CLTB Antibody
- Known as:
- CLTB Antibody
- Catalog number:
- XW-7978
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- CLTB Antibody
Related genes to: CLTB Antibody
- Gene:
- CLTB NIH gene
- Name:
- clathrin light chain B
- Previous symbol:
- -
- Synonyms:
- Lcb
- Chromosome:
- 5q35.2
- Locus Type:
- gene with protein product
- Date approved:
- 1990-10-16
- Date modifiied:
- 2016-01-18
Related products to: CLTB Antibody
Related articles to: CLTB Antibody
- β-Glucosidases (EC 3.2.1.21) are essential enzymes involved in biomass degradation and metabolic regulation, but the physiological roles of intracellular β-glucosidases in filamentous fungi remain incompletely understood. In this study, we characterized CbgA (AN10124) and CbgB (AN10375), two intracellular glycoside hydrolase family 1 β-glucosidases, in Aspergillus nidulans. Gene deletion and biochemical analyses demonstrated that CbgA is the predominant intracellular β-glucosidase. Loss of cbgA led to overactivation of cellulases, cellobiose-dependent accumulation of reddish-brown secondary metabolites, and a significant reduction in conidiation. Crucially, deletion of the cellobiose transporter gene cltB in the ΔcbgA background markedly attenuated these phenotypes, providing direct genetic evidence that the ΔcbgA-associated defects are driven by intracellular cellobiose accumulation rather than energy deficiency. Our findings identify CbgA as a critical "signal gatekeeper" that modulates the intensity of cellobiose-dependent induction. By maintaining the intracellular cellobiose pool within a physiological range, CbgA prevents secretory overload and maintains the metabolic balance between primary development and secondary metabolism. This study clarifies the coordination between nutrient transport and intracellular metabolism in shaping global regulatory outputs, suggesting that the targeted modulation of CbgA activity represents a potential strategy for optimizing cellulase production in fungal cell factories. KEY POINTS: CbgA negatively regulates cellulase expression by controlling intracellular cellobiose levels.Loss of cbgA leads to hyperpigmentation and reduced conidiation on cellobiose.Deletion of cltB alleviates ΔcbgA phenotypes, confirming the role of intracellular cellobiose. - Source: PubMed
Publication date: 2026/05/04
Yakabe ShunKadooka ChihiroMatsuzawa TomohikoKawai YuzukiNoguchi MasayukiHira DaisukeGoto MasatoshiOka Takuji - Cervical lymph node TB (CL-TB) is the most prevalent form of extra-pulmonary TB, yet it remains underdiagnosed in endemic settings due to non-specific symptoms and inconsistent diagnostic pathways. We aimed to identify socio-demographic and clinical predictors of CL-TB in patients attending a tertiary hospital in Bangladesh and evaluate the diagnostic yield of available tests. - Source: PubMed
Publication date: 2026/02/11
Luba F RGhosh PAnwar SDey B PBhowmick BArafat S MSaleh A AShomik M SMaruf SSagar S KAshaduzzaman MCeruti ASiegel MArpa COkuni J BSchneitler SMondal DAbd El Wahed A - Clathrin light chain B (CLTB) is one of the three light chain subunits of the clathrin complex. This study aims to elucidate the role of CLTB in the pathogenesis of hepatocellular carcinoma (HCC) and its clinical implications. Clinical and bioinformatic analyses reveal marked CLTB overexpression in HCC tissues. Genetic silencing of CLTB suppresses HCC cell proliferation, migration, and invasion, whereas its overexpression exacerbates malignant phenotypes. Mechanistically, CLTB activates NF-κB signaling to upregulate PCNA clamp-associated factor (PCLAF), thereby promoting small extracellular vesicle (sEV) uptake. Given that clathrin-mediated endocytosis is the key mechanism for sEV uptake, this study further investigated the functional implications of CLTB-enriched sEVs in tumor vascular remodeling. sEV-CLTB promotes endothelial angiogenesis, disrupts vascular integrity, and induces pulmonary vascular leakage by binding SH3 domain-containing kinase-binding protein 1 (SH3KBP1) and then inhibiting SH3KBP1 ubiquitination degradation. In patient-derived xenograft (PDX) models, combined therapy of clathrin inhibitor (chlorpromazine) or SH3KBP1 silencing with sorafenib suppresses tumor growth and reduces microvascular density. This study demonstrates that CLTB promotes HCC progression through the NF-κB-PCLAF signaling axis and sEV-mediated vascular remodeling, providing a mechanistic foundation for developing combination therapies targeting CLTB. - Source: PubMed
