m83 Search Results


bace  (Santa Cruz Biotechnology)
90
Santa Cruz Biotechnology bace
Dietary supplementation of vitamin D 3 aggravates AD pathology in APP/PS1 AD mice. (a) Serum 25(OH)D 3 levels in APP/PS1 (TG) and wild‐type (WT) mice. Mice were weaned at 4‐weeks of age (±3 days) and maintained on a vitamin D 3 ‐sufficient diet (600 IU/Kg of cholecalciferol). Serum vitamin D 3 levels were determined by 25(OH)D 3 enzyme‐linked immunosorbent assay (EMSA) at the indicated time points ( n = 5). Results are shown as mean ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001 by unpaired t ‐test. (b) WST‐1 cell viability assay. SH‐SY5Y cells were exposed to vitamin D 3 alone or Αβ (4 μM) plus vitamin D 3 (calcitriol or calcidiol) for 6 h prior to assays. Results are shown as mean ± SD. * p < 0.05 by One‐way ANOVA. (c) Western blot analysis of VDR, apoptotic and autophagic marker proteins in SH‐SY5Y cells exposed to Aβ42 or plus without or without Vitamin D 3 . SH‐SY5Y cells were treated with 4 μM Aβ42 alone or Aβ42 plus 10, 30, or 100 nM calcitriol for 6 h before harvesting cell lysates for analysis. (d) Representative immunofluorescent micrographs of gliosis (anti‐GFAP, GA5) and amyloid aggregates (anti‐Αβ, D54D2) in hippocampal tissues of APP/PS1 mice. 4.5‐month‐old APP/PS1 mice were fed with vitamin D 3 ‐supplemented (8044 IU/Kg cholecalciferol/day, Vit. D) or vitamin D 3 ‐sufficient diets (600 IU/Kg cholecalciferol/day, Ctrl) for 3 months before harvesting brain tissues for analysis. Sections of cortex or hippocampus were stained with the indicated antibodies. The average percentage of surface area with Αβ plaques in five consecutive sections per animal ( n = 4–7) was quantified by ImageJ in right panel. (e) Western blot analysis of Αβ production <t>and</t> <t>β‐secretase</t> 1 (BACE1) levels in hippocampal lysates of APP/PS1 mice supplemented with or without vitamin D 3. Densitometrical quantification of Aβ and <t>BACE</t> bands were normalized to GAPDH (right panel). (f) Cognitive performance for AD mice supplemented with vitamin D 3 . 4.5‐month‐old APP/PS1 mice were fed with vitamin D 3 –fortified (Vit. D) or vitamin D 3 ‐sufficient diets (Ctrl) for 7.5 months before Morris Water Maze. * p < 0.05 by One‐way ANOVA
Bace, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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m 83  (Santa Cruz Biotechnology)
88
Santa Cruz Biotechnology m 83
Dietary supplementation of vitamin D 3 aggravates AD pathology in APP/PS1 AD mice. (a) Serum 25(OH)D 3 levels in APP/PS1 (TG) and wild‐type (WT) mice. Mice were weaned at 4‐weeks of age (±3 days) and maintained on a vitamin D 3 ‐sufficient diet (600 IU/Kg of cholecalciferol). Serum vitamin D 3 levels were determined by 25(OH)D 3 enzyme‐linked immunosorbent assay (EMSA) at the indicated time points ( n = 5). Results are shown as mean ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001 by unpaired t ‐test. (b) WST‐1 cell viability assay. SH‐SY5Y cells were exposed to vitamin D 3 alone or Αβ (4 μM) plus vitamin D 3 (calcitriol or calcidiol) for 6 h prior to assays. Results are shown as mean ± SD. * p < 0.05 by One‐way ANOVA. (c) Western blot analysis of VDR, apoptotic and autophagic marker proteins in SH‐SY5Y cells exposed to Aβ42 or plus without or without Vitamin D 3 . SH‐SY5Y cells were treated with 4 μM