Polyclonal Rabbit FOXB1 per 2 Antibody
- Known as:
- Polyclonal Rabbit FOXB1 2 Antibody
- Catalog number:
- KA1336
- Product Quantity:
- 100ul
- Category:
- -
- Supplier:
- KareBay
- Gene target:
- Polyclonal Rabbit FOXB1 per 2 Antibody
Related genes to: Polyclonal Rabbit FOXB1 per 2 Antibody
- Gene:
- FOXB1 NIH gene
- Name:
- forkhead box B1
- Previous symbol:
- -
- Synonyms:
- HFKH-5, FKH5
- Chromosome:
- 15q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-22
- Date modifiied:
- 2015-08-25
Related products to: Polyclonal Rabbit FOXB1 per 2 Antibody
Related articles to: Polyclonal Rabbit FOXB1 per 2 Antibody
- Pacific oysters (Crassostrea gigas) are a major aquaculture species among molluscs worldwide, possessing significant ecological and economic value. The mechanism governing sex determination in oysters remains largely unknown. Fox transcription factors are key regulators of vital biological processes, controlling important functions such as tissue development and reproduction. This study presents a genome-wide identification and characterization of the Fox gene family in C. gigas. Through systematic identification, 16 Fox genes were discovered and classified into 13 subfamilies based on phylogenetic analysis and conservation domain analysis. Transcriptomic profiling revealed that FoxK2 and FoxG1 were significantly upregulated during the resting stage, whereas FoxG1 expression was higher in females and males throughout the active gametogenesis stage (P < 0.05). FoxE1 and FoxL2 exhibited elevated expression profiles during female maturation, whereas FoxO, FoxN4, and FoxK2 showed higher expression profiles during male maturation (P < 0.05). At the spawning stage, FoxE1 and FoxK2 were significantly expressed in females, whereas FoxJ1B and FoxK2 exhibited elevated expression in males (P < 0.05). Our findings indicate sexually dimorphic expression patterns of FoxB1, FoxE1, FoxL2, FoxP1, and FoxC1 and their gonad-specific functions. Our research has significant ecological implications for comprehending the sex determination process and offers fresh insights into the Fox gene regulation mechanisms in bivalves. - Source: PubMed
Publication date: 2026/03/22
Chen SitongLi QiHu BiyangDu Shaojun - Certain human mutations in the mitochondrial aldehyde dehydrogenase 4A1 (ALDH4A1) lead to a severe, paediatric form of epilepsy and developmental abnormalities, yet the precise molecular mechanism leading to the clinical phenotypes remains unexplained. ALDH4A1 metabolizes glutamic-γ-semialdehyde (GSA). Mutations in ALDH4A1, which lead to inactive enzyme variants, cause GSA to accumulate and vitamin B6 inactivation. Patients with severe ALDH4A1 deficiency have paediatric epilepsy and are resistant to prescribed therapies. We develop knock-in cell culture and mouse models of the S352L variant to help characterize this human pathology. The knock-in models show that ALDH4A1 is necessary for clearing a non-canonical substrate, 4-hydroxynonenal (4-HNE), without becoming inactivated, like the main clearance mechanism of 4-HNE, ALDH2, and that ALDH4A1 deficiency alters transcriptional profiles in genes that regulate brain development, including LGI1 and FOXB1. Protein levels, including those in the proline metabolic pathway (e.g., spermine synthase), are also downregulated in both S352L iPSCs and the brains of S352L homozygous mice. This work identifies additional metabolic and transcriptional pathways regulated by ALDH4A1, and potential pathways that can be targeted to treat patients with ALDH4A1 deficiency. - Source: PubMed
Publication date: 2026/03/14
Kraemer Benjamin RHeo GwangbeomChen Che-HongMochly-Rosen Daria - Leptin receptor-expressing hypothalamic neurons (LepR ) are key regulators of energy balance, yet a comprehensive, cell type-resolved, chromatin accessibility map of these neurons is lacking. We profiled ∼20,000 LepR nuclei using single-nucleus multiome (snRNA-seq/snATAC-seq), identifying 39 transcriptionally and epigenetically distinct clusters, including AgRP (two subtypes), Pomc (two subtypes), Foxb1, Irx5/3 (three subtypes), Nts, PNOC (two subtypes), Kiss1/Pdyn (KNDy, two subtypes), Ghrh, Tcf7l2, and Sf1/Nr5a1 (three subtypes) populations. We also identified three Glp1r-expressing clusters with the highest Lepr enrichment, each marked by distinct molecular signatures. Cluster-specific open chromatin regions (OCRs) delineated putative cis-regulatory elements unique to each LepR subtype. Mouse cell-type specific OCRs conserved in the human genome were identified; a subset were proximal to genes with high Human Genetic Evidence (HuGE) scores for obesity-related traits, overlapped obesity-associated GWAS loci, and/or coincided with eQTLs, including variants with the potential to influence human energy balance. Together, these data provide cell type-specific cis-regulatory atlas of LepR neuronal subtypes, including Glp1r/Lepr-enriched populations, and highlight evolutionarily conserved, subtype-specific regulatory elements, associated candidate genes, and putative functional variants that may modulate LepR subtype function and influence energy homeostasis and obesity susceptibility in humans. - Source: PubMed
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