rabbit polyclonal antibodies against enolase  (Cell Signaling Technology Inc)

Journal: International Journal of Molecular Sciences

Article Title: Proteomic Study Identifies Glycolytic and Inflammation Pathways Involved in Recurrent Otitis Media

doi: 10.3390/ijms21239291

Figure Lengend Snippet: Dysregulated proteins identified by mass spectrometry in RAOM compared to ATH.

Article Snippet: After protein transfer the membrane was blocked by treatment with 5% defatted milk in TBS-tween 20 and incubated overnight at 4 °C with 1:700 diluted primary rabbit polyclonal antibody against Transitional endoplasmic reticulum ATPase (VCP (Sigma-Aldrich; Merck KGaA, Darmstadt, Germany)), and with 1:800 diluted primary rabbit polyclonal antibody against Alpha-enolase (ENO1 (Sigma-Aldrich; Merck KGaA, Darmstadt, Germany)).

Techniques: Mass Spectrometry, Standard Deviation

Journal: International Journal of Molecular Sciences

Article Title: Proteomic Study Identifies Glycolytic and Inflammation Pathways Involved in Recurrent Otitis Media

doi: 10.3390/ijms21239291

Figure Lengend Snippet: Representative Western blotting analysis of VCP and ENO1 in ATH and RAOM. The intensities of the immunostained bands were normalized with the protein intensities measured by Red Ponceau from the same blot. The bar graph shows the relative quantitation (band density) of VCP and ENO1 in ATH and RAOM. Results are shown as a histogram (* indicates p < 0.05, while ** indicates p < 0.01 statistical difference) and each bar represents mean ± standard error.

Article Snippet: After protein transfer the membrane was blocked by treatment with 5% defatted milk in TBS-tween 20 and incubated overnight at 4 °C with 1:700 diluted primary rabbit polyclonal antibody against Transitional endoplasmic reticulum ATPase (VCP (Sigma-Aldrich; Merck KGaA, Darmstadt, Germany)), and with 1:800 diluted primary rabbit polyclonal antibody against Alpha-enolase (ENO1 (Sigma-Aldrich; Merck KGaA, Darmstadt, Germany)).

Techniques: Western Blot, Quantitation Assay

Journal: International Journal of Molecular Sciences

Article Title: Proteomic Study Identifies Glycolytic and Inflammation Pathways Involved in Recurrent Otitis Media

doi: 10.3390/ijms21239291

Figure Lengend Snippet: Schematic diagram displaying putative pathogenic mechanisms In ROAM (left side): bacterial infections (1) triggers neutrophils degranulation (2), but this is not effective due to lower PKM and HBB levels (black arrow downwards). Defective bacterial clearing (3) causes chronic infection (through formation of biofilm) in the median ear, with a consequent increase of NETs formation (4), due to higher proteasome activity provoked by increased VCP and CAP1 levels (black arrow upwards). Chronic bacterial infection of ear tissue (5) (red) establishes a milieu in which recurrent infections (6) are facilitated. In ATH (right side), TH-17 cells are activated (1) and switch to glycolytic metabolism (gray square), with increased levels of ALDOC and ENO1 (black arrow upwards). Activation of these cells causes increasing Interleukin-17 (IL-17) (2) production. This cytokine (3) could drive epithelial expression of granulopoietic and chemotactic factors such as Interleukin-8 (IL-8), Granulocyte Colony-Stimulating Factor (G-CSF) and Macrophage Inflammatory Proteins (MIP) (big arrow downwards) that could induce swelling of adenoidal tissue (4) (green), followed by upper airway obstruction. The imperfect oxygen intake could then trigger a self-sustained cycle (5) (dotted arrow), inducing furthermore a switch toward glycolytic metabolism (created with BioRender.com).

Article Snippet: After protein transfer the membrane was blocked by treatment with 5% defatted milk in TBS-tween 20 and incubated overnight at 4 °C with 1:700 diluted primary rabbit polyclonal antibody against Transitional endoplasmic reticulum ATPase (VCP (Sigma-Aldrich; Merck KGaA, Darmstadt, Germany)), and with 1:800 diluted primary rabbit polyclonal antibody against Alpha-enolase (ENO1 (Sigma-Aldrich; Merck KGaA, Darmstadt, Germany)).

Techniques: Infection, Activity Assay, Activation Assay, Expressing