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p62 351 (Bioss)

Name: p62 351
Brand: Bioss
Rating: 94 (15 reviews)

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Bioss p62 351
P62 351, supplied by Bioss, used in various techniques. Bioz Stars score: 94/100, based on 15 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 94 stars, based on 15 article reviews

p62 351 - by Bioz Stars, 2026-02

94/100 stars

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Journal: Autophagy

Article Title: Deregulated MTOR (mechanistic target of rapamycin kinase) is responsible for autophagy defects exacerbating kidney stone development

doi: 10.1080/15548627.2019.1635382

Figure Lengend Snippet: Antibodies used in this study.

Article Snippet: Antibodies Product SQSTM1/p62 (sequestosome 1) MBL, PM045 phosphorylated SQSTM1/p62 (Ser 351; p-SQSTM1) MBL, PM074 LGALS3/galectin-3 (lectin, galactose binding, soluble 3) Santa Cruz Biotechnology, sc-23,938 mono- and polyubiquitinylated conjugated monoclonal antibody (FK2) BML, PW8810 LAMP1 (lysosomal-associated membrane protein 1) Abcam, ab24170 MAP1LC3 (microtubule-associated protein 1 light chain 3) MBL, PM036 TOMM20 (mitochondrial translocase of outer mitochondrial membrane 20) MBL, ab78547 PINK1 (PTEN induced putative kinase 1) Proteintech, 23,274–1-AP PRKN/PARK2/PARKIN (parkin RBR E3 ubiquitin protein ligase) Cell Signaling Technology, #2132 TFEB (transcription factor EB) Proteintech, 13,372–1-AP RPS6KB1/p70S6K Cell Signaling Technology, #9202 phosphorylated RPS6KB1/p70S6K (p-RPS6KB1/p70S6K) Cell Signaling Technology, #9234 ULK1 (unc-51 like kinase 1) Cell Signaling Technology, #8054 Phosphorylated ULK1 (p-ULK1) Cell Signaling Technology, #14,202 LRP2/MEGALIN (low density lipoprotein receptor-related protein 2) Abcam, ab76969 AQP2 (aquaporin 2) Abcam, ab199975 SLC12A3/thiazide-sensitive NaCl Cotransporter Merck KGaA, AB3553 COX4I1 (cytochrome c oxidase subunit 4I1) Proteintech, 11,242–1-AP 4ʹ,6-diamidino-2-phenylindole (DAPI) Dojindo, 340–07971 ACTB/β-actin Sigma-Aldrich, A5316 histone H3 Abcam, ab1791 Open in a separate window Antibodies used in this study.

Techniques: Binding Assay

(A) Representative immunoblotting of LC3-I, LC3-II, phospho-p62 (Ser-351), p62, AMPK and GAPDH are shown. Full-size images of immunoblots are presented in S17-S21 Figs of S1 Data . (B) LC3-II/LC3-I was significantly increased in the PG-LPS group, and this increase was significantly attenuated by TAK-242. ** P < 0.01 vs. Control or # P < 0.05 vs. PG-LPS group by one-way ANOVA followed by the Tukey-Kramer post hoc test. (C) LC3-II expression was significantly increased in the PG-LPS group, and this increase was significantly attenuated by TAK-242. ** P < 0.01 vs. Control or # P < 0.05 vs. PG-LPS group by one-way ANOVA followed by the Tukey-Kramer post hoc test. (D) p62 phosphorylation (Ser-351) was significantly increased in the PG-LPS group, and this increase was significantly attenuated by TAK-242. ** P < 0.01 vs. Control or # P < 0.05 vs. PG-LPS group by one-way ANOVA followed by the Tukey-Kramer post hoc test. (E) p62 expression was similar among the four groups. NS, not significantly different from the Control ( P > 0.05) by one-way ANOVA followed by the Tukey-Kramer post hoc test. (F) AMPK (Thr-172) was significantly increased in the PG-LPS group, and this increase was significantly attenuated by TAK-242. * P < 0.05 vs. Control or ## P < 0.01 vs. PG-LPS group by one-way ANOVA followed by the Tukey-Kramer post hoc test. Data are means ± SD and representative immunoblots are shown. Data shows means ± SD and scattered dots show individual data.