Aβ42 alone or Aβ42 plus 10, 30, or 100 nM calcitriol for 6 h before harvesting cell lysates for analysis. (d) Representative immunofluorescent micrographs of gliosis (anti‐GFAP, GA5) and amyloid aggregates (anti‐Αβ, D54D2) in hippocampal tissues of APP/PS1 mice. 4.5‐month‐old APP/PS1 mice were fed with vitamin D 3 ‐supplemented (8044 IU/Kg cholecalciferol/day, Vit. D) or vitamin D 3 ‐sufficient diets (600 IU/Kg cholecalciferol/day, Ctrl) for 3 months before harvesting brain tissues for analysis. Sections of cortex or hippocampus were stained with the indicated antibodies. The average percentage of surface area with Αβ plaques in five consecutive sections per animal ( n = 4–7) was quantified by ImageJ in right panel. (e) Western blot analysis of Αβ production <t>and</t> <t>β‐secretase</t> 1 (BACE1) levels in hippocampal lysates of APP/PS1 mice supplemented with or without vitamin D 3. Densitometrical quantification of Aβ and <t>BACE</t> bands were normalized to GAPDH (right panel). (f) Cognitive performance for AD mice supplemented with vitamin D 3 . 4.5‐month‐old APP/PS1 mice were fed with vitamin D 3 –fortified (Vit. D) or vitamin D 3 ‐sufficient diets (Ctrl) for 7.5 months before Morris Water Maze. * p < 0.05 by One‐way ANOVA
M 83, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 88/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/m83/M83+(m)-PR/pmc03929097-307-27-28
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08536 cp/m '83 east  (Digital Research Inc)
90
Digital Research Inc 08536 cp/m '83 east
Dietary supplementation of vitamin D 3 aggravates AD pathology in APP/PS1 AD mice. (a) Serum 25(OH)D 3 levels in APP/PS1 (TG) and wild‐type (WT) mice. Mice were weaned at 4‐weeks of age (±3 days) and maintained on a vitamin D 3 ‐sufficient diet (600 IU/Kg of cholecalciferol). Serum vitamin D 3 levels were determined by 25(OH)D 3 enzyme‐linked immunosorbent assay (EMSA) at the indicated time points ( n = 5). Results are shown as mean ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001 by unpaired t ‐test. (b) WST‐1 cell viability assay. SH‐SY5Y cells were exposed to vitamin D 3 alone or Αβ (4 μM) plus vitamin D 3 (calcitriol or calcidiol) for 6 h prior to assays. Results are shown as mean ± SD. * p < 0.05 by One‐way ANOVA. (c) Western blot analysis of VDR, apoptotic and autophagic marker proteins in SH‐SY5Y cells exposed to Aβ42 or plus without or without Vitamin D 3 . SH‐SY5Y cells were treated with 4 μM Aβ42 alone or Aβ42 plus 10, 30, or 100 nM calcitriol for 6 h before harvesting cell lysates for analysis. (d) Representative immunofluorescent micrographs of gliosis (anti‐GFAP, GA5) and amyloid aggregates (anti‐Αβ, D54D2) in hippocampal tissues of APP/PS1 mice. 4.5‐month‐old APP/PS1 mice were fed with vitamin D 3 ‐supplemented (8044 IU/Kg cholecalciferol/day, Vit. D) or vitamin D 3 ‐sufficient diets (600 IU/Kg cholecalciferol/day, Ctrl) for 3 months before harvesting brain tissues for analysis. Sections of cortex or hippocampus were stained with the indicated antibodies. The average percentage of surface area with Αβ plaques in five consecutive sections per animal ( n = 4–7) was quantified by ImageJ in right panel. (e) Western blot analysis of Αβ production <t>and</t> <t>β‐secretase</t> 1 (BACE1) levels in hippocampal lysates of APP/PS1 mice supplemented with or without vitamin D 3. Densitometrical quantification of Aβ and <t>BACE</t> bands were normalized to GAPDH (right panel). (f) Cognitive performance for AD mice supplemented with vitamin D 3 . 4.5‐month‐old APP/PS1 mice were fed with vitamin D 3 –fortified (Vit. D) or vitamin D 3 ‐sufficient diets (Ctrl) for 7.5 months before Morris Water Maze. * p < 0.05 by One‐way ANOVA
