exposure to human developmental neurotoxicants (aluminum chloride, ethanol, and lead acetate) revealed that maternal lead acetate exposure also decreased numbers of SCN1B+ cells at weaning. Double immunohistochemistry with granule cell lineage markers revealed that immature and mature granule cells were SCN1B+. In addition, expression of sodium voltage-gated channel α-subunit genes, Scn1a and Scn8a, was reduced at weaning after maternal PTU exposure. These results indicate that SCN1B levels were suppressed in postmitotic granule cells in accordance with promoter-region hypermethylation of Scn1b. The resulting suppressed formation of intact voltage-gated sodium channels might be related to neurotoxicant-impaired neurogenesis and suppressed synaptic plasticity of granule cells. - Source: PubMed
Publication date: 2025/12/24
Ojiro RyotaTakahashi YasunoriTang QianSakamaki YuriShobudani MomokaZou XinyuKobayashi MioEbizuka YuriKigata TetsuhitoShibutani Makoto