Journal: Molecular Metabolism

Article Title: α-Parvin promotes glucose uptake and metabolism in skeletal muscle with minimal influence on hepatic insulin sensitivity

doi: 10.1016/j.molmet.2026.102322

Figure Lengend Snippet: Skeletal muscle αParvin improves glucose tolerance in lean mice. A ) Parf/f mice were crossed with human alpha actin-Cre mice to generate deletion of αParvin in skeletal muscle (mParKO). At 6 weeks of age mice were fed chow or HFD for 12 weeks to generate lean and DIO groups. The hyperinsulinemic-euglycemic clamp technique was performed after 12 weeks of diet intervention. B ) immunofluorescence imaging of αParvin was performed on OCT frozen sections of gastrocnemius muscle. The relative intensity was determined using ImageJ software. C ) Terminal body weight after 12 weeks of diet feeding. Intraperitoneal glucose tolerance test (2 g/kg body weight) was performed in D ) lean and E ) DIO mice after 10 weeks of diet feeding. Area under the curve was calculated and presented to the right of each glucose curve. Data are presented as mean ± SE. n = 5–18 mice/group. Panel B and AUC from Panel D and E, T test were conducted to test differences. Panel C, Two-way ANOVA with diet and genotype as factors was run to test for statistical differences. Glucose curves in panel D and E, Two-way repeated measures ANOVA with time and genotype as factors were run. Alpha was p < 0.05. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗∗p < 0.0001.

Article Snippet: To isolate the role of α-Parvin on hepatic and SkM insulin resistance, we developed hepatic (hParKO) and SkM (mParKO) specific α-Parvin knockdown mouse models. α-Parvin f/f mice were generously provided by Dr. Reinhard Fässler [ ]. α-Parvin f/f mice were crossed with mice expressing cre recombinase under control of the albumin promoter (Strain #:003574, Jackson Laboratory [ ]) to target hepatocytes or SkM specific human skeletal actin promoter (Strain#:006149, Jackson Laboratory [ ]) to target myocytes.

Techniques: Immunofluorescence, Imaging, Software

Journal: bioRxiv

Article Title: Targeted DNA methylation editing in vivo

doi: 10.64898/2026.02.26.708277

Figure Lengend Snippet: a . Schematic representation of the breeding strategy and the experimental setting for the characterization of the mouse lines that constitutively express dCas9-DNMT3 under ubiquitous β-actin promoter (ACT; dCas9) or the CAG promoter expression upon tamoxifen treatment (CAG; dCas9). b . Relative to Gapdh dCas9-DNMT3A expression assessed by qPCR in different organs of ACTB+/-; dCas9+/- (n=3-4 per organ) animals expressed as fold change compared to control ACTB-/-; dCas9+/- (n= 2-3 per organ) animals. c . Relative dCas9-DNMT3A assessed by qPCR in different organs of CAG+/-; dCas9+/- (n=3-4 per organ) animals expressed as fold change compared to control CAG-/-; dCas9+/- animals (n=7 per organ). Representative of immunofluorescence staining against EGFP in the striatum and quantification of the number of NeuN and/or EGFP positive neurons in the striatum of ( d ) ACTB+/-; dCas9+/- animals (n=7 and 5 animals for ACTB+/- and ACTB-/- groups, respectively), and ( e ) CAG+/-; dCas9+/- animals (n= 4 animals per group), scale bar: 200um (upper), 50um (lower). f . Schematics of the experimental design for the immunophenotyping of the lymph nodes and spleen in the ACTB+/-; dCas9+/- animals. g . Histograms of EGFP expression in myeloid ( left ) and lymphoid ( right ) cell subpopulations of representative EGFP-negative (null) and EGFP-positive (high) animals. Data is represented as Mean ± S.E.M, unpaired t-tests were performed ( b-e ). P-values are denoted: *p<0.05, **p<0.01, ***p< 0.001, ****p< 0.0001. Non-significant p-values are not represented.

Article Snippet: The original floxed dCas9-DNMT3A strain was bred with mice expressing CreER TM (Stock# 004682) under tamoxifen administration (named CAG-CreER TM ; dCas9-DNMT3A fl/fl ) or mice that were constitutively expressing Cre, utilizing the human β-Actin promoter, ACTB-Cre mice (Stock# 019099), purchased from the Jackson Laboratory.