08536 Cp/M '83 East, supplied by Digital Research Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/m83/08536+cp+m++83+east/10__1109_slash_mspec__1983__6501476-130-0-4
Average 90 stars, based on 1 article reviews
08536 cp/m '83 east - by Bioz Stars, 2026-10
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pseudopeptide inhibitor m83  (CS Bio Inc)
90
CS Bio Inc pseudopeptide inhibitor m83
Dietary supplementation of vitamin D 3 aggravates AD pathology in APP/PS1 AD mice. (a) Serum 25(OH)D 3 levels in APP/PS1 (TG) and wild‐type (WT) mice. Mice were weaned at 4‐weeks of age (±3 days) and maintained on a vitamin D 3 ‐sufficient diet (600 IU/Kg of cholecalciferol). Serum vitamin D 3 levels were determined by 25(OH)D 3 enzyme‐linked immunosorbent assay (EMSA) at the indicated time points ( n = 5). Results are shown as mean ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001 by unpaired t ‐test. (b) WST‐1 cell viability assay. SH‐SY5Y cells were exposed to vitamin D 3 alone or Αβ (4 μM) plus vitamin D 3 (calcitriol or calcidiol) for 6 h prior to assays. Results are shown as mean ± SD. * p < 0.05 by One‐way ANOVA. (c) Western blot analysis of VDR, apoptotic and autophagic marker proteins in SH‐SY5Y cells exposed to Aβ42 or plus without or without Vitamin D 3 . SH‐SY5Y cells were treated with 4 μM Aβ42 alone or Aβ42 plus 10, 30, or 100 nM calcitriol for 6 h before harvesting cell lysates for analysis. (d) Representative immunofluorescent micrographs of gliosis (anti‐GFAP, GA5) and amyloid aggregates (anti‐Αβ, D54D2) in hippocampal tissues of APP/PS1 mice. 4.5‐month‐old APP/PS1 mice were fed with vitamin D 3 ‐supplemented (8044 IU/Kg cholecalciferol/day, Vit. D) or vitamin D 3 ‐sufficient diets (600 IU/Kg cholecalciferol/day, Ctrl) for 3 months before harvesting brain tissues for analysis. Sections of cortex or hippocampus were stained with the indicated antibodies. The average percentage of surface area with Αβ plaques in five consecutive sections per animal ( n = 4–7) was quantified by ImageJ in right panel. (e) Western blot analysis of Αβ production <t>and</t> <t>β‐secretase</t> 1 (BACE1) levels in hippocampal lysates of APP/PS1 mice supplemented with or without vitamin D 3. Densitometrical quantification of Aβ and <t>BACE</t> bands were normalized to GAPDH (right panel). (f) Cognitive performance for AD mice supplemented with vitamin D 3 . 4.5‐month‐old APP/PS1 mice were fed with vitamin D 3 –fortified (Vit. D) or vitamin D 3 ‐sufficient diets (Ctrl) for 7.5 months before Morris Water Maze. * p < 0.05 by One‐way ANOVA
Pseudopeptide Inhibitor M83, supplied by CS Bio Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/m83/pseudopeptide+inhibitor+m83/pm32796025-74-1-12
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m83 transgenic mice  (Jackson Laboratory)
86
Jackson Laboratory m83 transgenic mice
