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Bioss anti lonp1 bs4245r
Anti Lonp1 Bs4245r, supplied by Bioss, used in various techniques. Bioz Stars score: 93/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 93 stars, based on 5 article reviews

anti lonp1 bs4245r - by Bioz Stars, 2026-05

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The expression of the UPR mt marker genes was reduced in the human IVDD tissue samples and increased in NP cells after IL-1β treatment. ( A ) The representing graphics of each Pfirrman grade was shown. The specific position of the obtained intervertebral disc tissue was indicated by arrows. ( B ) the UPR mt markers including LONP1, HSPA1A, HSPD1 and CLPP in the human IVDD tissue samples were detected by qRT-PCR. Pfirrman grade I ( n = 4), Pfirrman grade II ( n = 11), Pfirrman grade III ( n = 11), Pfirrman grade IV ( n = 8) and Pfirrman grade I ( n = 5). ( C ) Western blot to the UPR mt including LONP1, HSPA1A, HSPD1 and CLPP in the human IVDD tissue samples. Pfirrman grade I ( n = 3), Pfirrman grade II ( n = 3), Pfirrman grade III ( n = 3) and Pfirrman grade IV ( n = 3). ( D ) The quantitative analysis to the results of Western blot. ( E ) Western blot to mitophagy markers including Parkin, Pink1 and β-actin in the human IVDD tissue samples. Pfirrman grade I ( n = 3), Pfirrman grade II ( n = 3), Pfirrman grade III ( n = 3) and Pfirrman grade IV ( n = 3). ( F ) The quantitative analysis to the results of Western blot. Statistical significance was analyzed by one-way ANOVA followed by a post hoc Tukey’s test. All data were presented as mean ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001

Journal: Cell Biology and Toxicology

Article Title: The mitochondrial UPR induced by ATF5 attenuates intervertebral disc degeneration via cooperating with mitophagy

doi: 10.1007/s10565-024-09854-9

Figure Lengend Snippet: The expression of the UPR mt marker genes was reduced in the human IVDD tissue samples and increased in NP cells after IL-1β treatment. ( A ) The representing graphics of each Pfirrman grade was shown. The specific position of the obtained intervertebral disc tissue was indicated by arrows. ( B ) the UPR mt markers including LONP1, HSPA1A, HSPD1 and CLPP in the human IVDD tissue samples were detected by qRT-PCR. Pfirrman grade I ( n = 4), Pfirrman grade II ( n = 11), Pfirrman grade III ( n = 11), Pfirrman grade IV ( n = 8) and Pfirrman grade I ( n = 5). ( C ) Western blot to the UPR mt including LONP1, HSPA1A, HSPD1 and CLPP in the human IVDD tissue samples. Pfirrman grade I ( n = 3), Pfirrman grade II ( n = 3), Pfirrman grade III ( n = 3) and Pfirrman grade IV ( n = 3). ( D ) The quantitative analysis to the results of Western blot. ( E ) Western blot to mitophagy markers including Parkin, Pink1 and β-actin in the human IVDD tissue samples. Pfirrman grade I ( n = 3), Pfirrman grade II ( n = 3), Pfirrman grade III ( n = 3) and Pfirrman grade IV ( n = 3). ( F ) The quantitative analysis to the results of Western blot. Statistical significance was analyzed by one-way ANOVA followed by a post hoc Tukey’s test. All data were presented as mean ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001

Article Snippet: Lonp1 rabbit polyclonal antibody (Proteintech, Cat No. 15440–1-AP, 1:500, USA) and Clpp mouse polyclonal antibody (Santa Cruz, Cat. No. sc-271284, 1:100, USA) were incubated together.