Publication date: 2025/08/18
Sun XiaokeGuo JunchenZhao NingCui GuanghuaBai YunDing MeijuanXu YiYang Yu - Parkinson's disease is characterized by an abnormal accumulation of alpha synuclein (-syn) in different regions of the central nervous system. At present, only palliative pharmacological treatments are available for Parkinson´s disease. Immunotherapy is considered an alternative to treat Parkinson's disease, and plants are a convenient alternative platform for biopharmaceutical production. When compared to other systems, plants are particularly attractive because they offer cost-effectiveness, large-scale production, and enhanced safety. Therefore, this study aimed to establish a carrot cell suspension culture for the production of cLTB-Syn, a vaccine candidate against Parkinson's disease. The convenience of MS medium optimization was demonstrated. Transgenic callus cultures were maintained and adapted on solid MSU9 medium without phytohormones, followed by growth kinetics in suspension cultures. The maximum biomass yield was 15.8 ± 0.35 g/L DW at 14 days of culture, with a growth rate of µ = 0.1034/d and td = 6.7 days. The cLTB-Syn protein production reached a maximum value of 2.62 ± 0.03 µg/g DW, representing a 1.6-fold increase over the initial culture time. Finally, the presence of the transgene was confirmed by PCR, and the integrity of cLTB-Syn protein was determined by dot blot assays. This study presents evidence of a promising system for a toxin-free biopharmaceutical production, which has the potential to be scaled up for large manufacturing, at a low cost. - Source: PubMed
Publication date: 2025/06/03
Carreño-Campos ChristianZarate Sahara Dubraiicka ElgueaRomero-Maldonado AndreaVillarreal María LuisaRosales-Mendoza SergioOrtiz-Caltempa Anabel - Autism Spectrum Disorders (ASD) are complex and genetically heterogeneous neurodevelopmental conditions. Although alternative splicing (AS) has emerged as a potential contributor to ASD pathogenesis, its role in large-scale genomic studies has remained relatively unexplored. In this comprehensive study, we utilized computational tools to identify, predict, and validate splicing variants within a Spanish ASD cohort (360 trios), shedding light on their potential contributions to the disorder. We utilized SpliceAI, a newly developed machine-learning tool, to identify high-confidence splicing variants in the Spanish ASD cohort and applied a stringent threshold (Δ ≥ 0.8) to ensure robust confidence in the predictions. The in silico validation was then conducted using SpliceVault, which provided compelling evidence of the predicted splicing effects, using 335,663 reference RNA-sequencing (RNA-seq) datasets from GTEx v8 and the sequence read archive (SRA). Furthermore, ABSplice was employed for additional orthogonal in silico confirmation and to elucidate the tissue-specific impacts of the splicing variants. Notably, our analysis suggested the contribution of splicing variants within CACNA1I, CBLB, CLTB, DLGAP1, DVL3, KIAA0513, OFD1, PKD1, SLC13A3, and SCN2A. Complementary datasets, including more than 42,000 ASD cases, were employed for gene validation and gene ontology (GO) analysis. These analyses revealed potential tissue-specific effects of the splicing variants, particularly in adipose tissue, testis, and the brain. These findings suggest the involvement of these tissues in ASD etiology, which opens up new avenues for further functional testing. Enrichments in molecular functions and biological processes imply the presence of separate pathways and mechanisms involved in the progression of the disorder, thereby distinguishing splicing genes from other ASD-related genes. Notably, splicing genes appear to be predominantly associated with synaptic organization and transmission, in contrast to non-splicing genes (i.e., genes harboring de novo and inherited coding variants not predicted to alter splicing), which have been mainly implicated in chromatin remodeling processes. In conclusion, this study advances our comprehension of the role of AS in ASD and calls for further investigations, including in vitro validation and integration with multi-omics data, to elucidate the functional roles of the highlighted genes and the intricate interplay of the splicing process with other regulatory mechanisms and tissues in ASD. - Source: PubMed
Publication date: 2025/03/28
Dominguez-Alonso STubío-Fungueiriño MGonzález-Peñas JFernández-Prieto MParellada MArango CCarracedo ARodriguez-Fontenla C