Dietary supplementation of vitamin D 3 aggravates AD pathology in APP/PS1 AD mice. (a) Serum 25(OH)D 3 levels in APP/PS1 (TG) and wild‐type (WT) mice. Mice were weaned at 4‐weeks of age (±3 days) and maintained on a vitamin D 3 ‐sufficient diet (600 IU/Kg of cholecalciferol). Serum vitamin D 3 levels were determined by 25(OH)D 3 enzyme‐linked immunosorbent assay (EMSA) at the indicated time points ( n = 5). Results are shown as mean ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001 by unpaired t ‐test. (b) WST‐1 cell viability assay. SH‐SY5Y cells were exposed to vitamin D 3 alone or Αβ (4 μM) plus vitamin D 3 (calcitriol or calcidiol) for 6 h prior to assays. Results are shown as mean ± SD. * p < 0.05 by One‐way ANOVA. (c) Western blot analysis of VDR, apoptotic and autophagic marker proteins in SH‐SY5Y cells exposed to Aβ42 or plus without or without Vitamin D 3 . SH‐SY5Y cells were treated with 4 μM Aβ42 alone or Aβ42 plus 10, 30, or 100 nM calcitriol for 6 h before harvesting cell lysates for analysis. (d) Representative immunofluorescent micrographs of gliosis (anti‐GFAP, GA5) and amyloid aggregates (anti‐Αβ, D54D2) in hippocampal tissues of APP/PS1 mice. 4.5‐month‐old APP/PS1 mice were fed with vitamin D 3 ‐supplemented (8044 IU/Kg cholecalciferol/day, Vit. D) or vitamin D 3 ‐sufficient diets (600 IU/Kg cholecalciferol/day, Ctrl) for 3 months before harvesting brain tissues for analysis. Sections of cortex or hippocampus were stained with the indicated antibodies. The average percentage of surface area with Αβ plaques in five consecutive sections per animal ( n = 4–7) was quantified by ImageJ in right panel. (e) Western blot analysis of Αβ production <t>and</t> <t>β‐secretase</t> 1 (BACE1) levels in hippocampal lysates of APP/PS1 mice supplemented with or without vitamin D 3. Densitometrical quantification of Aβ and <t>BACE</t> bands were normalized to GAPDH (right panel). (f) Cognitive performance for AD mice supplemented with vitamin D 3 . 4.5‐month‐old APP/PS1 mice were fed with vitamin D 3 –fortified (Vit. D) or vitamin D 3 ‐sufficient diets (Ctrl) for 7.5 months before Morris Water Maze. * p < 0.05 by One‐way ANOVA
M83 Transgenic Mice, supplied by Jackson Laboratory, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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m83  (Jackson Laboratory)
86
Jackson Laboratory m83
Dietary supplementation of vitamin D 3 aggravates AD pathology in APP/PS1 AD mice. (a) Serum 25(OH)D 3 levels in APP/PS1 (TG) and wild‐type (WT) mice. Mice were weaned at 4‐weeks of age (±3 days) and maintained on a vitamin D 3 ‐sufficient diet (600 IU/Kg of cholecalciferol). Serum vitamin D 3 levels were determined by 25(OH)D 3 enzyme‐linked immunosorbent assay (EMSA) at the indicated time points ( n = 5). Results are shown as mean ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001 by unpaired t ‐test. (b) WST‐1 cell viability assay. SH‐SY5Y cells were exposed to vitamin D 3 alone or Αβ (4 μM) plus vitamin D 3 (calcitriol or calcidiol) for 6 h prior to assays. Results are shown as mean ± SD. * p < 0.05 by One‐way ANOVA. (c) Western blot analysis of VDR, apoptotic and autophagic marker proteins in SH‐SY5Y cells exposed to Aβ42 or plus without or without Vitamin D 3 . SH‐SY5Y cells were treated with 4 μM Aβ42 alone or Aβ42 plus 10, 30, or 100 nM calcitriol for 6 h before harvesting cell lysates for analysis. (d) Representative immunofluorescent micrographs of gliosis (anti‐GFAP, GA5) and amyloid