Techniques: Expressing, Marker, Quantitative RT-PCR, Western Blot

The expression of the UPR mt marker genes was also increased in NP cells after stress. ( A - B ) NP cells were treated with Vehicle or IL-1β (20 ng/ml) for 24 h and 48 h. ( A ) Western blot to the UPR mt markers such as Clpp, Hspa1a, Lonp1, Hspa9, Hspd1 and β-actin in NP cells after IL-1β treatment ( n = 3). ( B ) The quantitative analysis to the results of Western blot. ( C ) Western blot to the UPR mt markers such as Hspd1, Hspa1a, Clpp, Lonp1, and β-actin in NP cells ( n = 3). NP cells were treated with Vehicle or advanced glycation end products (AGEs, 200 μg/mL) for 24 h and 48 h. ( D ) The quantitative analysis to the results of Western blot. ( E ) Western blot to the UPR mt markers such as Hspd1, Hspa1a, Clpp, Lonp1, and β-actin in NP cells ( n = 3). NP cells were treated with Vehicle or hydrogen peroxide (H 2 O 2 , 100 μM) for 24 h and 48 h. ( F ) The quantitative analysis to the results of Western blot. ( G ) Immunofluorescence analysis to the UPR mt makers including Hspa1a and Clpp in NP cells after IL-1β treatment ( n = 3). NP cells were treated with Vehicle or IL-1β (20 ng/ml) for 48 h. Scale bars = 5 μm. Statistical significance was analyzed by one-way ANOVA followed by a post hoc Tukey’s test. All data were presented as mean ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001

Journal: Cell Biology and Toxicology

Article Title: The mitochondrial UPR induced by ATF5 attenuates intervertebral disc degeneration via cooperating with mitophagy

doi: 10.1007/s10565-024-09854-9

Figure Lengend Snippet: The expression of the UPR mt marker genes was also increased in NP cells after stress. ( A - B ) NP cells were treated with Vehicle or IL-1β (20 ng/ml) for 24 h and 48 h. ( A ) Western blot to the UPR mt markers such as Clpp, Hspa1a, Lonp1, Hspa9, Hspd1 and β-actin in NP cells after IL-1β treatment ( n = 3). ( B ) The quantitative analysis to the results of Western blot. ( C ) Western blot to the UPR mt markers such as Hspd1, Hspa1a, Clpp, Lonp1, and β-actin in NP cells ( n = 3). NP cells were treated with Vehicle or advanced glycation end products (AGEs, 200 μg/mL) for 24 h and 48 h. ( D ) The quantitative analysis to the results of Western blot. ( E ) Western blot to the UPR mt markers such as Hspd1, Hspa1a, Clpp, Lonp1, and β-actin in NP cells ( n = 3). NP cells were treated with Vehicle or hydrogen peroxide (H 2 O 2 , 100 μM) for 24 h and 48 h. ( F ) The quantitative analysis to the results of Western blot. ( G ) Immunofluorescence analysis to the UPR mt makers including Hspa1a and Clpp in NP cells after IL-1β treatment ( n = 3). NP cells were treated with Vehicle or IL-1β (20 ng/ml) for 48 h. Scale bars = 5 μm. Statistical significance was analyzed by one-way ANOVA followed by a post hoc Tukey’s test. All data were presented as mean ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001

Techniques: Expressing, Marker, Western Blot, Immunofluorescence

NR promote the level of the UPR mt in NP cells. (A-C) NP cells were divided into 3 groups and treated with 0 ng/ml, 10 ng/ml and 20 ng/ml IL-1β for 48 h respectively. Each group was subdivided into 4 groups and treated with 0, 0.2, 0.5 and 1 mM NR for 6 h respectively after IL-1β treatments. ( A ) Western blot to the UPR mt markers such as Lonp1, Hspa4, Hspd1 and Clpp in NP cells ( n = 3). ( B ) The quantitative analysis to the results of Western blot. ( C ) the UPR mt makers such as Lonp1, Hspa4, Hspd1 and Clpp in NP cells were detected by qRT-PCR ( n = 5). ( D ) Immunofluorescence analysis to the UPR mt makers including Hspa4 and Hspa9 in NP cells after IL-1β treatment ( n = 3). NP cells were divided into 2 groups and treated with 0 ng/ml and 20 ng/ml IL-1β for 48 h respectively. Each group was subdivided into 2 groups and treated with 0 and 1 mM NR for 6 h respectively after IL-1β treatments. Scale bars = 20 μm. ( E ) Cellular ATP level ( F ) NAD + concentrations in NP cells ( n = 5). NP cells were divided into 2 groups and treated with 0 ng/ml and 20 ng/ml IL-1β for 48 h respectively. Each group was subdivided into 2 groups and treated with 0 and 1 mM NR for 6 h respectively after IL-1β treatments. ( G ) The relative expression of Parkin, Pink1, Sqstm1, Clpp, Lonp1 and Hspd1 were determined by Western blot in the mitochondria of NP cells ( n = 3). NP cells were divided into 2 groups and treated with 0 ng/ml and 20 ng/ml IL-1β for 48 h respectively. Each group was subdivided into 2 groups and treated with 0 and 1 mM NR for 6 h respectively after IL-1β treatments. The experimental grouping settings were indicated. ( H ) The quantitative analysis to the results of Western blot. Statistical significance was analyzed by one-way ANOVA followed by a post hoc Tukey’s test. All data were presented as mean ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001

