Hsp40 (Hdj1), DyLight 488 Conjugate Rabbit pAb
- Known as:
- Hsp40 (Hdj1), DyLight 488 Conjugate Rabbit pAb
- Catalog number:
- ASASPA400488F
- Product Quantity:
- 200 µg
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- Hsp40 (Hdj1) DyLight 488 Conjugate Rabbit pAb
Related genes to: Hsp40 (Hdj1), DyLight 488 Conjugate Rabbit pAb
- Gene:
- DNAJB1 NIH gene
- Name:
- DnaJ heat shock protein family (Hsp40) member B1
- Previous symbol:
- HSPF1
- Synonyms:
- Hsp40, Sis1, RSPH16B
- Chromosome:
- 19p13.12
- Locus Type:
- gene with protein product
- Date approved:
- 1996-10-02
- Date modifiied:
- 2015-11-19
Related products to: Hsp40 (Hdj1), DyLight 488 Conjugate Rabbit pAb
guanine nucleotide binding protein alpha inhibiting activity polypeptide 1 (GNAI1) polyclonal antibody kinase suppressor of ras (KSR) polyclonal antibody(Alpha)_ 1 _ antitrypsin (A1AT) POLYCLONAL Rabbit anti_human(Alpha)_ Feto Protein (AFP) POLYCLONAL Rabbit anti_human(Alpha)_ Feto Protein (AFP) POLYCLONAL Rabbit anti_human(Alpha)_1_ antitrypsin (A1AT) POLYCLONAL Rabbit anti_human(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2(Arg6,β-cyclohexyl-Ala8,D-Tic16,Arg17,Cys18)-Atrial Natriuretic Factor (6-18) amide (mouse, rabbit, rat)
A71915 98% C69H116N26O15S2 CAS:(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host Rabbit(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host: Rabbit(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host: Rabbit(Arg8)-Vasopressin - EIA Kit (H - sr, pl), Host Rabbit, Extraction-free, CE-marked(Arg8)-Vasopressin - EIA Kit (H - sr, pl), Host RabbitExtraction-freeCE-marked(Arg8)-Vasopressin - EIA Kit (H - sr, pl), Host: Rabbit, Extraction-free, CE-marked Related articles to: Hsp40 (Hdj1), DyLight 488 Conjugate Rabbit pAb
- Fibrolamellar hepatocellular carcinoma (FLC) and combined hepatocellular-cholangiocarcinoma (cHCC-CCA) are rare primary liver cancers for which limited evidence is available to guide clinical management. cHCC-CCA could arises in the context of chronic liver disease and shares epidemiological and molecular features with both hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (iCCA), reflecting its intermediate biological and clinical position between these two entities. Its diagnosis remains challenging particularly when based on tumor biopsy specimens. Surgical resection remains the standard of care when feasible. Liver transplantation, trans-arterial chemoembolization, ablation, or selective internal radiation therapy have been used in selected cases. For advanced disease, systemic treatments commonly used for HCC or CCA have been applied in real-world practice, including platinum-based chemotherapy, tyrosine kinase inhibitors, and more recently immunotherapy. In addition, molecularly guided therapies have been explored, as targetable genetic alterations can be identified in a subset of cHCC-CCA. In contrast, FLC typically arises in non-cirrhotic livers of young patients and is frequently associated with metastatic disease, including lymph node involvement. At the molecular level, FLC is characterized by the presence of the DNAJB1-PRKACA fusion and by elevated serum procalcitonin secreted by the tumor. Surgical resection remains the cornerstone of treatment when feasible, but data guiding systemic therapy in unresectable cases are limited. Several regimens, including gemcitabine-oxaliplatin, lenvatinib, and immunotherapy, have been evaluated. More recently, clinical trials have reported antitumor activity with combinations of immunotherapy and vaccines targeting the DNAJB1-PRKACA fusion. To improve patient care, since cHCC-CCA and FLC are rare subtypes of liver cancer, we need to compile prospective samples and clinical data from the patients, including their response to any type of treatment at the national and international levels. - Source: PubMed
Publication date: 2026/08/13