Journal: bioRxiv

Article Title: Role of TLR4 signaling on Porphyromonas gingivalis LPS-induced cardiac dysfunction in mice

doi: 10.1101/2021.10.07.463544

Figure Lengend Snippet: (A) Representative immunoblotting of LC3-I, LC3-II, phospho-p62 (Ser-351), p62, AMPK and GAPDH are shown. Full-size images of immunoblots are presented in S17-S21 Figs of S1 Data . (B) LC3-II/LC3-I was significantly increased in the PG-LPS group, and this increase was significantly attenuated by TAK-242. ** P < 0.01 vs. Control or # P < 0.05 vs. PG-LPS group by one-way ANOVA followed by the Tukey-Kramer post hoc test. (C) LC3-II expression was significantly increased in the PG-LPS group, and this increase was significantly attenuated by TAK-242. ** P < 0.01 vs. Control or # P < 0.05 vs. PG-LPS group by one-way ANOVA followed by the Tukey-Kramer post hoc test. (D) p62 phosphorylation (Ser-351) was significantly increased in the PG-LPS group, and this increase was significantly attenuated by TAK-242. ** P < 0.01 vs. Control or # P < 0.05 vs. PG-LPS group by one-way ANOVA followed by the Tukey-Kramer post hoc test. (E) p62 expression was similar among the four groups. NS, not significantly different from the Control ( P > 0.05) by one-way ANOVA followed by the Tukey-Kramer post hoc test. (F) AMPK (Thr-172) was significantly increased in the PG-LPS group, and this increase was significantly attenuated by TAK-242. * P < 0.05 vs. Control or ## P < 0.01 vs. PG-LPS group by one-way ANOVA followed by the Tukey-Kramer post hoc test. Data are means ± SD and representative immunoblots are shown. Data shows means ± SD and scattered dots show individual data.

Article Snippet: The primary antibodies against p62 (1:1000, #PM045) and phospho-p62 (1:500, Ser-351) (#PM074MS) were purchased from MBL (Nagoya, Japan) and the primary antibodies against NOX4, 1:1000, #ab133303) and NOX2 (1:1000, #ab80508) were purchased from Abcam (Cambridge, UK).

Techniques: Western Blot, Expressing

Journal: Autophagy

Article Title: Deregulated MTOR (mechanistic target of rapamycin kinase) is responsible for autophagy defects exacerbating kidney stone development

doi: 10.1080/15548627.2019.1635382

Figure Lengend Snippet: Antibodies used in this study.

Article Snippet: phosphorylated SQSTM1/p62 (Ser 351; p-SQSTM1) , MBL, PM074.

Techniques: Binding Assay, Membrane, Ubiquitin Proteomics

(A) Confocal immunofluorescence microscopy of liver sections from the indicated mice at 3 months of age using antibodies to p62 and the mitochondrial protein PDH. Boxed regions are enlarged. (B) Cells that show p62 accumulation are quantified. Values represent the average ± SEM (n=3 mice). (C and D) Confocal microscopy of liver sections using antibodies to p62 and PDH along with ubiquitin (C) or LC3 (D). (E) Western blotting of livers isolated from the indicated mice at 3 months of age using antibodies p62 and GAPDH. Quantification of band intensity. Values are average ± SEM (n=3 mice). (F) Summary of the data. (G) Plasmids carrying Su9-mCherry-GFP were delivered to the livers of control, Alb-Drp1KO, and Alb-Drp1Opa1KO mice via hydrodynamic tail vein injection. Four days after injection, the livers were analyzed by confocal microscopy. (H) The mitophagy index was determined by measuring the relative area of mCherry fluorescence that did not overlap with GFP fluorescence over the total area of mCherry fluorescence in each cell using NIH ImageJ software and set 1 in the control mice. Values are average ± SEM (n=3–4 mice). Statistical analysis was performed using Student’s t-test: *p<0.05, **p< 0.01, ***p< 0.001. See also Figure S2.

