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Proteintech non fat milk
Non Fat Milk, supplied by Proteintech, used in various techniques. Bioz Stars score: 95/100, based on 176 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/vdac1/VDAC1%2F2+Antibody/pmc12993230-67-5-20
Average 95 stars, based on 176 article reviews

non fat milk - by Bioz Stars, 2026-09

95/100 stars

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Incubation:

Article Title: Ceritinib Induces Mitochondrial Fragmentation in Thyroid Cancer Cells by Targeting Drp-1.
Article Snippet: Mitochondrial dynamics play a crucial role in thyroid cancer progression by regulating apoptosis, metabolism, and oxidative stress.. Ceritinib, a tyrosine kinase inhibitor, shows potential anticancer effects; however, its impact on mitochondrial function in thyroid cancer remains obscure.. Herein, we aim to investigate the impact of ceritinib on the mitochondrial functionality in TPC‐1 thyroid carcinoma cells and the underlying mechanism.

Article Title: Disruption of sphingolipid metabolism triggers lung vascular inflammation and aging-like changes under hypoxia through VDAC1-mediated mitochondrial DNA release.
Article Snippet: With the growing demand for travel and diverse occupational activities, people now have more opportunities to be exposed to high-altitude environments.. Low atmospheric pressure and hypobaric hypoxia pose significant health challenges to individuals in high-altitude areas [1].. Hypoxia is a primary driver of physiological and pathological changes [2].

Article Title: Hematopoietic Cell Kinase Promotes Cerebral Ischemic Injury and Mitochondrial Dysfunction via p38 Activation in Ischemic Stroke.
Article Snippet: Ischemic stroke is a leading cause of death and permanent disability worldwide.. There is an urgent need to identify novel therapeutic targets.. Through bioinformatics analysis of Gene Expression Omnibus (GEO) datasets and the construction of protein–protein interaction (PPI) network, we identified hematopoietic cell kinase (HCK) as a key regulatory factor in ischemic stroke.

Western Blot:

Article Title: Parkinson's disease-associated PLA2G6 protects IP3R1 protein to control ER-mitochondria tethering and Ca 2+ transfer.
Article Snippet: Immunoblotting signals were detected using a chemiluminescence reagent (Invitrogen, 32106) and quantified via ImageJ. .. The antibodies used for immunoblotting included PLA2G6 (Abcam, ab259950, 1:1000), GRP75 (Santa Cruz, sc-133137, 1:500), VDAC1 (Proteintech, 55259-1-AP, 1:1000), Sigma1R (CST, 61994, 1:1000), COX IV (ABclonal, A11631, 1:1000), Calreticulin (ABclonal, A20986, 1:1000), IP3R1 (ABclonal, A21471, 1:1000), MFN2 (Abcam, ab124773, 1:1000), TOM40 (ABclonal, A3213, 1:1000), TOM20 (CST, 42406S, AR TI CL E IN P RE SS 1:1000), TIM23 (Proteintech, 11123-1-AP, 1:1000), ubiquitin (Santa Cruz, sc-8017, 1:500), ERLIN2 (ABclonal, A0781, 1:1000), NDUFA9 (ABclonal, A3196, 1:1000), pS129 (CST, 23706, 1:1000), GSK3β (ABclonal, A2081, 1:1000), DJ-1 (Proteintech, 68915-6-Ig, 1:1000), GFP (HUABIO, ET1607-31, 1:2000), LAMP1 (Santa Cruz, sc-20011, 1:500) and GAPDH (Proteintech, 60004-1-Ig, 1:5000). .. For Co-IP assays, proteins were extracted from cells and mouse ventral midbrains using 1% NP-40 lysis buffer (Beyotime, P0013F) supplemented with a protease inhibitor cocktail (MCE, HY-K0010) on ice for 30 minutes.