Techniques: Expressing, Control, Immunofluorescence, Staining

Journal: bioRxiv

Article Title: ADAM17 Deletion Protects Against Type1 Diabetes-Associated Kidney Injury by Modulating Inflammatory and Fibrotic Pathways

doi: 10.64898/2026.02.05.704041

Figure Lengend Snippet: Reduced macrophage infiltration and chemokine-associated inflammation. (A) F4/80 + -macrophages quantified and normalized to glomerular area; (B) representative images of cell infiltration at 200x magnification where grey arrows indicate F4/80 + cells; (C) Ccl5 expression after 20 weeks of follow up; (D) renal Ccl2/MCP-1 gene expression; (E) MCP-1 protein levels normalized to β-actin; (F) representative Western blot images. Data are presented as mean ± SEM. Groups: non-diabetic (NoDB); diabetic (DB); wild-type (WT); Adam17 knockout (ADAM17_KO). *p≤0.05 vs. NoDB.

Article Snippet: A tamoxifen-inducible global Adam17 knockout (Adam17_KO) mouse model was generated by crossing Adam17flox/flox mice (kindly provided by Dr. Raines, Washington University, Saint Louis, MO, USA) with a murine line carrying a Cre recombinase-Estrogen Receptor fusion gene under the control of β-Actin promoter (β-Actin–Cre-ER) obtained from the Jackson Laboratory (Bar Harbor, ME, USA), allowing inducible deletion of Adam17 in all cell types.

Techniques: Expressing, Gene Expression, Western Blot, Knock-Out

Journal: bioRxiv

Article Title: ADAM17 Deletion Protects Against Type1 Diabetes-Associated Kidney Injury by Modulating Inflammatory and Fibrotic Pathways

doi: 10.64898/2026.02.05.704041

Figure Lengend Snippet: Selective modulation of stress-related signaling pathways. (A–B) p-Akt/Akt analysis and representative Western blot images for pAkt and Akt; (C–D) SIRT3 protein normalized to β-actin and representative Western blot images; (E-F) FOXO3 protein bands normalized to β-actin and representative Western blot images. Data are presented as mean ± SEM. Groups: non-diabetic (NoDB); diabetic (DB); wild-type (WT); Adam17 knockout (ADAM17_KO). *p≤0.05 DB vs NoDB.

Article Snippet: A tamoxifen-inducible global Adam17 knockout (Adam17_KO) mouse model was generated by crossing Adam17flox/flox mice (kindly provided by Dr. Raines, Washington University, Saint Louis, MO, USA) with a murine line carrying a Cre recombinase-Estrogen Receptor fusion gene under the control of β-Actin promoter (β-Actin–Cre-ER) obtained from the Jackson Laboratory (Bar Harbor, ME, USA), allowing inducible deletion of Adam17 in all cell types.

Techniques: Protein-Protein interactions, Western Blot, Knock-Out

Journal: bioRxiv

Article Title: ADAM17 Deletion Protects Against Type1 Diabetes-Associated Kidney Injury by Modulating Inflammatory and Fibrotic Pathways

doi: 10.64898/2026.02.05.704041

Figure Lengend Snippet: Global Adam17 deletion limits fibrotic remodeling. (A, C) Fibrosis due to α-SMA staining and quantification on cortex kidney sections as shown in the microphotographs at 200x magnification; (B) α-SMA protein bands compared with GAPDH bands in a representative Western blot image; (D-E) Galectin-3 protein bands normalized to β-actin and representative bands in Western blot images; (F) Microphotographies of Gal3 localized by immunohistochemistry at 100x and 400x magnification. Data are presented as mean ± SEM. Groups: non-diabetic (NoDB); diabetic (DB); wild-type (WT); Adam17 knockout (ADAM17_KO). *p≤0.05 vs. NoDB.

Article Snippet: A tamoxifen-inducible global Adam17 knockout (Adam17_KO) mouse model was generated by crossing Adam17flox/flox mice (kindly provided by Dr. Raines, Washington University, Saint Louis, MO, USA) with a murine line carrying a Cre recombinase-Estrogen Receptor fusion gene under the control of β-Actin promoter (β-Actin–Cre-ER) obtained from the Jackson Laboratory (Bar Harbor, ME, USA), allowing inducible deletion of Adam17 in all cell types.

Techniques: Staining, Western Blot, Immunohistochemistry, Knock-Out