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
- To investigate the clinicopathological and molecular features of fibrolamellar hepatocellular carcinoma (FL-HCC). The clinicopathological and prognostic information of 9 FL-HCC cases diagnosed at the Fudan University Shanghai Cancer Center, Shanghai, China from January 2018 to December 2024 were collected and analyzed. The FL-HCC samples were examined with immunohistochemical staining, fluorescence in situ hybridization (FISH), and RNA-based next-generation sequencing (NGS). The related literature was also reviewed. There were 3 males and 6 females. The patients' age was 18.0 (10.5, 26.0) years. One of the 9 patients had slightly elevated serum AFP level, and 2 patients had current infection of hepatitis B virus. Five cases occurred in the left lobe of the liver, 3 cases in the right lobe of the liver, and 1 case had multiple lesions involving both the left and right lobes. The tumor sizes ranged from 4.0 to 21.4 cm. Microscopically, neoplastic cells were mainly arranged in sheets or nests, separated by dense collagen bundles frequently arranged in cord-like or parallel lamellae. The tumor cells were large and polygonal, with abundant granular and eosinophilic cytoplasm, large vesicular nuclei, and prominent nucleoli. All tumor cells expressed CK7, HepPar-1, and Arg-1. Molecular analysis revealed that 6 cases harbored the DNAJB1::PRKACA gene fusion by NGS, while the other 3 cases showed PRKACA gene rearrangement by FISH using a break-apart probe. The follow-up period ranged from 7 to 80 months. One patient was lost to follow-up after diagnosis, 3 patients survived without recurrence, 1 patient relapsed with lung metastasis, and 4 patients died of the disease. FL-HCC is a rare type of hepatocellular carcinoma characterized by laminated intratumoral fibrous stroma and specific fusion (DNAJB1::PRKACA) or rearrangement of the PRKACA gene. - Source: PubMed
Weng W WBao HZhang MTan CNi S JHuang DJi GYao Q LBai Q MZhou X YSheng W QWang L - In 2024, we published a paper which described the identification of the fusion DNAJB1::PRKACA kinase in young patients with aggressive hepatoblastoma (HBL) and with biliary atresia (BA). In our study, we used sensitive molecular and cellular techniques and found that about 70% of our analyzed HBL samples showed varying levels of DNAJB1::PRKACA expression. In total, 15-20% of those fusion-positive HBL samples had DNAJB1::PRKACA levels comparable to those observed in FLC, whereas the remaining samples exhibited lower kinase levels. Palaz et al. analyzed five HBL datasets and one BA RNA-Seq dataset with Arriba and found no DNAJB1::PRKACA fusion transcript. Based on their analysis, the authors concluded that DNAJB1::PRKACA is not expressed in HBL patients. They further stated that the identification of DNAJB1::PRKACA fusion in either HBL or BA requires orthogonal molecular validation to confirm the fusion event at the DNA or RNA level. Therefore, we conducted Sanger sequencing on RT-PCR products from several fusion-positive HBL samples and three BA samples. Both HBL and BA cases showed the presence of the DNAJB1::PRKACA fusion transcript, identical to that detected in FLC. These results verify that DNAJB1::PRKACA is present in some HBL and BA patients, as has already been demonstrated using sensitive molecular and cellular techniques. Arriba analysis of current RNA-Seq data may not be sensitive enough for detecting low DNAJB1::PRKACA levels in HBL cases, especially if they are mixed with fusion-negative HBL specimens. Thus, we found that several independent methods, such as immunoanalysis and RT-PCR sequencing, effectively detect DNAJB1::PRKACA in HBL and BA cases. Our study also highlights that detecting low levels of DNAJB1::PRKACA requires individual analysis of HBL and BA patients within the same study, using FLC as the control. - Source: PubMed
Publication date: 2026/08/21
Fleifil YasmeenGulati RuhiJennings KatherineMiethke AlexanderBondoc AlexanderTiao GregoryKarns RebekahTimchenko LubovTimchenko Nikolai - We read with great interest the article by Fleifil et al [...]. - Source: PubMed
Publication date: 2026/08/19
Palaz FahreddinYu XuanxuanBruner JuliaFeely MichaelCai GuoshuaiDuarte SergioZarrinpar Ali - 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