Journal: Cell metabolism

Article Title: Mitochondrial Stasis Reveals p62-mediated Ubiquitination in Parkin-independent Mitophagy and Mitigates Nonalcoholic Fatty Liver Disease

doi: 10.1016/j.cmet.2018.06.014

Figure Lengend Snippet: (A) Confocal immunofluorescence microscopy of liver sections from the indicated mice at 3 months of age using antibodies to p62 and the mitochondrial protein PDH. Boxed regions are enlarged. (B) Cells that show p62 accumulation are quantified. Values represent the average ± SEM (n=3 mice). (C and D) Confocal microscopy of liver sections using antibodies to p62 and PDH along with ubiquitin (C) or LC3 (D). (E) Western blotting of livers isolated from the indicated mice at 3 months of age using antibodies p62 and GAPDH. Quantification of band intensity. Values are average ± SEM (n=3 mice). (F) Summary of the data. (G) Plasmids carrying Su9-mCherry-GFP were delivered to the livers of control, Alb-Drp1KO, and Alb-Drp1Opa1KO mice via hydrodynamic tail vein injection. Four days after injection, the livers were analyzed by confocal microscopy. (H) The mitophagy index was determined by measuring the relative area of mCherry fluorescence that did not overlap with GFP fluorescence over the total area of mCherry fluorescence in each cell using NIH ImageJ software and set 1 in the control mice. Values are average ± SEM (n=3–4 mice). Statistical analysis was performed using Student’s t-test: *p<0.05, **p< 0.01, ***p< 0.001. See also Figure S2.

Article Snippet: The following primary antibodies were used: Drp1 (611113; BD Biosciences), Opa1 (612607; BD Biosciences), PDH (ab110333; Abcam), GAPDH (MA5-15738; Thermo), Tim44 (612582; BD Transduction Laboratories), Tim23 (611223; BD Transduction Laboratories), Tom20 (sc-11415; Santa Cruz Biotechnology), mitofusin 1 (ab57602; Abcam), mitofusin 2 (ab56889; Abcam), HA (600-401-384; Rockland), VDAC (4866; Cell Signaling Technology), HSP60 (12165; Cell Signaling Technology), E-cadherin (14472; Cell Signaling Technology), p62 (GP-62C; Progen), ubiquitin (z0458; DAKO), phospho-p62 (serine 351) (PM074; MBL International), LC3 (PM036; MBL) and Keap1 (10503-2-AP; Proteintech).

Techniques: Immunofluorescence, Microscopy, Confocal Microscopy, Western Blot, Isolation, Injection, Fluorescence, Software

(A) Liver sections of the indicated mice were analyzed at 3 months of age using confocal microscopy using anti-PDH antibodies. Boxed regions are enlarged. (B) Individual mitochondrial size (n=887 mitochondria from 4 control mice, 654 from 3 Alb-Drp1KO mice, 611 from 3 ParkinKO mice, 640 from 3 Alb-Drp1ParkinKO mice). (C) Average size of mitochondria. Error bars indicate SEM (n=3–4 mice). (D) Confocal microscopy of liver sections using antibodies to p62 and PDH. (E) Cells that showed p62 accumulation are quantified. Values represent the average ± SEM (n=3 mice). (F and H) Confocal microscopy of liver sections using antibodies to p62 and PDH together with ubiquitin (F) or LC3 (H). (G) Cells that showed ubiquitin accumulation are quantified. Values represent the average ± SEM (n=3 mice). (I) Summary of the data. Statistical analysis was performed using Student’s t-test: **p< 0.01, ***p< 0.001. See also Figure S3.

Journal: Cell metabolism

Article Title: Mitochondrial Stasis Reveals p62-mediated Ubiquitination in Parkin-independent Mitophagy and Mitigates Nonalcoholic Fatty Liver Disease

doi: 10.1016/j.cmet.2018.06.014

Figure Lengend Snippet: (A) Liver sections of the indicated mice were analyzed at 3 months of age using confocal microscopy using anti-PDH antibodies. Boxed regions are enlarged. (B) Individual mitochondrial size (n=887 mitochondria from 4 control mice, 654 from 3 Alb-Drp1KO mice, 611 from 3 ParkinKO mice, 640 from 3 Alb-Drp1ParkinKO mice). (C) Average size of mitochondria. Error bars indicate SEM (n=3–4 mice). (D) Confocal microscopy of liver sections using antibodies to p62 and PDH. (E) Cells that showed p62 accumulation are quantified. Values represent the average ± SEM (n=3 mice). (F and H) Confocal microscopy of liver sections using antibodies to p62 and PDH together with ubiquitin (F) or LC3 (H). (G) Cells that showed ubiquitin accumulation are quantified. Values represent the average ± SEM (n=3 mice). (I) Summary of the data. Statistical analysis was performed using Student’s t-test: **p< 0.01, ***p< 0.001. See also Figure S3.

