anti kcc3 antibody if  (Bioss)

Journal: iScience

Article Title: DNA repair factor KAT5 prevents ischemic acute kidney injury through glomerular filtration regulation

doi: 10.1016/j.isci.2021.103436

Figure Lengend Snippet: KAT5-mediated increase in KCC3 expression is associated with the preconditioning effect via attenuation of TGF (A) Real-time RT-PCR analysis of KCC3 (Slc12a6), KCC4 (Slc12a7), and Slc26a6 expression in the kidney cortex of wild-type control mice following IR according to the experimental protocol as shown in Figure 1 (n = 3–5 per groups). (B) Real-time RT-PCR analysis of KCC3 (Slc12a6), KCC4 (Slc12a7), and Slc26a6 expression in the kidney cortex of KOs and controls. (C) Real-time RT-PCR analysis of KCC3 expression in the kidney cortex following IR injury with preconditioning 12 weeks prior to the IR. (D) Real-time RT-PCR analysis of KCC3 expression in the kidney cortex following IR injury in KOs. (E) Representative photomicrographs of immunofluorescence double staining of KCC3 (green)/AQP1 (red) in kidney cortex. Scale bar, 50 μm. (F) (Left) Representative photomicrographs of immunofluorescence (IF) double staining of KCC3 (green)/AQP1 (red) 1 day after IR with or without KCC3 plasmid injection. (Right) Real-time RT-PCR analysis of KCC3 in the kidney cortex of 1 day after IR with or without KCC3 plasmid injection. (G) Serum creatinine and UN of WT mice 1 day after IR with or without KCC3 plasmid injection. (H) (Left panels) Representative photographs of immunofluorescent double staining of γH2AX (green) and AQP1 (red) in human biopsy samples with non-AKI or AKI. AKI, acute kidney injury. (Right panel) The number of γH2AX-positive cells in AQP1-positive PT cells. (I) (Left panels) Representative photographs of immunofluorescent staining of KCC3 (green) and AQP1 (red) in human biopsy samples with non-AKI or AKI. (Right panel) The ratio of KCC3 positive area/cortex except glomerular area. (J) (Left panel) Correlation between eGFR and the ratio of KCC3 positive area/cortex except glomerular area. (Right panel) Correlation between the number of γH2AX and AQP1 double-positive cells and the ratio of KCC3 positive area/cortex except glomerular area. The clinical data presented in . Scale bar, 50 μm. Data represent the mean ± SEM. ∗p < 0.05, ∗∗p < 0.01 versus controls, ##p < 0.01 versus the respective groups.

Article Snippet: Anti-KCC3 antibody (IF) , Bioss , Cat# BS-11952R.

Techniques: Expressing, Quantitative RT-PCR, Immunofluorescence, Double Staining, Plasmid Preparation, Injection, Staining

Journal: iScience

Article Title: DNA repair factor KAT5 prevents ischemic acute kidney injury through glomerular filtration regulation

doi: 10.1016/j.isci.2021.103436

Figure Lengend Snippet: KAT5 regulates KCC3 expression through an epigenetic mechanism In vitro analysis using cultured human tubular epithelial cells (HK2 cells). (A) Experimental protocol. HK2 cells were treated with antimycin A (AMA) for 1 h and analyzed 24 h after AMA treatment without (Ax1) or with (Ax2) the pretreatment of AMA 72 h prior to the injury. pCMV-KAT5 expression plasmid was transfected to AMA-treated HK2 cells 72 h after AMA treatment and analyzed 24 h after transfection (Ax1+KAT5). KAT5 knockdown experiment was performed using siRNA before the AMA treatment (siRNA + Ax2). (B) Time course of ATP levels after AMA treatment. Decreased ATP levels after AMA treatment gradually recovered and reached plateau almost 8 h after starting the treatment. (C) KAT5 expression of indicated groups: (left) real-time RT-PCR; (right) western blots. (D and E) KCC3 expression of indicated groups: (left) real-time RT-PCR; (right) western blots. (F) Chromatin accessibility assay of the KCC3 promoter region. (G) Quantitative ChIP assay performed using IgG and KAT5 antibodies. Data was normalized to input fraction, and the results were relative to that of IgG which was set 1. Data represent the mean ± SEM. ∗p < 0.05, ∗∗p < 0.01 versus controls. #p < 0.05 versus the respective groups, ##p < 0.01 versus the respective groups.

Article Snippet: Anti-KCC3 antibody (IF) , Bioss , Cat# BS-11952R.

Techniques: Expressing, In Vitro, Cell Culture, Plasmid Preparation, Transfection, Quantitative RT-PCR, Western Blot

Journal: iScience

Article Title: DNA repair factor KAT5 prevents ischemic acute kidney injury through glomerular filtration regulation

doi: 10.1016/j.isci.2021.103436

Figure Lengend Snippet: A scheme of the ischemic preconditioning effect via KAT5 (Upper panel) IR injury causes proximal tubular (PT) cell damage, which induces a decrease in KCC3 expression as well as KAT5-mediated DNA damage repair, leading reduced Cl − reabsorption in PT cells and increased Cl − delivery to macula densa. It triggers activation of TGF via elevated adenosine concentration, which causes vasoconstriction of afferent arterioles and decreased GFR. (Lower panel) When IR injury occurs following preconditioning, promoted KAT5 expression causes accelerated DNA damage repair and protection from apoptosis as well as restoration of KCC3 expression through epigenetic mechanism, which induces increased Cl − reabsorption in PT cells and reduced Cl − delivery to macula densa. It causes attenuation of TGF activation with reduced adenosine concentration and maintained GFR. IR: ischemic reperfusion, PC: preconditioning, GFR: glomerular filtration rate.

Article Snippet: Anti-KCC3 antibody (IF) , Bioss , Cat# BS-11952R.

Techniques: Expressing, Activation Assay, Concentration Assay, Filtration

Journal: iScience

Article Title: DNA repair factor KAT5 prevents ischemic acute kidney injury through glomerular filtration regulation

doi: 10.1016/j.isci.2021.103436

Figure Lengend Snippet:

Article Snippet: Anti-KCC3 antibody (IF) , Bioss , Cat# BS-11952R.

Techniques: Recombinant, Transfection, Lysis, Microarray, Expressing, Software

Journal: iScience

Article Title: DNA repair factor KAT5 prevents ischemic acute kidney injury through glomerular filtration regulation

doi: 10.1016/j.isci.2021.103436

Figure Lengend Snippet:

Article Snippet: Anti-KCC3 antibody (IF) , Bioss , Cat# BS-11952R.

Techniques: Recombinant, Transfection, Lysis, Microarray, Expressing, Software