Polyclonal Rabbit DNAJC17 Antibody
- Known as:
- Polyclonal Rabbit DNAJC17 Antibody
- Catalog number:
- KA1082
- Product Quantity:
- 100ul
- Category:
- -
- Supplier:
- KareBay
- Gene target:
- Polyclonal Rabbit DNAJC17 Antibody
Ask about this productRelated genes to: Polyclonal Rabbit DNAJC17 Antibody
- Gene:
- DNAJC17 NIH gene
- Name:
- DnaJ heat shock protein family (Hsp40) member C17
- Previous symbol:
- -
- Synonyms:
- FLJ10634
- Chromosome:
- 15q15.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-06-30
- Date modifiied:
- 2019-02-19
Related products to: Polyclonal Rabbit DNAJC17 Antibody
Related articles to: Polyclonal Rabbit DNAJC17 Antibody
- Molecular chaperones including the heat-shock protein 70-kilodalton (HSP70) family and the J-domain containing protein (JDP) co-chaperones maintain homeostatic balance in eukaryotic cells through regulation of the proteome. The expansive JDP family helps direct specific HSP70 functions, yet loss of single JDP-encoding genes is widely tolerated by mammalian cells, suggesting a high degree of redundancy. By contrast, essential JDPs might carry out HSP70-independent functions or fill cell-context dependent, highly specialized roles within the proteostasis network. Using a genetic screen of JDPs in human cancer cell lines, we found the RNA recognition motif (RRM) containing DNAJC17 to be pan-essential and investigated the contribution of its structural domains to biochemical and cellular function. We found that the RRM exerts an auto-inhibitory effect on the ability of DNAJC17 to allosterically activate ATP hydrolysis by HSP70. The J-domain, but neither the RRM nor a distal C-terminal alpha helix are required to rescue cell viability after loss of endogenous DNAJC17. Knockdown of DNAJC17 leads to relatively few conserved changes in the abundance of individual mRNAs, but instead deranges gene expression through exon skipping, primarily of genes involved in cell cycle progression. Concordant with cell viability experiments, the C-terminal portions of DNAJC17 are dispensable for restoring splicing and G2-M progression. Overall, our findings identify essential cellular JDPs and suggest that diversification in JDP structure extends the HSP70-JDP system to control divergent processes such as RNA splicing. Future investigations into the structural basis for auto-inhibition of the DNAJC17 J-domain and the molecular regulation of splicing by these components may provide insights on how conserved biochemical mechanisms can be programmed to fill unique, non-redundant cellular roles and broaden the scope of the proteostasis network. - Source: PubMed
Publication date: 2026/05/20
Allegakoen David VSahu Pushpendra KKwong KristenMorales JacquelineBivona Trever GSabnis Amit J - To describe an advanced case of pentosan polysulfate sodium (PPS)-associated retinopathy with extensive macular and peripheral retinal involvement following prolonged high-dose exposure. - Source: PubMed
Publication date: 2025/12/10
Zhao Aaron TWibbelsman Turner DCalotti MartinRichards Collin JVrabec Tamara R - Cytoplasmic aggregation and concomitant dysfunction of the prion-like, RNA-binding protein TDP-43 underpin several fatal neurodegenerative diseases, including amyotrophic lateral sclerosis. To elucidate endogenous defenses, we systematically scoured the entire human Hsp70 network for buffers of TDP-43 toxicity. We identify 30 J-domain proteins (2 DNAJAs, 10 DNAJBs, 18 DNAJCs), 6 Hsp70s, and 5 nucleotide-exchange factors that mitigate TDP-43 toxicity. Specific chaperones reduce TDP-43 aggregate burden and detoxify diverse synthetic or disease-linked TDP-43 variants. Sequence-activity mapping unveiled unexpected, modular mechanisms of chaperone-mediated protection. Typically, DNAJBs collaborate with Hsp70 to suppress TDP-43 toxicity, whereas DNAJCs act independently. In human cells, specific chaperones increase TDP-43 solubility and enhance viability under proteotoxic stress. Strikingly, spliceosome-associated DNAJC8 and DNAJC17 retain TDP-43 in the nucleus and promote liquid-phase behavior. Thus, we disambiguate a diverse chaperone arsenal embedded in the human proteostasis network that counters TDP-43 toxicity and illuminate mechanistic gateways for therapeutic intervention in TDP-43 proteinopathies. - Source: PubMed