Journal: Cell Biology and Toxicology

Article Title: The mitochondrial UPR induced by ATF5 attenuates intervertebral disc degeneration via cooperating with mitophagy

doi: 10.1007/s10565-024-09854-9

Figure Lengend Snippet: NR promote the level of the UPR mt in NP cells. (A-C) NP cells were divided into 3 groups and treated with 0 ng/ml, 10 ng/ml and 20 ng/ml IL-1β for 48 h respectively. Each group was subdivided into 4 groups and treated with 0, 0.2, 0.5 and 1 mM NR for 6 h respectively after IL-1β treatments. ( A ) Western blot to the UPR mt markers such as Lonp1, Hspa4, Hspd1 and Clpp in NP cells ( n = 3). ( B ) The quantitative analysis to the results of Western blot. ( C ) the UPR mt makers such as Lonp1, Hspa4, Hspd1 and Clpp in NP cells were detected by qRT-PCR ( n = 5). ( D ) Immunofluorescence analysis to the UPR mt makers including Hspa4 and Hspa9 in NP cells after IL-1β treatment ( n = 3). NP cells were divided into 2 groups and treated with 0 ng/ml and 20 ng/ml IL-1β for 48 h respectively. Each group was subdivided into 2 groups and treated with 0 and 1 mM NR for 6 h respectively after IL-1β treatments. Scale bars = 20 μm. ( E ) Cellular ATP level ( F ) NAD + concentrations in NP cells ( n = 5). NP cells were divided into 2 groups and treated with 0 ng/ml and 20 ng/ml IL-1β for 48 h respectively. Each group was subdivided into 2 groups and treated with 0 and 1 mM NR for 6 h respectively after IL-1β treatments. ( G ) The relative expression of Parkin, Pink1, Sqstm1, Clpp, Lonp1 and Hspd1 were determined by Western blot in the mitochondria of NP cells ( n = 3). NP cells were divided into 2 groups and treated with 0 ng/ml and 20 ng/ml IL-1β for 48 h respectively. Each group was subdivided into 2 groups and treated with 0 and 1 mM NR for 6 h respectively after IL-1β treatments. The experimental grouping settings were indicated. ( H ) The quantitative analysis to the results of Western blot. Statistical significance was analyzed by one-way ANOVA followed by a post hoc Tukey’s test. All data were presented as mean ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001

Techniques: Western Blot, Quantitative RT-PCR, Immunofluorescence, Expressing

Atf5 mediated UPR mt process to regulate NP cells. ( A ) NP cells were transfected with si-NC, si-Atf5-1 and si- Atf5-2 respectively ( n = 3). NP cells were treated with 0 or 20 ng/ml IL-1β treatment for 48 h. The experimental grouping settings were indicated. ( B ) NP cells were transfected with OE-NC, OE-Atf5 ( n = 3). ( C ) Western blot to the UPR mt markers such as Hspd1, Hspa1a, Clpp, Lonp1, and β-actin in NP cells ( n = 3). The experimental grouping settings were indicated. ( D ) The quantitative analysis to the results of Western blot. ( E ) Lysotracker and mitotracker staining were performed to assess the delivery of mitochondria to lysosome. The experimental grouping settings were indicated. ( F ) Flow cytometry to NP cell apoptosis ( n = 3). ( G ) The quantitative analysis to the results of Flow cytometry. The experimental grouping settings were indicated. Scale bars = 5 μm. Statistical significance was analyzed by one-way ANOVA followed by a post hoc Tukey’s test. All data were presented as mean ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001

