Journal: Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc

Article Title: Hepatic adenomas with synchronous or metachronous fibrolamellar carcinomas: both are characterized by LFABP loss.

doi: 10.1038/modpathol.2016.59

Figure Lengend Snippet: Figure 4 PRKAR1A expression in fibrolamellar carcinomas. (a) The fibrolamellar carcinoma negative for the DNAJB1- PRKACA fusion shows loss of PRKAR1A expression. (b) In contrast, fibrolamellar carcinomas with the DNAJB1-PRKACA fusion show retained expression of PRKAR1A.

Article Snippet: Five micron-thick sections were cut from the tissue block and immunohistochemistry performed using antibodies to Arginase-1(predilute, clone SP156; Cell Marque), HepPar1 (predilute, clone OCH1E5; Ventana), cytokeratin 7 (1:100, Clone OV-TL 12/30; Dako), CD68 (clone KP1, 1:50-1:100; Dako), PRKAR1A (1:2000, clone OTI6C7; Origene Technologies), LFABP (1:50, rabbit polyclonal; Abcam), CRP (1:2000, clone Y284; Abcam), SAA (1:2000, clone mc1; Dako), Glutamine synthetase (1:2000, clone GS-6; Millipore), and beta catenin (predilute, clone 14; Ventana).

Techniques: Expressing

Journal: bioRxiv

Article Title: IR-B deficiency and fatty acid dysregulation accelerate prostate cancer progression via PI3K/AKT signaling

doi: 10.64898/2026.01.30.702723

Figure Lengend Snippet: (A) Volcano plot showing differentially expressed genes between LL H (control) and pLL +H prostate DLP lobes. (B) Hierarchical clustering and heatmap of significantly differentially expressed genes; enriched gene ontology (GO) terms indicated. (C) Bubble plot of enriched KEGG pathways for upregulated genes. (D) Real-time PCR quantification of IRS-1, IRS-2, IRS-3, and IGF2 mRNA in LL H and pLL +H prostate DLP lobes. mean ± SEM. (E) Western blot analysis of p- IR, total IR, p- IRS, total IRS1, p- AKT, total AKT, and PI3K protein in LL, pLL + , LL H and pLL +H prostate DLP lobes. (F) Heatmap showing differential metabolites between pLL +H and LL H mice. (G) Classification of metabolite type in prostate DLP lobes of LL H and pLL +H mice. (H) Volcano plot of significantly differential metabolites; fatty acids highlighted.

Article Snippet: The following primary antibodies were used: IRS, phospho-IRS1(Tyr896), GSK3β and phospho-GSK3β(Ser9), GPR120, GLUT1, Bcl-2, BAX (Abbkine, USA); IR and phospho-IR, AR, AKT1 and phospho-AKT, PI3K p85 alpha, GAPDH (Proteintech, Wuhan, China); Ki-67 (Cell Signaling Technology, USA); GLUT12 (Boster Bioengineering Co., Ltd., Wuhan); GSK3α/β and phospho-GSK3β (Y216) and phosphor-GSK3α (Y279) (Abcam,USA).

Techniques: Control, Real-time Polymerase Chain Reaction, Western Blot

Journal: bioRxiv

Article Title: IR-B deficiency and fatty acid dysregulation accelerate prostate cancer progression via PI3K/AKT signaling

doi: 10.64898/2026.01.30.702723

Figure Lengend Snippet: (A & B) Western blot and quantification showing AR expression reduced by ω-3 and increased by ω-6. (C & D) Western blot and quantification of p -PI3K, PI3K, p -AKT, and AKT at 3 and 6 months; ω-3 decreases phosphorylation, ω-6 increases it. (E, F, G, & H) Western blot and quantification of BCL2 and BAX at 3 and 6 months. ω-3 increases pro-apoptotic BAX and decreases anti-apoptotic BCL2, ω-6 shows opposite pattern. (I & J) Western blot of cultured cells treated with EPA, DHA, or AA, corfirming protein expression treads. Data mean ± SEM. *p<0.05, **p<0.01, ***p<0.001.

Article Snippet: The following primary antibodies were used: IRS, phospho-IRS1(Tyr896), GSK3β and phospho-GSK3β(Ser9), GPR120, GLUT1, Bcl-2, BAX (Abbkine, USA); IR and phospho-IR, AR, AKT1 and phospho-AKT, PI3K p85 alpha, GAPDH (Proteintech, Wuhan, China); Ki-67 (Cell Signaling Technology, USA); GLUT12 (Boster Bioengineering Co., Ltd., Wuhan); GSK3α/β and phospho-GSK3β (Y216) and phosphor-GSK3α (Y279) (Abcam,USA).

Techniques: Western Blot, Expressing, Phospho-proteomics, Cell Culture

Journal: bioRxiv

Article Title: IR-B deficiency and fatty acid dysregulation accelerate prostate cancer progression via PI3K/AKT signaling

doi: 10.64898/2026.01.30.702723

Figure Lengend Snippet: Left: Dysregulation of IR isoforms mediates cell proliferation and glucose metabolism via PI3K/AKT signaling in Hi-Myc mice. Right: IR-B knockout leads to glucose metabolism disorder and compensatory increase of ω-3 polyunsaturated fatty acids, which upregulate GPR120 expression and enhance glucose uptake through GLUT1.

Article Snippet: The following primary antibodies were used: IRS, phospho-IRS1(Tyr896), GSK3β and phospho-GSK3β(Ser9), GPR120, GLUT1, Bcl-2, BAX (Abbkine, USA); IR and phospho-IR, AR, AKT1 and phospho-AKT, PI3K p85 alpha, GAPDH (Proteintech, Wuhan, China); Ki-67 (Cell Signaling Technology, USA); GLUT12 (Boster Bioengineering Co., Ltd., Wuhan); GSK3α/β and phospho-GSK3β (Y216) and phosphor-GSK3α (Y279) (Abcam,USA).

Techniques: Knock-Out, Expressing

Journal: Endocrine-Related Cancer

Article Title: Defects of the Carney complex gene (PRKAR1A) in odontogenic tumors

doi: 10.1530/erc-15-0094

Figure Lengend Snippet: Figure 1 Ideogram of the cytogenetic bands of chromosome 17 and polymorphic microsatellite markers and representative results of PRKAR1A loss of heterozygosity (LOH). (A) Polymorphic DNA markers located on the long arm of chromosome 17, including D17S1882 (17q24.1), D17S942 (17q24.2), D17S940 (17q24.2), and D17S2182 (17q24.3), which are used to assess LOH at the PRKAR1A genetic locus. (B and C) Loss of the long allele at marker D17S1882 in the mesenchyme of case 3 (B) and in the tumor of case 5 (C) as compared with matched normal DNA. *short allele, **long allele. A full colour version of this figure is available at http://dx.doi.org/10.1530/ ERC-15-0094.

Article Snippet: Immunohistochemical reactions Published by Bioscientifica Ltd. E n d o cr in e -R e la te d C a n ce r were performed using a mouse MAB against the PRKAR1A protein (clone 6C7) (OriGene, Rockville, MD, USA).

Techniques: Marker