Ask about this productRelated genes to: CLPB Blocking Peptide
- Gene:
- CLPB NIH gene
- Name:
- ClpB homolog, mitochondrial AAA ATPase chaperonin
- Previous symbol:
- -
- Synonyms:
- HSP78, SKD3, FLJ13152, ANKCLB
- Chromosome:
- 11q13.4
- Locus Type:
- gene with protein product
- Date approved:
- 2005-10-04
- Date modifiied:
- 2019-04-23
Related products to: CLPB Blocking Peptide
Related articles to: CLPB Blocking Peptide
- The present study aimed to elucidate whether the metabolic effects of the probiotic bacterium 4597 depend on melanocortin receptor (MCR) signaling. The response to a 3-week intragastric treatment with the bacterial suspension or total protein extract was compared between genetically similar mouse sub-strains but with different MCR sensitivity: KK and KK.Cg-Ay/a (KK-Ay)-the latter overproducing Agouti protein. Treatment of KK mice with protein extract stimulated energy expenditure and carbohydrate oxidation but reduced lipid oxidation, leptin level, pancreatic weight, and hypothalamic insulin and leptin receptor mRNA expression. Live bacteria in KK mice reduced food intake and stimulated hypothalamic mRNA expression of proopiomelanocortin, Agouti-related peptide, and insulin receptors. In the sub-strain KK-Ay, probiotics had no effect on the aforementioned metabolic parameters. -based probiotics improved glucose tolerance and decreased body fat and liver glycogen in both mouse sub-strains. Activation of MC4R by protein extract was revealed by in vitro study using β-arrestin recruitment. These findings confirm beneficial effects of the bacteria and show that, for several parameters, the bacterial protein extract may be more effective than bacterial suspension. Differential responses to the treatment between the mouse sub-strains, particularly in energy metabolism, as well as in vitro data, indicate that the effects of are mediated by MCR signaling. - Source: PubMed
Publication date: 2026/08/03
Zolotarev Vasiliy AMurovets Vladimir OSozontov Egor ASepp Anastasia LLukina Ekaterina AKhropycheva Raisa PThomas BenjaminFetissov Sergueï O - The evolving field of fetal neurology can offer insights into early nervous system development through antenatal dynamic ultrasonography and maternal perception of movements. The spectrum of abnormal fetal movements ranges from fetal akinesia, often associated with arthrogryposis multiplex congenita (AMC), to increased repetitive movements, typically indicating fetal seizures. Nonepileptic hyperkinetic movement disorders of the fetus are rarely documented. Here, we report a female infant who had clonus-like movements in utero and postnatally. Antenatal ultrasonography revealed polyhydramnios, fetal growth restriction, and repetitive clonus-like movements (∼5 Hz), which the mother perceived as frequently "shaking" her. The infant required resuscitation and intubation at delivery. AMC, ectrodactyly, cataract, axial hypotonia, and absent primitive reflexes were noted, along with persistent high-frequency, low-amplitude clonus-like movements without accompanying ictal epileptic activity on the EEG. Laboratory findings included markedly elevated serum creatine kinase levels attributed to sustained contractions, severe neutropenia, and 3-methylglutaconic aciduria. Despite supportive care, she died of respiratory failure on day 15. Whole-exome sequencing established the diagnosis as caseinolytic peptidase B deficiency, an autosomal recessive primary mitochondrial disorder caused by pathogenic variants in the nuclear-encoded gene. This is a unique case of AMC, paradoxically occurring with hyperkinesia rather than with global hypokinesia, but the hyperkinetic movement repertoire is limited and restrictive. This case underlines the diagnostic value of integrating antenatal history and imaging with detailed postnatal phenotyping by a multidisciplinary team in neurometabolic disorders. - Source: PubMed
Publication date: 2026/07/24
