Human Parvalbumin a PVALB
- Known as:
- Human Parvalbumin a PVALB
- Catalog number:
- CG44
- Product Quantity:
- l0
- Category:
- -
- Supplier:
- Novoprotein
- Gene target:
- Human Parvalbumin PVALB
Related genes to: Human Parvalbumin a PVALB
- Gene:
- MB NIH gene
- Name:
- myoglobin
- Previous symbol:
- -
- Synonyms:
- PVALB
- Chromosome:
- 22q12.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-10-05
- Gene:
- PVALB NIH gene
- Name:
- parvalbumin
- Previous symbol:
- -
- Synonyms:
- D22S749
- Chromosome:
- 22q12.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2017-05-31
Related products to: Human Parvalbumin a PVALB
Related articles to: Human Parvalbumin a PVALB
- Medial ganglionic eminence-derived inhibitory γ-aminobutyric acid (GABAergic) pallial interneurons (MGE-pINs) are essential regulators of cortical circuits, and their dysfunction is associated with neurological disorders. We developed human MGE-pINs from pluripotent stem cells for the treatment of drug-resistant epilepsy. Here, we analyzed xenografted MGE-pINs from human pluripotent stem cells (hMGE-pINs) over the lifespan of host mice in healthy and epileptic environments using single-nuclei RNA sequencing. Comparative transcriptomics against endogenous human brain datasets revealed that 97% of grafted cells developed into somatostatin (SST) and parvalbumin (PVALB) subtypes, including populations that exhibit selective vulnerability in Alzheimer's disease. Transplanted hMGE-pINs demonstrated rapid emergence of subclass features, progressing through distinct transcriptional states sequentially involving neuronal migration, synapse organization, and membrane maturation. We present molecular, electrophysiological, and morphological data that collectively confirm the derivation of diverse bona fide human SST and PVALB subtypes, providing a high-fidelity model to study hMGE-pIN development as well as a compositional atlas for regenerative cell therapy applications. - Source: PubMed
Publication date: 2025/07/11
Bershteyn MarinaZhou HongjunFuentealba LuisChen ChunSubramanyam GeethaCherkowsky DanielSevilla Eric StevenHampel PhilipSalvatierra JuanSezan MelizMaury YvesHavlicek StevenKriks SonjaLee SeonokAu WaiWatson MichaelKuzmenko OlgaGrimmett Maria ElenaVogel AlexandraPorkka FionaQiu YuechenNesterova AnastasiaAnderson DerekFeld Brianna GHosford VictoriaJung Ji-HyeKowal TiaBulfone AlessandroBanik GautamPriest CatherinePalop Jorge JNicholas Cory R - Sensory feedback is required for the stable execution of learned motor skills, and its loss can severely disrupt motor performance. The neural mechanisms that mediate sensorimotor stability have been extensively studied at systems and physiological levels, yet relatively little is known about how disruptions to sensory input alter the molecular properties of associated motor systems. Songbird courtship song, a model for skilled behavior, is a learned and highly structured vocalization that is destabilized following deafening. Here, we sought to determine how the loss of auditory feedback modifies gene expression and its coordination across the birdsong sensorimotor circuit. To facilitate this system-wide analysis of transcriptional responses, we developed a gene expression profiling approach that enables the construction of hundreds of spatially-defined RNA-sequencing libraries. Using this method, we found that deafening preferentially alters gene expression across birdsong neural circuitry relative to surrounding areas, particularly in premotor and striatal regions. Genes with altered expression are associated with synaptic transmission, neuronal spines, and neuromodulation and show a bias toward expression in glutamatergic neurons and class GABAergic interneurons. We also found that connected song regions exhibit correlations in gene expression that were reduced in deafened birds relative to hearing birds, suggesting that song destabilization alters the inter-region coordination of transcriptional states. Finally, lesioning LMAN, a forebrain afferent of RA required for deafening-induced song plasticity, had the largest effect on groups of genes that were also most affected by deafening. Combined, this integrated transcriptomics analysis demonstrates that the loss of peripheral sensory input drives a distributed gene expression response throughout associated sensorimotor neural circuitry and identifies specific candidate molecular and cellular mechanisms that support the stability and plasticity of learned motor skills. - Source: PubMed