Publication date: 2025/05/10
Barbieri Edward MLinsenmeier MiriamWhiteman Katherine RCheng YanBraganza SylvanneCopley Katie EMiranda-Castrodad PaolaLewis BrennenVillafañe KevinAmado Defne ADavidson Beverly LShorter James - Low birth weight in newborns is of multifactorial origin (fetal, maternal, placental, and environmental factors), and in one-third of cases, the cause is of unknown origin, with high infant morbidity and mortality. The main treatment for regaining weight and height in children with low birth weight is the application of growth hormones. However, their role as a protective factor to prevent an increase in body composition and the development of metabolic diseases is still poorly understood. : A case-control study was conducted in a cohort of patients consulted at the CES Pediatric Endocrinology Clinic, Medellín, Colombia, between 2008 and 2018. We evaluated sociodemographic and clinical variables. Additionally, the identification of differential patterns of genomic methylation between cases (treated with growth hormone) and controls (without growth hormone treatment) was performed. The groups were compared using Fisher's exact test for qualitative variables and Student's -test for the difference in means in independent samples. The correlation was evaluated with the Pearson coefficient. Regarding clinical manifestations, body mass index (BMI) was higher in children who did not receive growth hormone treatment, higher doses of growth hormone treatment helped reduce body mass index (R: -0.21, and = 0.067), and the use of growth hormone was related to a decrease in triglyceride blood concentrations ( = 0.06); these results tended towards significance. Regarding genome-wide methylation patterns, the following genes were found to be hypermethylated: , and . Meanwhile, the following genes were found hypomethylated: , and . Using growth hormone as a treatment in SGA newborns helps regain weight and height. Additionally, it could be a protective factor against the increase in adolescent body composition. - Source: PubMed
Publication date: 2025/05/23
Velásquez Juan M AlfaroVásquez Trespalacios Elsa MariaUrrego RodrigoArroyave Toro María CMontilla Velásquez María Del PilarSoto Cecilia Maria DíazVélez Juan C ZuluagaJaramillo Henríquez VerónicaFlórez Jorge Emilio SalazarMonroy Fernando PPalacio Mosquera Hernando AlirioVélez Gómez SaraPelaez Sánchez Ronald Guillermo - As the world's largest farmed marine animal, oysters have enormous economic and ecological value. However, mass summer mortality caused by high temperature poses a significant threat to the oyster industry. To investigate the molecular mechanisms underlying heat adaptation and improve the heat tolerance ability in the oyster, we conducted genome-wide association analysis (GWAS) analysis on the F generation derived from the hybridization of relatively heat-tolerant ♀ and heat-sensitive ♂, which are the dominant cultured species in southern and northern China, respectively. Acute heat stress experiment (semi-lethal temperature 42 °C) demonstrated that the F population showed differentiation in heat tolerance, leading to extremely differentiated individuals (approximately 20% of individuals die within the first four days with 10% survival after 14 days). Genome resequencing and GWAS of the two divergent groups had identified 18 significant SNPs associated with heat tolerance, with 26 candidate genes located near these SNPs. Eleven candidate genes that may associate with the thermal resistance were identified, which were classified into five categories: temperature sensor (), transcriptional factor (), protein ubiquitination (, , ), heat shock subfamily (, ), and transporters (, , , ). The expressional differentiation of the above genes between and under sublethal temperature (37 °C) further supports their crucial role in coping with high temperature. Our results will contribute to understanding the molecular mechanisms underlying heat tolerance, and provide genetic markers for heat-resistance breeding in the oyster industry. - Source: PubMed
Publication date: 2023/12/21
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