Journal: Cell Biology and Toxicology

Article Title: The mitochondrial UPR induced by ATF5 attenuates intervertebral disc degeneration via cooperating with mitophagy

doi: 10.1007/s10565-024-09854-9

Figure Lengend Snippet: Atf5 mediated UPR mt process to regulate NP cells. ( A ) NP cells were transfected with si-NC, si-Atf5-1 and si- Atf5-2 respectively ( n = 3). NP cells were treated with 0 or 20 ng/ml IL-1β treatment for 48 h. The experimental grouping settings were indicated. ( B ) NP cells were transfected with OE-NC, OE-Atf5 ( n = 3). ( C ) Western blot to the UPR mt markers such as Hspd1, Hspa1a, Clpp, Lonp1, and β-actin in NP cells ( n = 3). The experimental grouping settings were indicated. ( D ) The quantitative analysis to the results of Western blot. ( E ) Lysotracker and mitotracker staining were performed to assess the delivery of mitochondria to lysosome. The experimental grouping settings were indicated. ( F ) Flow cytometry to NP cell apoptosis ( n = 3). ( G ) The quantitative analysis to the results of Flow cytometry. The experimental grouping settings were indicated. Scale bars = 5 μm. Statistical significance was analyzed by one-way ANOVA followed by a post hoc Tukey’s test. All data were presented as mean ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001

Techniques: Transfection, Western Blot, Staining, Flow Cytometry

Silencing of Pink1 reduced the protective effect of NR on NP cells. ( A ) NP cells were transfected with si-NC, si-Pink1-1 and si-Pink1-2 respectively ( n = 3). NP cells were treated with 0 or 20 ng/ml IL-1β treatment for 48 h. The experimental grouping settings were indicated. ( B ) The quantitative analysis to the results of Western blot. ( C ) Western blot to the UPR mt markers including Lonp1, Hspd1, Clpp and β-actin in NP cells ( n = 3). The experimental grouping settings were indicated. ( D ) The quantitative analysis to the results of Western blot. ( E ) Western blot to Bcl-2, Bax, Cleaved-caspase 3, Cleaved-caspase 9, LC3-II and β-actin in NP cells ( n = 3). ( F ) The quantitative analysis to the results of Western blot. ( G ) TUNEL assays to NP cell apoptosis ( n = 3). The experimental grouping settings were indicated. NP cells were transfected with si-NC or si-Pink1, treated with 0 ng/ml and 20 ng/ml IL-1β for 48 h and then treated with 0 and 1 mM NR for 6 h. The experimental grouping settings were indicated. Scale bars = 50 μm. ( H ) The quantitative analysis to the results of TUNEL assays. Statistical significance was analyzed by one-way ANOVA followed by a post hoc Tukey’s test. All data were presented as mean ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001

Journal: Cell Biology and Toxicology

Article Title: The mitochondrial UPR induced by ATF5 attenuates intervertebral disc degeneration via cooperating with mitophagy

doi: 10.1007/s10565-024-09854-9

Figure Lengend Snippet: Silencing of Pink1 reduced the protective effect of NR on NP cells. ( A ) NP cells were transfected with si-NC, si-Pink1-1 and si-Pink1-2 respectively ( n = 3). NP cells were treated with 0 or 20 ng/ml IL-1β treatment for 48 h. The experimental grouping settings were indicated. ( B ) The quantitative analysis to the results of Western blot. ( C ) Western blot to the UPR mt markers including Lonp1, Hspd1, Clpp and β-actin in NP cells ( n = 3). The experimental grouping settings were indicated. ( D ) The quantitative analysis to the results of Western blot. ( E ) Western blot to Bcl-2, Bax, Cleaved-caspase 3, Cleaved-caspase 9, LC3-II and β-actin in NP cells ( n = 3). ( F ) The quantitative analysis to the results of Western blot. ( G ) TUNEL assays to NP cell apoptosis ( n = 3). The experimental grouping settings were indicated. NP cells were transfected with si-NC or si-Pink1, treated with 0 ng/ml and 20 ng/ml IL-1β for 48 h and then treated with 0 and 1 mM NR for 6 h. The experimental grouping settings were indicated. Scale bars = 50 μm. ( H ) The quantitative analysis to the results of TUNEL assays. Statistical significance was analyzed by one-way ANOVA followed by a post hoc Tukey’s test. All data were presented as mean ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001