Techniques: Confocal Microscopy

(A) Liver sections of the indicated mice were analyzed at 3 months of age using confocal microscopy with anti-PDH antibodies. Boxed regions are enlarged. (B) Individual mitochondrial size (n=619 mitochondria from 3 control mice, 595 from 3 Alb-Drp1KO mice, 583 from 3 p62KO mice, 614 from 3 Alb-Drp1p62KO mice). (C) Average size of mitochondria. Error bars indicate SEM (n=3 mice). (D) Confocal microscopy of liver sections using antibodies to p62 and PDH along with ubiquitin. The p62 signals disappeared in p62KO and Drp1p62KO hepatocytes, demonstrating the specificity of the anti-p62 antibodies. (E) Confocal microscopy of liver sections using antibodies to ubiquitin and LC3. Dotted lines outline single cells. (F) Quantification of cells showing the accumulation of ubiquitin. Values are average ± SEM (n=3–4 mice). (G) Quantification of cells that show colocalization of ubiquitin to LC3 (n=3 mice). (H) Summary of the data. Statistical analysis was performed using Student’s t-test: *p< 0.05, **p< 0.01.

Journal: Cell metabolism

Article Title: Mitochondrial Stasis Reveals p62-mediated Ubiquitination in Parkin-independent Mitophagy and Mitigates Nonalcoholic Fatty Liver Disease

doi: 10.1016/j.cmet.2018.06.014

Figure Lengend Snippet: (A) Liver sections of the indicated mice were analyzed at 3 months of age using confocal microscopy with anti-PDH antibodies. Boxed regions are enlarged. (B) Individual mitochondrial size (n=619 mitochondria from 3 control mice, 595 from 3 Alb-Drp1KO mice, 583 from 3 p62KO mice, 614 from 3 Alb-Drp1p62KO mice). (C) Average size of mitochondria. Error bars indicate SEM (n=3 mice). (D) Confocal microscopy of liver sections using antibodies to p62 and PDH along with ubiquitin. The p62 signals disappeared in p62KO and Drp1p62KO hepatocytes, demonstrating the specificity of the anti-p62 antibodies. (E) Confocal microscopy of liver sections using antibodies to ubiquitin and LC3. Dotted lines outline single cells. (F) Quantification of cells showing the accumulation of ubiquitin. Values are average ± SEM (n=3–4 mice). (G) Quantification of cells that show colocalization of ubiquitin to LC3 (n=3 mice). (H) Summary of the data. Statistical analysis was performed using Student’s t-test: *p< 0.05, **p< 0.01.

Techniques: Confocal Microscopy

(A) Liver sections of the indicated mice were analyzed at 3 months of age using confocal microscopy using antibodies to PDH, phospho-p62(S351) and p62. Boxed regions are enlarged. 87.9% of p62-positive mitochondria were also positive for the p62 phosphorylation (n=1048 mitochondria). (B) Liver sections were analyzed using confocal microscopy using anti-PDH antibodies, Keap1, and p62. Boxed regions are enlarged. (C) Cells that show Keap1 accumulation on mitochondria are quantified. Values represent the average ± SEM (n=3–5 mice). (D) Western blotting of livers using antibodies to p62, Keap1 and GAPDH. Quantification of band intensity is shown. Values are average ± SEM (n=3 mice). (E) Summary of the data. (F and G) Plasmids carrying WT p62-MffTM or Keap1-interaction-defective (KID) p62-MffTM were delivered to the livers of Alb-Drp1p62KO mice via hydrodynamic tail vein injection. Four days after injection, the livers were analyzed by confocal fluorescence microscopy. Quantification of p62 that overlapped with Keap1 (F) and ubiquitin (G) is shown. Values are average ± SEM (n=3 mice). Statistical analysis was performed using Student’s t-test: *p< 0.05, **p< 0.01, ***p< 0.001.

