DARPP-32 (Phospho-Thr34) Polyclonal Antibody
- Known as:
- DARPP-32 (Phospho-Thr34) Polyclonal Antibody
- Catalog number:
- 12369
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- DARPP-32 (Phospho-Thr34) Polyclonal Antibody
Related products to: DARPP-32 (Phospho-Thr34) Polyclonal Antibody
Related articles to: DARPP-32 (Phospho-Thr34) Polyclonal Antibody
- - Source: PubMed
- We present the clinicopathologic, immunohistochemical, and molecular findings of 27 primary cutaneous apocrine carcinomas (PCACs). Most patients were men (67%), and the axilla was the most common site (52%). Regional lymph node metastasis was seen in 14 patients (56%), and both lymph node and distant metastasis were seen in 1 patient (4%). Eight patients (32%) were deceased at last follow-up. PCACs exhibit various morphologies, including papillary, tubular, cribriform, solid, and signet ring cell/histiocytoid. The signet ring cell/histiocytoid morphology was seen adjacent to a tubular component in 6 cases (22%). An in situ component was seen in 14 cases (52%). Perineural invasion and lymphovascular invasion were seen in 9 cases (33%) and 6 cases (22%), respectively. All PCACs showed diffuse and strong androgen receptor (AR) expression (23/23, 100%); estrogen receptor (6/25, 24%) and progesterone receptor (4/23, 17%) expression was seen in subset of cases. Six cases showed 3+ HER2 expression; 3 cases showed HER2/ERBB2 amplification. Gross cystic disease fluid protein 15 expression was seen in 20 of 20 cases (100%). Adipophilin was seen in 1 of 15 cases (7%), keratin 5/6 in 13 of 17 cases (76.5%), and mammaglobin in 5 of 16 cases (31%). Targeted DNA sequencing and fusion assays were performed on 12 and 9 cases, respectively. Recurrently mutated genes include ERBB2 (5/11, 45%), KMT2C (5/11, 45%), PIK3CA (3/12, 25%), TP53 (2/12, 17%), and SETD2 (2/11, 17%). One case harbored both an ERBB2::PPP1R1B fusion and an AR-V7 splice variant. Another case harbored only an AR-V7 splice variant; a RARA intronic deletion was seen in 1 case. In summary, PCACs frequently occur in the axilla of men, demonstrate a variety of histomorphologies, and may have an in situ component; they are AR+, estrogen receptor positive or negative, and progesterone receptor positive or negative and can have HER2/ERBB2 amplification. ERBB2, KMT2C, and PIK3CA recurrent alterations were observed. These findings may allow for both distinction from histopathologic mimics and for the use of targeted therapy. - Source: PubMed
Publication date: 2026/09/07
Moran Jakob M TShore Karen TDias-Santagata DoraLaga Alvaro CHosler Gregory AFujimoto MasakazuMochel Mark CHoang Mai P - has been implicated in tumor progression in several malignancies; however, population-level genetic evidence supporting its role in intrahepatic cholangiocarcinoma (ICC) remains limited. This study aimed to investigate the association between and ICC risk and prognosis using genetic and multi-omics analyses. Multiple public datasets were integrated, including finn-b-C3_LIVER_INTRAHEPATIC_BILE_DUCTS, ebi-a-GCST90018583, eqtl-a-ENSG00000131771, GSE138709, The Cancer Genome Atlas (TCGA)-ICC, and FU-iCCA. Two-sample Mendelian randomization (MR) was performed to evaluate the genetic association between expression and ICC risk. expression patterns were further characterized using single-cell and bulk transcriptomic analyses. Expression validation was conducted using TCGA-ICC data and tissue microarray immunohistochemistry. Survival analyses were performed using the FU-iCCA cohort and institutional clinical samples. MR analysis identified as significantly associated with increased ICC risk ( < 0.05, OR > 1), and sensitivity analyses supported the robustness of the results. Single-cell analysis demonstrated enrichment of PPP1R1B expression in malignant cell populations. Bulk transcriptomic datasets and immunohistochemical validation confirmed elevated PPP1R1B expression in tumor tissues. High PPP1R1B expression was significantly associated with poorer overall survival. Genetic and multi-omics evidence supports PPP1R1B as a risk-associated and potential prognostic biomarker in ICC, providing a translational genomics framework for future biomarker development. These findings complement previously reported functional studies and strengthen the biological relevance of in ICC. - Source: PubMed
Publication date: 2026/07/25