Techniques: Transfection, Western Blot, TUNEL Assay

NR might attenuate the IVDD of rat. Rats were divided randomly into sham operation group and unbalanced dynamic group. Sham operation groups were subdivided into NR (-) and NR ( +) (400 mg/kg/day) group. Per group included six rats. ( A ) Schematic diagram of animal experimental schedule. ( B ) T2-weighted MRI of IVDD models from each group at 16 weeks ( n = 6). ( C ) Pfirrmann MRI scores for T2-weighted MRIs of IVDD models from each group at 4 months ( n = 30). Each rat including L1-2, L2-3, L3-4, L4-5 and L5-6 were evaluated by Pfirrmann MRI scores according to T2-weighted MRIs ( n = 30). Each rat had a total of five segments of intervertebral discs evaluated by Pfirrmann MRI scores according to T2-weighted MRIs. There were six rats in each group, with a total of 30 segments intervertebral discs. ( D ) Safranin O-fast green staining showed the structure of the intervertebral disc ( n = 6). Scale bars = 200 μm and 2.5 μm. ( E ) Western blot to Bcl-2, Bax, Cleaved-caspase 9, Nqo1, Homx1 and β-actin in the tissue samples of rat IVDD ( n = 3). ( F ) The quantitative analysis to the results of Western blot. ( G ) Western blot to the UPR mt markers such as Clpp, Hspa1a, Lonp1 and mitophagy markers such as Pink1, Parkin, sqstm1 and β-actin in the tissue samples of rat IVDD ( n = 3). ( H ) The quantitative analysis to the results of Western blot. ( I ) Immunohistochemical examination of the UPR mt markers including Clpp and Lonp1 in the tissue samples of rat IVDD ( n = 6). Scale bars = 200 μm and 2.5 μm. ( J ) The quantitative analysis to the results of Immunohistochemistry.Statistical significance was analyzed by one-way ANOVA followed by a post hoc Tukey’s test. All data were presented as mean ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001

Journal: Cell Biology and Toxicology

Article Title: The mitochondrial UPR induced by ATF5 attenuates intervertebral disc degeneration via cooperating with mitophagy

doi: 10.1007/s10565-024-09854-9

Figure Lengend Snippet: NR might attenuate the IVDD of rat. Rats were divided randomly into sham operation group and unbalanced dynamic group. Sham operation groups were subdivided into NR (-) and NR ( +) (400 mg/kg/day) group. Per group included six rats. ( A ) Schematic diagram of animal experimental schedule. ( B ) T2-weighted MRI of IVDD models from each group at 16 weeks ( n = 6). ( C ) Pfirrmann MRI scores for T2-weighted MRIs of IVDD models from each group at 4 months ( n = 30). Each rat including L1-2, L2-3, L3-4, L4-5 and L5-6 were evaluated by Pfirrmann MRI scores according to T2-weighted MRIs ( n = 30). Each rat had a total of five segments of intervertebral discs evaluated by Pfirrmann MRI scores according to T2-weighted MRIs. There were six rats in each group, with a total of 30 segments intervertebral discs. ( D ) Safranin O-fast green staining showed the structure of the intervertebral disc ( n = 6). Scale bars = 200 μm and 2.5 μm. ( E ) Western blot to Bcl-2, Bax, Cleaved-caspase 9, Nqo1, Homx1 and β-actin in the tissue samples of rat IVDD ( n = 3). ( F ) The quantitative analysis to the results of Western blot. ( G ) Western blot to the UPR mt markers such as Clpp, Hspa1a, Lonp1 and mitophagy markers such as Pink1, Parkin, sqstm1 and β-actin in the tissue samples of rat IVDD ( n = 3). ( H ) The quantitative analysis to the results of Western blot. ( I ) Immunohistochemical examination of the UPR mt markers including Clpp and Lonp1 in the tissue samples of rat IVDD ( n = 6). Scale bars = 200 μm and 2.5 μm. ( J ) The quantitative analysis to the results of Immunohistochemistry.Statistical significance was analyzed by one-way ANOVA followed by a post hoc Tukey’s test. All data were presented as mean ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001

Techniques: Staining, Western Blot, Immunohistochemical staining, Immunohistochemistry

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