aggregates (anti‐Αβ, D54D2) in hippocampal tissues of APP/PS1 mice. 4.5‐month‐old APP/PS1 mice were fed with vitamin D 3 ‐supplemented (8044 IU/Kg cholecalciferol/day, Vit. D) or vitamin D 3 ‐sufficient diets (600 IU/Kg cholecalciferol/day, Ctrl) for 3 months before harvesting brain tissues for analysis. Sections of cortex or hippocampus were stained with the indicated antibodies. The average percentage of surface area with Αβ plaques in five consecutive sections per animal ( n = 4–7) was quantified by ImageJ in right panel. (e) Western blot analysis of Αβ production <t>and</t> <t>β‐secretase</t> 1 (BACE1) levels in hippocampal lysates of APP/PS1 mice supplemented with or without vitamin D 3. Densitometrical quantification of Aβ and <t>BACE</t> bands were normalized to GAPDH (right panel). (f) Cognitive performance for AD mice supplemented with vitamin D 3 . 4.5‐month‐old APP/PS1 mice were fed with vitamin D 3 –fortified (Vit. D) or vitamin D 3 ‐sufficient diets (Ctrl) for 7.5 months before Morris Water Maze. * p < 0.05 by One‐way ANOVA
M83, supplied by Jackson Laboratory, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/m83/m83/us12521398-143-8-9
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lenovo thinkcentre m83 pc  (Lenovo Inc)
86
Lenovo Inc lenovo thinkcentre m83 pc
Dietary supplementation of vitamin D 3 aggravates AD pathology in APP/PS1 AD mice. (a) Serum 25(OH)D 3 levels in APP/PS1 (TG) and wild‐type (WT) mice. Mice were weaned at 4‐weeks of age (±3 days) and maintained on a vitamin D 3 ‐sufficient diet (600 IU/Kg of cholecalciferol). Serum vitamin D 3 levels were determined by 25(OH)D 3 enzyme‐linked immunosorbent assay (EMSA) at the indicated time points ( n = 5). Results are shown as mean ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001 by unpaired t ‐test. (b) WST‐1 cell viability assay. SH‐SY5Y cells were exposed to vitamin D 3 alone or Αβ (4 μM) plus vitamin D 3 (calcitriol or calcidiol) for 6 h prior to assays. Results are shown as mean ± SD. * p < 0.05 by One‐way ANOVA. (c) Western blot analysis of VDR, apoptotic and autophagic marker proteins in SH‐SY5Y cells exposed to Aβ42 or plus without or without Vitamin D 3 . SH‐SY5Y cells were treated with 4 μM Aβ42 alone or Aβ42 plus 10, 30, or 100 nM calcitriol for 6 h before harvesting cell lysates for analysis. (d) Representative immunofluorescent micrographs of gliosis (anti‐GFAP, GA5) and amyloid aggregates (anti‐Αβ, D54D2) in hippocampal tissues of APP/PS1 mice. 4.5‐month‐old APP/PS1 mice were fed with vitamin D 3 ‐supplemented (8044 IU/Kg cholecalciferol/day, Vit. D) or vitamin D 3 ‐sufficient diets (600 IU/Kg cholecalciferol/day, Ctrl) for 3 months before harvesting brain tissues for analysis. Sections of cortex or hippocampus were stained with the indicated antibodies. The average percentage of surface area with Αβ plaques in five consecutive sections per animal ( n = 4–7) was quantified by ImageJ in right panel. (e) Western blot analysis of Αβ production <t>and</t> <t>β‐secretase</t> 1 (BACE1) levels in hippocampal lysates of APP/PS1 mice supplemented with or without vitamin D 3. Densitometrical quantification of Aβ and <t>BACE</t> bands were normalized to GAPDH (right panel). (f) Cognitive performance for AD mice supplemented with vitamin D 3 . 4.5‐month‐old APP/PS1 mice were fed with vitamin D 3 –fortified (Vit. D) or vitamin D 3 ‐sufficient diets (Ctrl) for 7.5 months before Morris Water Maze. * p < 0.05 by One‐way ANOVA
