Journal: medRxiv

Article Title: Elevated levels of IL-6 in IgA nephropathy patients are induced by an epigenetically-driven mechanism triggered by viral and bacterial RNA

doi: 10.1101/2022.03.05.22271944

Figure Lengend Snippet: (A) ELISA assay showed significant increased levels of IL-6 in IgAN patients with VTRNA2-1/PKR/CREB activated pathway respect to healthy group. (B) An IL-6 increase was found in T-IgAN patients with VTRNA2-1/PKR/CREB activated pathway compared to TP group, even if not statistically significant. Both the levels of pPKR (C) and pCREB (D) significantly correlated with IL-6 levels in IgAN patients (r=0.97, p= 0.0006 and r=0.89, p=0.0064, respectively). Data are representative of 8 independent experiments (means ±SEM; * p-value < 0.05).

Article Snippet: Colorimetric Cell-Based ELISA assays were used to detect the levels of CREB/pCREB (CREB (Phospho-Ser142) Aviva Systems Biology, USA), and PKR/pPKR (PKR (Phospho-Thr258) Aviva Systems Biology, USA).

Techniques: Enzyme-linked Immunosorbent Assay

Journal: iScience

Article Title: Peripheral amylin modulation rebalances brain glycolysis and Tau-Ser214 phosphorylation via cAMP-PKA signaling

doi: 10.1016/j.isci.2026.115157

Figure Lengend Snippet: ATF4 signaling, glucose transporters and amino acid responses in low vs. high brain amylin under metabolic stress (A and B) Top seven canonical pathways from ingenuity pathways analysis (A) and (B) top five GO biological processes enriched in hA i−OFF vs. hA ON brains. (C) Brain ATF4 levels in hA ON , hA i−OFF , hA OFF , and hA i−ON mice. Main effect of animal model, p = 0.0049. (D) Aspartate to asparagine ratio in brain tissues from hA ON , hA i−OFF , hA OFF , and hA i−ON mice. Main effect of animal model, p < 0.0001. (E) Correlation between brain amylin and ATF4, with mice stratified by normal (126.1 ± 3.15 mg/dL) or high (154.4 ± 5.39 mg/dL) glucose. (F–I) Statistical modeling comparing molecular outcomes (cAMP and ATF4) of changes in plasma amylin vs. insulin levels in same mice. (J and K) GLUT1 and GLUT3 levels in brain tissues from hA ON , hA i−OFF , hA OFF , and hA i−ON mice as a function of blood glucose levels. Measurements were performed in duplicate. Results are shown as individual data points and/or mean ± s.e.m. and statistical analyses were performed using One-way ANOVA followed by Tukey’s multiple-comparisons test (C and D).

Article Snippet: ATF4 , Proteintech , KE00147.

Techniques: Animal Model, Clinical Proteomics

Journal: iScience

Article Title: Peripheral amylin modulation rebalances brain glycolysis and Tau-Ser214 phosphorylation via cAMP-PKA signaling

doi: 10.1016/j.isci.2026.115157

Figure Lengend Snippet: Pancreatic amylin regulation reduces amylin-cAMP-PKA overactivation and tau-Aβ coupling: molecular evidence (A and B) Representative confocal microscopy images comparing neuronal pS214-tau in cortical sections from hA ON vs. hA OFF mice ( n = 5 slices/mouse from n = 3 mice/group). (C–F) In the same mice as in , , , , , , and , average brain amylin level vs. average pS214-tau (C) and average brain tissue PKA activity vs. average pS214-tau (D) along with correlation analyses between brain tissue Aβ 42 and pT31-tau in hA ON vs. hA i−OFF mice (E) and hA OFF vs. hA i−ON mice (F). (G) Heat maps comparing the brain tissue levels of inflammatory cytokines (IL-1β, IL-6, TNF-α, IFN-γ, and CXCL1) in hA i−OFF mice vs. hA ON littermates. (H) Same as in (G) for hA i−ON mice compared to hA OFF littermates. (I) In same mice, principal component (PC) analysis of amylin, AD markers (Aβ 40, Aβ 42 , pTau, and total tau), neuroinflammation (IL-1β, IL-6, TNF-α, IFN-γ, and CXCL1), and metabolic covariates (glucose, G6P, cAMP, and ATF4). (J) PC loading plot suggesting that clustering is largely driven by contributions of amylin, cAMP and Aβ covariates to the main principal component (PC1), whereas G6P and tau pathology drive the variation on PC2. (K) Schematic diagram (using BioRender): toggling amylin secretion under pre-diabetic stress bidirectionally regulates brain glucose metabolism and memory. Excess amylin amplifies amylin-cAMP-PKA signaling, suppresses astrocytic glycolysis and promotes tau phosphorylation, tau-Aβ coupling and neuroinflammation, whereas restricting brain amylin preserves metabolic function and memory.

Article Snippet: ATF4 , Proteintech , KE00147.

Techniques: Confocal Microscopy, Activity Assay, Phospho-proteomics

Journal: Neurochemical Research

Article Title: Morin Improves Cognitive Deficits in an in Vivo Model of Vascular Dementia by Modulating the N-methyl-D-aspartate Receptor Signaling Pathways

doi: 10.1007/s11064-026-04717-7

Figure Lengend Snippet: Morin modulated the expression of NMDA receptors in the hippocampus of VaD rats. a the expression levels of NR1 ; b the expression levels of NR2A ; c the expression levels of NR2B ; d the expression levels of NR1 protein; e the expression levels of NR2A protein; f the expression levels of NR2B protein; g protein levels of p-CREB; h protein levels of p-CAMK2A; i protein levels of p-CAMK2D. Protein levels of NR1, NR2A, and NR2B were quantified by ELISA. Data are presented as mean ± SD ( n = 8 per group). Statistical analysis was performed by one-way ANOVA with Tukey’s post-hoc test (data met assumptions of normality and homoscedasticity)/Kruskal-Wallis with Dunn’s test (data did not meet assumptions). * indicates a significant difference from the Sham group; # indicates a significant difference 2VO group; *# indicates a significant difference from both the Sham and 2VO groups, with a p-value of less than 0.05 considered statistically significant

Article Snippet: The phosphorylation status of another key NMDAR downstream effector, CREB at Ser133 (p-CREB), was quantified in hippocampal homogenates using a commercial ELISA kit (Phospho-CREB [Ser133] ELISA Kit, Boster Bio, #EKC2382).

Techniques: Expressing, Enzyme-linked Immunosorbent Assay