Chen ZhuomiaoyuCao FumeiLi Zhao - The growing number of omics datasets in public repositories provides an opportunity to enhance data reusability through data integration; however, complex statistical barriers often hinder the effective combination of independent studies. To address this problem, we present MetaOmixTools, an interactive web-based suite that streamlines the meta-analysis of ranked feature lists and functional enrichment profiles. The platform integrates 2 primary modules-MetaRank and MetaEnrich-within a code-free environment. MetaRank generates robust consensus rankings from multiple lists by implementing weighted (e.g., rank product) and unweighted (e.g., robust rank aggregation) strategies, while MetaEnrich performs functional meta-analyses by combining probability values from individual overrepresentation analyses using established statistical techniques. Using case studies, we established consensus rankings for acute spinal cord injury across heterogeneous platforms, identifying conserved inflammatory marker genes in the up-regulated gene list (e.g., , , and ) and synaptic loss genes in the down-regulated gene list (e.g., , , and ), and also characterized inverse functional intersections between melanoma brain metastasis and neurodegenerative diseases. By providing intuitive, real-time visualization and reproducible workflows, MetaOmixTools empowers the research community to extract consistent biological insights from multistudy data. We have made MetaOmixTools freely available at https://bioinfo.cipf.es/metaomixtools/. - Source: PubMed
Publication date: 2026/06/30
Grillo-Risco RubénTiurin Maksym KupchykPerpiñá-Clérigues CarlaCordero Felipe Francisco JJuárez Samuel LozanoIglesia-Vayá MaríaGarcía-García Francisco - Huntington disease (HD) is a progressive neurodegenerative disease caused by an expanded CAG repeat in the () gene, leading to the accumulation of mutant HTT (mHTT). IL17A (interleukin 17A), a proinflammatory cytokine primarily secreted by Th17 and γδ T cells, has been implicated in immune-mediated neurodegeneration. However, the role of IL17A in the pathogenesis of HD remains poorly understood. Here, we identify IL17A as a critical pathogenic factor in HD that promotes neuroinflammation, mHTT aggregation, and autophagy-lysosomal dysfunction. IL17A disrupts autophagic flux by downregulating CTSB and CTSD, inducing SQSTM1/p62 and MAP1LC3B-II/LC3-II accumulation, and impairing lysosomal reformation. Mechanistically, IL17A suppresses lysosomal biogenesis by inhibiting the nuclear translocation of TFE3. This regulation occurs via a novel GSK3B/GSK-3β-TFE3 signaling pathway. Therapeutic neutralization of IL17A with a monoclonal antibody (IL17A mAb) ameliorates disease phenotypes in R6/2 HD mice, improving motor performance, extending survival, and reducing gliosis. IL17A mAb also attenuates mHTT aggregation and enhances neuroprotective signaling, as evidenced by increased expression of DLG4/PSD-95, phosphorylated CREB1, and BDNF. Moreover, IL17A mAb restores autophagy-lysosomal function by facilitating the clearance of protein aggregates and upregulating lysosomal enzymes and biogenesis markers, including CTSB, CTSD, PIP5K1A, and LAMP2. These findings establish IL17A as a key modulator of HD pathophysiology and highlight IL17A inhibition as a promising therapeutic strategy for targeting autophagy-lysosomal dysfunction in HD. 3-MA; 3-methyladenine; Aβ, amyloid beta; AIF1/Iba1, allograft inflammatory factor 1; ALP, autophagy-lysosomal pathway; ALR, autophagic lysosomal reformation; ATG7, autophagy related 7; ATG5, autophagy related 5; Baf A1, bafilomycin A1; BBB, blood-brain barrier; BDNF, brain derived neurotrophic factor; CSF, cerebrospinal fluid; CTSB, cathepsin B; CTSD, cathepsin D; DLG4/PSD-95, discs large MAGUK scaffold protein 4; GFAP, glial fibrillary acidic protein; GSK3B/GSK-3β, glycogen synthase kinase 3 beta; HD, Huntington disease; HTT, huntingtin; ICV, intracerebroventricular; IL17A, interleukin 17A; IL17A mAb, IL17A monoclonal antibody; IL17RA, interleukin 17 receptor A; IV, intravenous; LAMP2, lysosomal-associated membrane protein 2; MAP1LC3B/LC3B, microtubule-associated protein 1 light chain 3 beta; mHTT, mutant HTT; RBFOX3/NeuN, RNS binding protein, fox-1 homolog (C. elegans) 3; p-CREB1/CREB, phospho-cAMP responsive element binding protein 1; PIP5K1A, phosphatidylinositol-4-phosphate 5-kinase, type 1 alpha; PPP1R1B/DARPP-32, protein phosphatase 1 regulatory inhibitor subunit 1B; rIL17A, recombinant IL17A; SQS, self-quenched substrate; SQSTM1/p62, sequestosome 1; MAPT/tau, microtubule-associated protein tau; TDG, tideglusib; TFE3, transcript factor E3; TFEB, transcript factor EB; Th17, T helper 17; TX-100, Triton X-100; WT, wild-type. - Source: PubMed
Publication date: 2026/08/18
Chen Kai-PoJu Tz-Chuen