Lenovo Thinkcentre M83 Pc, supplied by Lenovo Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/m83/lenovo+m83+pc+thinkcentre/pmc12851487-65-5-5
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homozygous m83  (Jackson Laboratory)
86
Jackson Laboratory homozygous m83
Dietary supplementation of vitamin D 3 aggravates AD pathology in APP/PS1 AD mice. (a) Serum 25(OH)D 3 levels in APP/PS1 (TG) and wild‐type (WT) mice. Mice were weaned at 4‐weeks of age (±3 days) and maintained on a vitamin D 3 ‐sufficient diet (600 IU/Kg of cholecalciferol). Serum vitamin D 3 levels were determined by 25(OH)D 3 enzyme‐linked immunosorbent assay (EMSA) at the indicated time points ( n = 5). Results are shown as mean ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001 by unpaired t ‐test. (b) WST‐1 cell viability assay. SH‐SY5Y cells were exposed to vitamin D 3 alone or Αβ (4 μM) plus vitamin D 3 (calcitriol or calcidiol) for 6 h prior to assays. Results are shown as mean ± SD. * p < 0.05 by One‐way ANOVA. (c) Western blot analysis of VDR, apoptotic and autophagic marker proteins in SH‐SY5Y cells exposed to Aβ42 or plus without or without Vitamin D 3 . SH‐SY5Y cells were treated with 4 μM Aβ42 alone or Aβ42 plus 10, 30, or 100 nM calcitriol for 6 h before harvesting cell lysates for analysis. (d) Representative immunofluorescent micrographs of gliosis (anti‐GFAP, GA5) and amyloid aggregates (anti‐Αβ, D54D2) in hippocampal tissues of APP/PS1 mice. 4.5‐month‐old APP/PS1 mice were fed with vitamin D 3 ‐supplemented (8044 IU/Kg cholecalciferol/day, Vit. D) or vitamin D 3 ‐sufficient diets (600 IU/Kg cholecalciferol/day, Ctrl) for 3 months before harvesting brain tissues for analysis. Sections of cortex or hippocampus were stained with the indicated antibodies. The average percentage of surface area with Αβ plaques in five consecutive sections per animal ( n = 4–7) was quantified by ImageJ in right panel. (e) Western blot analysis of Αβ production <t>and</t> <t>β‐secretase</t> 1 (BACE1) levels in hippocampal lysates of APP/PS1 mice supplemented with or without vitamin D 3. Densitometrical quantification of Aβ and <t>BACE</t> bands were normalized to GAPDH (right panel). (f) Cognitive performance for AD mice supplemented with vitamin D 3 . 4.5‐month‐old APP/PS1 mice were fed with vitamin D 3 –fortified (Vit. D) or vitamin D 3 ‐sufficient diets (Ctrl) for 7.5 months before Morris Water Maze. * p < 0.05 by One‐way ANOVA
Homozygous M83, supplied by Jackson Laboratory, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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m83 crispr activation plasmid  (Santa Cruz Biotechnology)
N/A
CRISPR/Cas9 KO Plasmids consists of M83-specific 20 nt guide RNA sequences derived from the GeCKO (v2) library. For CRISPR gene knockout, gRNA sequences direct the Cas9 protein to induce a site-specific double strand break (DSB)
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m83 crispr/cas9 ko plasmid  (Santa Cruz Biotechnology)
N/A
CRISPR/Cas9 KO Plasmids consists of M83-specific 20 nt guide RNA sequences derived from the GeCKO (v2) library. For CRISPR gene knockout, gRNA sequences direct the Cas9 protein to induce a site-specific double strand break (DSB)