Ubiquitin Proteomics:

Article Title: USP30 alleviates intestinal ischemia-reperfusion injury by deubiquitinating MFN2 mediating the mitochondrial endoplasmic reticulum pathway.
Article Snippet: Intestinal ischemia-reperfusion (IIR) injury can cause intestinal barrier damage, systemic inflammatory response, and high mortality.. The key mechanism is the disorder of the mitochondrial-endoplasmic reticulum network.. Ubiquitin-specific peptidase 30 (USP30), located on the outer mitochondrial membrane, can reverse the partial ubiquitination of Parkin substrates or completely remove the ubiquitin chain to maintain mitochondrial function.

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$SS-31 reduces radiation-induced mitochondrial-related apoptosis proteins in H9C2 cells and hiPSC-CMs . (A, C) Representative western blot images showing the expression of mitochondrial apoptosis-related proteins Bax and Bcl-2 in H9C2 cells (A) and hiPSC-CMs (C). (B, D) Quantification of corresponding protein expression levels, n = 3–10. Experimental groups include control, SS-31 treatment, 10 Gy radiation, and 10 Gy radiation plus SS-31 treatment, as indicated in the figure. (E) Representative western blot images of cytochrome c (Cyt c) distribution. Protein levels were analyzed in isolated mitochondrial and cytosolic fractions. (F) Quantitative analysis of Cyt c expression. Cyt c levels were normalized to VDAC1 for the mitochondrial fraction and β-actin for the cytosolic fraction. n = 3–4. All data are presented as mean ± SEM. * P < 0.05 vs control; ** P < 0.01 vs control; # P < 0.05 vs irradiation; ## P < 0.01 vs irradiation.$

Journal: Journal of Radiation Research

Article Title: Mitochondrial-targeted SS-31 peptide attenuates radiation-induced cardiomyocyte senescence

doi: 10.1093/jrr/rrag048

Figure Lengend Snippet: SS-31 reduces radiation-induced mitochondrial-related apoptosis proteins in H9C2 cells and hiPSC-CMs . (A, C) Representative western blot images showing the expression of mitochondrial apoptosis-related proteins Bax and Bcl-2 in H9C2 cells (A) and hiPSC-CMs (C). (B, D) Quantification of corresponding protein expression levels, n = 3–10. Experimental groups include control, SS-31 treatment, 10 Gy radiation, and 10 Gy radiation plus SS-31 treatment, as indicated in the figure. (E) Representative western blot images of cytochrome c (Cyt c) distribution. Protein levels were analyzed in isolated mitochondrial and cytosolic fractions. (F) Quantitative analysis of Cyt c expression. Cyt c levels were normalized to VDAC1 for the mitochondrial fraction and β-actin for the cytosolic fraction. n = 3–4. All data are presented as mean ± SEM. * P < 0.05 vs control; ** P < 0.01 vs control; # P < 0.05 vs irradiation; ## P < 0.01 vs irradiation.

Article Snippet: Membranes were blocked with 1% BSA or 1% non-fat milk in tris-buffered saline with Tween 20 (TBST) for 1 hour at room temperature, followed by overnight incubation at 4°C with the following primary antibodies: TNFα (MILLIPORE, AB1837P, 1:2000), IL-6 (Sigma, SAB5700632, 1:2000), p16 (Invitrogen, PA5–20379, 1:2000), p21 (Invitrogen, 14–6715-81, 1:2000), Bax (Invitrogen MA5–14003, 1:1000), Bcl-2 (Abcam, ab196495, 1:2000), Lamin B1 (CST, 13435, 1:2000), Caspase 7 (CST, 9492S, 1:2000), Caspase 8 (CST, 4790S, 1:2000), Caspase 9 (CST, 9508S, 1:1000), Cytochrome c (Medchemexpress, HY- P80102 , 1:3000), VDAC1 (Medchemexpress, HY- P80369 , 1:3000), OxPhos Rodent WB Antibody Cocktail (Invitrogen, 45–8099, 1:2000), or β-actin (Bio-techne, MAB8929, 1:5000).