Gallant MatteoDecraecker MarieZiol MarianneCalderaro JulienRonot MaximeZucman-Rossi JessicaNault Jean-Charles - Heat shock cognate protein 70 (Hsc70) is a 71 kDa molecular chaperone belonging to the Hsp70 family of heat shock proteins. These proteins act as ATP-dependent molecular machines that assist protein folding under both physiological and stress conditions such as hypoxia, heat shock, and pH fluctuations. In addition to general chaperone functions, Hsc70 performs specialized roles, including uncoating clathrin-coated vesicles, facilitating protein transport into organelles, and targeting proteins for lysosomal degradation. Members of the Hsp70 family are known to form dimers and higher oligomers, but the structural organization and functional relevance of these assemblies remain poorly understood. Earlier studies also suggested that J-domain proteins (JDPs) can promote Hsp70 dimerization. In this study, we used chemical cross-linking, high-resolution Fourier transform mass spectrometry (FTMS), 15N isotopic labeling, and advanced data analysis to investigate the structural organization of Hsc70 dimers. Cross-link-derived distance restraints enabled structural modeling of Hsc70 monomers and dimers using AlphaLink2. Our results reveal distinct ATP- and ADP-state dimer conformations that coexist in equilibrium. In the presence of the cochaperone DnaJB1, we observed a shift in the dimer-monomer equilibrium, accompanied by enhanced ATP hydrolysis and formation of intermediate species. These findings demonstrate that the Hsc70 dimer population is structurally heterogeneous and depends on nucleotide state and cochaperone interactions. - Source: PubMed
Melikov AleksandrViliuga VsevolodKavan DanielKukačka ZdeněkMayer Matthias PNovák Petr - Acute myeloid leukemia (AML) is a malignancy characterized by abnormal myeloid proliferation. Despite therapeutic advances, relapse is frequent. Understanding the tumor microenvironment (TME), particularly the dysfunction and interactions of natural killer (NK) cells, is essential for improving immunotherapeutic strategies such as chimeric antigen receptor T-cell (CAR-T) and chimeric antigen receptor natural killer cell (CAR-NK) therapies. - Source: PubMed
Li JunyiZhu HuoyanYe ChaoqiongXu ShengnanWu ZhihuaDeng Yuping - The global emergence of monkeypox virus (MPXV) highlights the urgent need for a deeper understanding of host-pathogen interactions. Although transcriptional responses to MPXV infection have been characterized, the role of epitranscriptomic regulation particularly N6‑methyladenosine (m6A) modification remains largely unexplored. - Source: PubMed
Publication date: 2026/07/18
Tang RuixiaHuang JindiYu WenhaiLu ShuaiyaoZhou JienanDing KaiyunWang JunbinTang CongFu XiaoqingDu TingfuSun Qiangming - Type 2 diabetes mellitus (T2DM) and sarcopenia demonstrate a significant comorbidity, particularly in the elderly, yet the molecular mechanisms linking them, especially through oxidative stress, remain incompletely understood. This study aimed to identify oxidative stress-related hub genes involved in T2DM-associated sarcopenia (T2DS) by integrating single-cell RNA sequencing (scRNA-seq) and bulk RNA-seq data with machine learning. We analyzed scRNA-seq datasets (GSE244515, GSE268953) to characterize cellular heterogeneity and bulk RNA-seq datasets (GSE202295, GSE226151) for differential expression. Cell type annotation revealed key involvement of neuromuscular junctions and myofibers. Functional enrichment analyses highlighted pathways like the proteasome, TNF signaling, and ubiquitin-mediated proteolysis. From an initial set of oxidative stress-related genes, a comprehensive machine learning framework comprising 127 algorithm combinations was employed. The Lasso+Stepglm[both] model identified 12 candidate genes. Subsequent Protein-Protein Interaction (PPI) network analysis refined this to seven core hub genes: TNFRSF1B, PSMA2, UBE2D1, UBE2N, HSP90AA1, RAD23A, and DNAJB1. These genes are functionally interconnected, primarily implicating TNFRSF1B-mediated inflammatory signaling that activates the ubiquitin-proteasome system, leading to enhanced protein degradation-a key pathway in muscle atrophy. ROC curve analysis confirmed the strong diagnostic value of these hub genes across training, test, and external validation sets. Our findings systematically reveal novel oxidative stress-related hub genes and mechanisms in T2DS, providing potential biomarkers and therapeutic targets for this debilitating condition. - Source: PubMed
Publication date: 2026/07/07
Zhu GuangwenZou KaiLiang YiXie LitingChen Qiu