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m83 lentiviral activation particles  (Santa Cruz Biotechnology)
N/A
CRISPR/Cas9 KO Plasmids consists of M83-specific 20 nt guide RNA sequences derived from the GeCKO (v2) library. For CRISPR gene knockout, gRNA sequences direct the Cas9 protein to induce a site-specific double strand break (DSB)
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m83 shrna (h) lentiviral particles  (Santa Cruz Biotechnology)
N/A
Gene Silencers generally consist of pools of three to five target-specific 19-25 nucleotide sequences in length. For independent verification of M83 gene silencing results, individual duplex components or plasmids are also available upon request. Suitable
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Image Search Results


Dietary supplementation of vitamin D 3 aggravates AD pathology in APP/PS1 AD mice. (a) Serum 25(OH)D 3 levels in APP/PS1 (TG) and wild‐type (WT) mice. Mice were weaned at 4‐weeks of age (±3 days) and maintained on a vitamin D 3 ‐sufficient diet (600 IU/Kg of cholecalciferol). Serum vitamin D 3 levels were determined by 25(OH)D 3 enzyme‐linked immunosorbent assay (EMSA) at the indicated time points ( n = 5). Results are shown as mean ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001 by unpaired t ‐test. (b) WST‐1 cell viability assay. SH‐SY5Y cells were exposed to vitamin D 3 alone or Αβ (4 μM) plus vitamin D 3 (calcitriol or calcidiol) for 6 h prior to assays. Results are shown as mean ± SD. * p < 0.05 by One‐way ANOVA. (c) Western blot analysis of VDR, apoptotic and autophagic marker proteins in SH‐SY5Y cells exposed to Aβ42 or plus without or without Vitamin D 3 . SH‐SY5Y cells were treated with 4 μM Aβ42 alone or Aβ42 plus 10, 30, or 100 nM calcitriol for 6 h before harvesting cell lysates for analysis. (d) Representative immunofluorescent micrographs of gliosis (anti‐GFAP, GA5) and amyloid aggregates (anti‐Αβ, D54D2) in hippocampal tissues of APP/PS1 mice. 4.5‐month‐old APP/PS1 mice were fed with vitamin D 3 ‐supplemented (8044 IU/Kg cholecalciferol/day, Vit. D) or vitamin D 3 ‐sufficient diets (600 IU/Kg cholecalciferol/day, Ctrl) for 3 months before harvesting brain tissues for analysis. Sections of cortex or hippocampus were stained with the indicated antibodies. The average percentage of surface area with Αβ plaques in five consecutive sections per animal ( n = 4–7) was quantified by ImageJ in right panel. (e) Western blot analysis of Αβ production and β‐secretase 1 (BACE1) levels in hippocampal lysates of APP/PS1 mice supplemented with or without vitamin D 3. Densitometrical quantification of Aβ and BACE bands were normalized to GAPDH (right panel). (f) Cognitive performance for AD mice supplemented with vitamin D 3 . 4.5‐month‐old APP/PS1 mice were fed with vitamin D 3 –fortified (Vit. D) or vitamin D 3 ‐sufficient diets (Ctrl) for 7.5 months before Morris Water Maze. * p < 0.05 by One‐way ANOVA

Journal: Aging Cell

Article Title: Vitamin D supplementation worsens Alzheimer's progression: Animal model and human cohort studies

doi: 10.1111/acel.13670