Publication date: 2023/06/07
Colquitt Bradley MLi KellyGreen FoadVeline RobertBrainard Michael S - Protein design is able to create artificial proteins with advanced functions, and computer simulation plays a key role in guiding the rational design. In the absence of structural evidence for cytoglobin (Cgb) with an intramolecular disulfide bond, we recently designed a de novo disulfide bond in myoglobin (Mb) based on structural alignment (i.e., V21C/V66C Mb double mutant). To provide deep insight into the regulation role of the Cys21-Cys66 disulfide bond, we herein perform molecular dynamics (MD) simulation of the fluoride-protein complex by using a fluoride ion as a probe, which reveals detailed interactions of the fluoride ion in the heme distal pocket, involving both the distal His64 and water molecules. Moreover, we determined the kinetic parameters of fluoride binding to the double mutant. The results agree with the MD simulation and show that the formation of the Cys21-Cys66 disulfide bond facilitates both fluoride binding to and dissociating from the heme iron. Therefore, the combination of theoretical and experimental studies provides valuable information for understanding the structure and function of heme proteins, as regulated by a disulfide bond. This study is thus able to guide the rational design of artificial proteins with tunable functions in the future. - Source: PubMed
Publication date: 2020/04/04
Yin Lu-LuXu Jia-KunWang Xiao-JuanGao Shu-QinLin Ying-Wu - We have previously reported genome-wide significant linkage of bipolar disorder to a region on 22q12.3 near the marker D22S278. Towards identifying the susceptibility gene, we have conducted a fine-mapping association study of the region in two independent family samples, an independent case-control sample and a genome-wide association dataset. Two hundred SNPs were first examined in a 5 Mb region surrounding the D22S278 marker in a sample of 169 families and analyzed using PLINK. The peak of association was a haplotype near the genes stargazin (CACNG2), intraflagellar transport protein homolog 27 (IFT27) and parvalbumin (PVALB; P = 4.69 × 10(-4)). This peak overlapped a significant haplotype in a family based association study of a second independent sample of 294 families (P = 1.42 × 10(-5)). Analysis of the combined family sample yielded statistically significant evidence of association to a rare three SNP haplotype in the gene IFT27 (P = 8.89 × 10(-6)). Twelve SNPs comprising these haplotypes were genotyped in an independent sample of 574 bipolar I cases and 550 controls. Statistically significant association was found for a haplotype window that overlapped the region from the first two family samples (P = 3.43 × 10(-4)). However, analyses of the two family samples using the program LAMP, found no evidence for association in this region, but did yield significant evidence for association to a haplotype 3' of CACNG2 (P = 1.76 × 10(-6)). Furthermore, no evidence for association was found in a large genome-wide association dataset. The replication of association to overlapping haplotypes in three independent datasets suggests the presence of a bipolar disorder susceptibility gene in this region. - Source: PubMed
Publication date: 2012/10/04
Nissen StephanieLiang SherriShehktman TatyanaKelsoe John R Greenwood Tiffany ANievergelt Caroline MMcKinney RebeccaShilling Paul DSmith Erin NSchork Nicholas JBloss Cinnamon SNurnberger John IEdenberg Howard JForoud TatianaKoller Daniel LGershon Elliot SLiu ChunyuBadner Judith AScheftner William ALawson William BNwulia Evaristus AHipolito MariaCoryell WilliamRice JohnByerley WilliamMcMahon Francis JBerrettini Wade HPotash James BZandi Peter PMahon Pamela BMcInnis Melvin GZöllner SebastianZhang PengCraig David WSzelinger SzabolicsBarrett Thomas BSchulze Thomas G