Techniques: Western Blot, Expressing, Control, Isolation, Irradiation

$NAD + restoration prevents VDAC1 oligomerization‐mediated mtDNA leakage and cGAS/STING pathway activation in AD. (A, B) Enzymatic activities of isocitrate dehydrogenase (ICDH) (A; n = 6 per group) and α‐ketoglutarate dehydrogenase (α‐KGDH) (B; n ≥5 per group) in mitochondrial‐enriched fractions from cerebral vessel‐enriched fractions of APPwt, APPwt + NR, APPtg, and APPtg + NR mice. (C) Citrate accumulation in mitochondrial‐enriched fractions from cerebral vessel‐enriched fractions of APP/PS1 mice, which was significantly increased compared to APPwt controls and normalized following NAD + restoration ( n ≥5 per group). (D) Immunoblot analysis showing enhanced VDAC1 oligomerization in cerebral vessel‐enriched fractions from APP/PS1 mice, which was markedly suppressed by NR treatment. (E) Quantification of cytosolic mtDNA fragments ( D‐loop , Non‐Numt , and Cox1 ) in Aβ‐treated bEnd.3 endothelial cells with or without VBIT‐4 (VDAC1 oligomerization inhibitor) treatment ( n = 4 per group). (F) Representative immunoblot showing VDAC1 oligomerization in Aβ‐treated bEnd.3 cells, which was suppressed by NR or VBIT‐4 treatment. (G) Immunoblot and densitometric quantification showing decreased expression of cGAS, STING, and phosphorylated TBK1 and IRF3 following VBIT‐4 treatment in Aβ‐treated bEnd.3 cells ( n = 4 per group). Data are presented as mean ± SEM. Statistical analyses were performed using one‐way ANOVA followed by Tukey's multiple comparisons test. P ‐values are indicated in the figure.$

Journal: Alzheimer's & Dementia

Article Title: Endothelial NAD + depletion drives vascular senescence and neuroinflammation via mtDNA‐cGAS/STING‐CD38 signaling in Alzheimer's disease

doi: 10.1002/alz.71423

Figure Lengend Snippet: NAD + restoration prevents VDAC1 oligomerization‐mediated mtDNA leakage and cGAS/STING pathway activation in AD. (A, B) Enzymatic activities of isocitrate dehydrogenase (ICDH) (A; n = 6 per group) and α‐ketoglutarate dehydrogenase (α‐KGDH) (B; n ≥5 per group) in mitochondrial‐enriched fractions from cerebral vessel‐enriched fractions of APPwt, APPwt + NR, APPtg, and APPtg + NR mice. (C) Citrate accumulation in mitochondrial‐enriched fractions from cerebral vessel‐enriched fractions of APP/PS1 mice, which was significantly increased compared to APPwt controls and normalized following NAD + restoration ( n ≥5 per group). (D) Immunoblot analysis showing enhanced VDAC1 oligomerization in cerebral vessel‐enriched fractions from APP/PS1 mice, which was markedly suppressed by NR treatment. (E) Quantification of cytosolic mtDNA fragments ( D‐loop , Non‐Numt , and Cox1 ) in Aβ‐treated bEnd.3 endothelial cells with or without VBIT‐4 (VDAC1 oligomerization inhibitor) treatment ( n = 4 per group). (F) Representative immunoblot showing VDAC1 oligomerization in Aβ‐treated bEnd.3 cells, which was suppressed by NR or VBIT‐4 treatment. (G) Immunoblot and densitometric quantification showing decreased expression of cGAS, STING, and phosphorylated TBK1 and IRF3 following VBIT‐4 treatment in Aβ‐treated bEnd.3 cells ( n = 4 per group). Data are presented as mean ± SEM. Statistical analyses were performed using one‐way ANOVA followed by Tukey's multiple comparisons test. P ‐values are indicated in the figure.

Article Snippet: To specifically inhibit VDAC1 oligomerization, bEnd.3 cells were pretreated with VBIT‐4 (10 μM; MedChemExpress, #HY‐101966) for 24 h in serum‐reduced medium before being subjected to Aβ challenge.

Techniques: Activation Assay, Western Blot, Expressing