Journal: Cell metabolism

Article Title: Mitochondrial Stasis Reveals p62-mediated Ubiquitination in Parkin-independent Mitophagy and Mitigates Nonalcoholic Fatty Liver Disease

doi: 10.1016/j.cmet.2018.06.014

Figure Lengend Snippet: (A) Liver sections of the indicated mice were analyzed at 3 months of age using confocal microscopy using antibodies to PDH, phospho-p62(S351) and p62. Boxed regions are enlarged. 87.9% of p62-positive mitochondria were also positive for the p62 phosphorylation (n=1048 mitochondria). (B) Liver sections were analyzed using confocal microscopy using anti-PDH antibodies, Keap1, and p62. Boxed regions are enlarged. (C) Cells that show Keap1 accumulation on mitochondria are quantified. Values represent the average ± SEM (n=3–5 mice). (D) Western blotting of livers using antibodies to p62, Keap1 and GAPDH. Quantification of band intensity is shown. Values are average ± SEM (n=3 mice). (E) Summary of the data. (F and G) Plasmids carrying WT p62-MffTM or Keap1-interaction-defective (KID) p62-MffTM were delivered to the livers of Alb-Drp1p62KO mice via hydrodynamic tail vein injection. Four days after injection, the livers were analyzed by confocal fluorescence microscopy. Quantification of p62 that overlapped with Keap1 (F) and ubiquitin (G) is shown. Values are average ± SEM (n=3 mice). Statistical analysis was performed using Student’s t-test: *p< 0.05, **p< 0.01, ***p< 0.001.

Techniques: Confocal Microscopy, Western Blot, Injection, Fluorescence, Microscopy

(A) Plasmids carrying HA-Rbx1 were delivered to the livers of control, Alb-Drp1KO, Alb-Drp1p62KO, and Alb-Drp1Opa1KO mice via hydrodynamic tail vein injection. Eight hours after injection, the livers were analyzed by confocal immunofluorescence microscopy with antibodies to PDH, HA, and p62. (B) Mouse embryonic fibroblasts were infected with lentiviruses expressing scramble or two independent Rbx1 shRNAs. Six days after infection, whole cell lysates were analyzed by Western blotting with antibodies to Rbx1, PDH and GAPDH. Quantification of band intensity is shown. Values are average ± SEM (n=3 experiments). (C and D) Plasmids expressing the indicated shRNAs along with GFP were introduced to the livers of Alb-Drp1KO mice (C) and Alb-Drp1ParkinKO mice (D) using tail vein injection. Four days after injection, the livers were analyzed by confocal microscopy with antibodies to GFP and HA. Quantification of GFP-positive cells that have the accumulation of ubiquitin is shown. Values are average ± SEM (n=3–4 mice). (E) Model for p62-mediated mitochondrial ubiquitination. p62 recruits Keap1 and Rbx1 to mitochondria to promote ubiquitination in Drp1KO hepatocytes. p62 also connects mitochondria to autophagosomes through interactions with ubiquitin and LC3. Statistical analysis was performed using Student’s t-test: *p<0.05, **p< 0.01. See also Figure S4.

Journal: Cell metabolism

Article Title: Mitochondrial Stasis Reveals p62-mediated Ubiquitination in Parkin-independent Mitophagy and Mitigates Nonalcoholic Fatty Liver Disease

