Journal: Cell Death Discovery

Article Title: GPER1 reduces skin inflammation by inhibiting keratinocyte proliferation

doi: 10.1038/s41420-026-03059-1

Figure Lengend Snippet: Representative images of biopsy sections from healthy and psoriasis patients immunostained with anti-GPER1 ( a ) and anti-pCREB ( b ). Sections were examined under a Leica microscope DMC6200 equipped with a Leica DFC 280 digital camera. No staining was observed when primary antibodies were omitted. Magnification at 20X and 40X (scale bar 100 µm and 50 µm, respectively). CL Cornified layer, SL Spinous layer, D dermis.

Article Snippet: Afterward, sections were immunostained with rabbit polyclonal antibody to GPER1 (Sigma-Aldrich, #SAB2700363, 1/100), or rabbit monoclonal anti-pCREB (Cell Signaling Technology, #9198, 1/800), followed by 1/100 dilution of biotinylated anti-rabbit secondary antibody (Dako, E0432) and then by the ImmunoCruz goat ABC Staining System (#sc-2023, Santa Cruz Biotechnology).

Techniques: Microscopy, Staining

Journal: Nucleic Acids Research

Article Title: Disruption of a six-nucleotide miRNA motif improves PKD1 dosage and ameliorates polycystic kidney disease

doi: 10.1093/nar/gkaf1538

Figure Lengend Snippet: Pkd1 RC*17/− allele disrupts the c-Myc–miR-17–mitochondrial axis in cystic kidneys. Shotgun label-free quantitative proteomics was performed to assess global proteomic profiles of kidneys from 18-day-old Pkd1 +/+ , Pkd1 RC/− , and Pkd1 RC*17/− mice ( n = 3, each group). ( A ) Comparative differential expression analysis depicts a global trend where a substantial portion of dysregulated protein expression (adjusted P < .05) in Pkd1 RC/− kidneys compared to Pkd1 +/+ kidneys was improved in Pkd1 RC*17/− kidneys. ( B ) Top pathways (based on z -score ≥6 in at least one comparison group) that underlie the proteomic changes observed in Pkd1 RC/− compared to Pkd1 +/+ kidneys, and Pkd1 RC*17/− compared to Pkd1 RC/− kidneys. The ingenuity pathway analysis software was used for the predictions. Expression of metabolic, proliferative, and RNA processing pathways were improved in Pkd1 RC*17/− compared to Pkd1 RC/− kidneys. ( C ) Immunoblot analysis showing reduced pMTOR and pCREB expression, and increased expression of oxidative phosphorylation complex (OXPHOS) components in Pkd1 RC*17/− compared to Pkd1 RC/− kidneys ( n = 3). (D, E) Phospho-histone H3 (pHH3, pink) immunofluorescence staining ( D ) and subsequent quantification ( E ) demonstrated reduced proliferation in Pkd1 RC*17/− compared to Pkd1 RC/− kidneys ( n = 4 each). The slides were counterstained with DAPI (blue). (F–I) qRT-PCR analysis showing expression of primary miR-17 transcript ( F ), mature miR-17 and miR-20a ( G ), mature miR-21 ( H ), and cMyc ( I ) in kidneys of 18-day-old Pkd1 +/+ , Pkd1 RC/− , and Pkd1 RC*17/− mice ( n = 3). The c-Myc/miR-17 axis remained elevated in Pkd1 RC*17/− kidneys, whereas expression of miR-21, a cyst-pathogenic miRNA, was improved. ( J ) Immunoblot analysis showing equivalent expression of cMyc protein in kidneys of 18-day-old Pkd1 RC/− and Pkd1 RC*17/− mice ( n = 3). Actin serves as the loading control; Error bars indicate SEM. Statistics: ANOVA with Tukey’s (A, F–I), and Unpaired, two-tailed t -test (E, J).

Article Snippet: Primary antibodies used: PC1 (7E12 Santa Cruz, #sc-130554), PC2 (PKD-RRC), AQP2 (Sigma–Aldrich, #A7310), Beta-Actin (Sigma–Aldrich, #A3854), Mannose Receptor (Abcam, #ab64693), Alpha Smooth Muscle (Sigma–Aldrich, #F377), Phospho-mTOR (Cell Signaling, #2971), pCREB (Cell Signaling, #9198), Total OXPHOS Rodent WB Antibody Cocktail (Abcam, #ab110413), and c-Myc (Abcam, #ab185656).

Techniques: Quantitative Proteomics, Expressing, Comparison, Software, Western Blot, Phospho-proteomics, Immunofluorescence, Staining, Quantitative RT-PCR, Control, Two Tailed Test