Yıldız YılmazÇetin Faruk Seyfettinİyigün İremUnal SuleŞimşek Kiper Pelin ÖzlemDeren ÖzgürHaliloğlu Göknur - ClpB, an ATP-dependent molecular chaperone belonging to the Hsp100/Clp subfamily of AAA+ ATPases, plays a crucial role in protein disaggregation, thereby enhancing bacterial survival under stress conditions. Despite its well-conserved function in prokaryotes, the specific contributions of ClpB to the pathogenesis of the ruminant pathogen Mycoplasma bovis remain largely unexplored. In this study, we identified and functionally characterized a ClpB homolog in M. bovis. Biochemical assays confirmed that the recombinant ClpB protein exhibits intrinsic ATPase activity and, in cooperation with the DnaK chaperone system, efficiently mediates protein disaggregation in vitro. Through genome-wide transposon mutagenesis of the M. bovis HB0801 strain, we generated ClpB-deficient mutants that maintained normal growth kinetics and morphology at 37 °C but exhibited significant growth defects under thermal and oxidative stress conditions. Phenotypic analysis demonstrated that ClpB disruption attenuated key virulence traits, including impaired adhesion to host cells, marked reduction in biofilm formation, diminished pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) expression in BoMac cells. Furthermore, the reduced virulence of the ClpB mutant was investigated by DIA proteomic analyses, which revealed that the ClpB mutant strain altered distinct protein expression patterns related to proteostasis, including phosphotransferase system, serine-type peptidase activity, serine hydrolase activity, and chaperone-mediated protein folding that contribute to the stress response and virulence. These findings collectively demonstrate that ClpB serves as a multifunctional virulence determinant in M. bovis, orchestrating stress adaptation, host-pathogen interactions, and pathogenic potential through modulation of both protein quality control systems and virulence-associated pathways. - Source: PubMed
Publication date: 2026/07/13
Zhang HuiLu DoukunZhao GangChen XiChen YingyuHu ChangminZhang HuanrongGuo AizhenYang Falong - Impaired mitochondrial proteostasis underlies a broad spectrum of diseases, yet effective therapies remain limited. Here we show that deficiency of HTRA2, a mitochondrial intermembrane space protease, can be rescued by hypoxia therapy. Using an Htra2 mutant mouse model that displays severe neurodegeneration and early lethality, we find that continuous hypoxia rescues striatal degeneration and extends lifespan. Mechanistically, we demonstrate that HTRA2 forms a functional complex with the disaggregase CLPB. Loss of function of either protein drives aggregation of intermembrane space-facing subunits of complex I of the electron transport chain, resulting in secondary complex I dysfunction. These changes impair tissue oxygen consumption and probably cause pathological hyperoxia, which is corrected by hypoxia. Together, these findings define a proteostasis pathway linking intermembrane space quality control to complex I function and expand the potential of hypoxia therapy to secondary complex I disease. - Source: PubMed
Publication date: 2026/07/08
Garg AnkurDesousa Brandon RRoy RajuFlis AmyBlume Skyler YAbe YoheiMelo Arthur ACupo Ryan RGrigorean GabrielaSouthworth Daniel RShorter JamesJain Isha H - Staphylococcus aureus (S. aureus) is a major foodborne pathogen frequently associated with the contamination of milk and dairy products. It persists in dairy-processing environments by tolerating diverse environmental stresses and forming biofilms on equipment surfaces. While quorum-sensing (QS) systems are known to regulate bacterial physiology, their specific contributions to stress adaptation in the context of dairy processing remain poorly understood. In this study, Δagr, ΔluxS, and ΔagrΔluxS mutants were constructed in a methicillin-resistant S. aureus (MRSA) background to evaluate contributions of the Agr and LuxS QS systems to survive under food-associated stress conditions. Deletion of agr significantly reduced survival under oxidative, acid, heat, and desiccation stresses, while enhancing biofilm formation. In contrast, luxS deletion selectively impaired tolerance to heat and desiccation without affecting biofilm formation. Additionally, the ΔagrΔluxS double mutant largely phenocopied the Δagr mutant, exhibiting a further decrease in heat and desiccation tolerance, suggesting an additive effect between the 2 systems. Furthermore, integrated transcriptomic analysis and RT-qPCR validation not only confirmed the phenotypic observations at the genetic level but also revealed Agr-dominant regulation of stress-response pathways, including molecular chaperones (clpC, clpB, dnaK, groESL), acid-resistance genes (ureABCD), and desiccation-associated genes, whereas LuxS exhibited a more selective effect on heat- and desiccation-related responses. In conclusion, these findings identify Agr as a central regulator of stress adaptation in S. aureus and suggest that targeting QS systems may be a viable strategy to reduce bacterial persistence in dairy production and processing environments. - Source: PubMed
Publication date: 2026/07/03
Wang HuiMa KaiShen JiaweiZhang BingtaoZhang SijingWang XinciYang XinxingXue Ting