doi: 10.1016/j.cmet.2018.06.014

Figure Lengend Snippet: (A) Plasmids carrying HA-Rbx1 were delivered to the livers of control, Alb-Drp1KO, Alb-Drp1p62KO, and Alb-Drp1Opa1KO mice via hydrodynamic tail vein injection. Eight hours after injection, the livers were analyzed by confocal immunofluorescence microscopy with antibodies to PDH, HA, and p62. (B) Mouse embryonic fibroblasts were infected with lentiviruses expressing scramble or two independent Rbx1 shRNAs. Six days after infection, whole cell lysates were analyzed by Western blotting with antibodies to Rbx1, PDH and GAPDH. Quantification of band intensity is shown. Values are average ± SEM (n=3 experiments). (C and D) Plasmids expressing the indicated shRNAs along with GFP were introduced to the livers of Alb-Drp1KO mice (C) and Alb-Drp1ParkinKO mice (D) using tail vein injection. Four days after injection, the livers were analyzed by confocal microscopy with antibodies to GFP and HA. Quantification of GFP-positive cells that have the accumulation of ubiquitin is shown. Values are average ± SEM (n=3–4 mice). (E) Model for p62-mediated mitochondrial ubiquitination. p62 recruits Keap1 and Rbx1 to mitochondria to promote ubiquitination in Drp1KO hepatocytes. p62 also connects mitochondria to autophagosomes through interactions with ubiquitin and LC3. Statistical analysis was performed using Student’s t-test: *p<0.05, **p< 0.01. See also Figure S4.

Techniques: Injection, Immunofluorescence, Microscopy, Infection, Expressing, Western Blot, Confocal Microscopy

(A) Control Opa1flox/flox mice and Alb-Opa1KO mice were fed a methionine- and choline-deficient diet (MCD diet) for six weeks. Liver sections from these mice were analyzed by confocal microscopy with antibodies to PDH, ubiquitin, and p62. (B) Individual mitochondrial sizes were analyzed (n=602 mitochondria from 3 control mice, 639 from 3 MCD-diet-fed control mice, and 692 from 3 MCD-diet-fed Alb-Opa1KO mice). Red lines indicate averages. (C and D) Cells that show the accumulation of p62 (C) and ubiquitin (D) are quantified. Values represent the average ± SEM (n=3 mice). (E) Liver sections from the same set of mice in (A) were analyzed by confocal microscopy with antibodies to PDH, Keap1, and p62. 86.5% of p62-positive mitochondria were also positive for Keap1 (n=37 mitochondria). (F) Blood levels of ALT were measured before and during administration at 2, 4, and 6 weeks. ALT activity levels for each mouse were normalized to that obtained before MCD diet administration. Values are average ± SEM (n=3–5 mice). Statistical analysis was performed using Student’s t-test: *p< 0.05, **p< 0.01, ***p<0.001.

Journal: Cell metabolism

Article Title: Mitochondrial Stasis Reveals p62-mediated Ubiquitination in Parkin-independent Mitophagy and Mitigates Nonalcoholic Fatty Liver Disease

doi: 10.1016/j.cmet.2018.06.014

Figure Lengend Snippet: (A) Control Opa1flox/flox mice and Alb-Opa1KO mice were fed a methionine- and choline-deficient diet (MCD diet) for six weeks. Liver sections from these mice were analyzed by confocal microscopy with antibodies to PDH, ubiquitin, and p62. (B) Individual mitochondrial sizes were analyzed (n=602 mitochondria from 3 control mice, 639 from 3 MCD-diet-fed control mice, and 692 from 3 MCD-diet-fed Alb-Opa1KO mice). Red lines indicate averages. (C and D) Cells that show the accumulation of p62 (C) and ubiquitin (D) are quantified. Values represent the average ± SEM (n=3 mice). (E) Liver sections from the same set of mice in (A) were analyzed by confocal microscopy with antibodies to PDH, Keap1, and p62. 86.5% of p62-positive mitochondria were also positive for Keap1 (n=37 mitochondria). (F) Blood levels of ALT were measured before and during administration at 2, 4, and 6 weeks. ALT activity levels for each mouse were normalized to that obtained before MCD diet administration. Values are average ± SEM (n=3–5 mice). Statistical analysis was performed using Student’s t-test: *p< 0.05, **p< 0.01, ***p<0.001.

Techniques: Confocal Microscopy, Activity Assay

Journal: Cell metabolism

Article Title: Mitochondrial Stasis Reveals p62-mediated Ubiquitination in Parkin-independent Mitophagy and Mitigates Nonalcoholic Fatty Liver Disease

doi: 10.1016/j.cmet.2018.06.014

Figure Lengend Snippet: KEY RESOURCES TABLE

Techniques: Recombinant, Protease Inhibitor, Modification, Transfection, Activity Assay, Ligation, SYBR Green Assay, Plasmid Preparation, shRNA, Sequencing, Software

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