Figure Lengend Snippet: Dietary supplementation of vitamin D 3 aggravates AD pathology in APP/PS1 AD mice. (a) Serum 25(OH)D 3 levels in APP/PS1 (TG) and wild‐type (WT) mice. Mice were weaned at 4‐weeks of age (±3 days) and maintained on a vitamin D 3 ‐sufficient diet (600 IU/Kg of cholecalciferol). Serum vitamin D 3 levels were determined by 25(OH)D 3 enzyme‐linked immunosorbent assay (EMSA) at the indicated time points ( n = 5). Results are shown as mean ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001 by unpaired t ‐test. (b) WST‐1 cell viability assay. SH‐SY5Y cells were exposed to vitamin D 3 alone or Αβ (4 μM) plus vitamin D 3 (calcitriol or calcidiol) for 6 h prior to assays. Results are shown as mean ± SD. * p < 0.05 by One‐way ANOVA. (c) Western blot analysis of VDR, apoptotic and autophagic marker proteins in SH‐SY5Y cells exposed to Aβ42 or plus without or without Vitamin D 3 . SH‐SY5Y cells were treated with 4 μM Aβ42 alone or Aβ42 plus 10, 30, or 100 nM calcitriol for 6 h before harvesting cell lysates for analysis. (d) Representative immunofluorescent micrographs of gliosis (anti‐GFAP, GA5) and amyloid aggregates (anti‐Αβ, D54D2) in hippocampal tissues of APP/PS1 mice. 4.5‐month‐old APP/PS1 mice were fed with vitamin D 3 ‐supplemented (8044 IU/Kg cholecalciferol/day, Vit. D) or vitamin D 3 ‐sufficient diets (600 IU/Kg cholecalciferol/day, Ctrl) for 3 months before harvesting brain tissues for analysis. Sections of cortex or hippocampus were stained with the indicated antibodies. The average percentage of surface area with Αβ plaques in five consecutive sections per animal ( n = 4–7) was quantified by ImageJ in right panel. (e) Western blot analysis of Αβ production and β‐secretase 1 (BACE1) levels in hippocampal lysates of APP/PS1 mice supplemented with or without vitamin D 3. Densitometrical quantification of Aβ and BACE bands were normalized to GAPDH (right panel). (f) Cognitive performance for AD mice supplemented with vitamin D 3 . 4.5‐month‐old APP/PS1 mice were fed with vitamin D 3 –fortified (Vit. D) or vitamin D 3 ‐sufficient diets (Ctrl) for 7.5 months before Morris Water Maze. * p < 0.05 by One‐way ANOVA

Article Snippet: The antibodies used in this study are listed as follows: VDR (C20), Santa Cruz Biotechnology, Cat# sc‐1008; VDR(D6), Santa Cruz, Biotechnology Cat# sc‐1313; GAPDH, GeneTex, Cat# GTX10011; PARP‐1/2 (H‐250), Santa Cruz Biotechnology, Cat# sc‐715; LC3B, Cell Signaling Technology, Cat# 4108; Beta‐Amyloid‐1‐16 antibody, BioLegend, Cat# 803014; β‐Amyloid Antibody, Cell Signaling Technology, Cat# 245; BACE (M‐83), Santa Cruz Biotechnology, Cat# sc‐10748; GFAP (Clone SP78), MybioSourse, Cat# MBS302899; GFAP (GA5), Cell Signaling Technology, Cat# 3670; p53 (DO‐1) Santa Cruz Biotechnology Cat# sc‐12; Cat# sc‐13985; Phospho‐SQSTM1/p62 (Ser349), Cell Signaling Technology, Cat# 95697; SQATM1/p62 (GT1478), Thermo Fisher Scientific, Cat# MA5–27800; TNF‐α (D2D4) XP® Rabbit mAb, Cell Signaling Technology, Cat# 1194; Alexa 488 chicken anti‐rabbit IgG (H + L), Thermo Fisher Scientific, Cat# A‐21441; Alexa 594 chicken anti‐goat IgG (H + L), Thermo Fisher Scientific Cat# A‐2146; Peroxidase‐AffiniPure Goat Anti‐Rabbit IgG (H + L), Jackson ImmunoResearch Labs, Cat# 111‐035‐144; Peroxidase‐AffiniPure Goat Anti‐Mouse IgG (H + L), Jackson ImmunoResearch Labs, Cat# 115‐035‐14; Peroxidase‐AffiniPure Rabbit Anti‐Goat IgG (H + L), Jackson ImmunoResearch Labs, Cat# 305‐035‐003; Mouse anti‐Rabbit light chain; HRP conjugate, Millipore, at# MAB201P; HRP‐conjugated AffiniPure Mouse Anti‐Rabbit IgG Light Chain, Bclonal Cat# AS061.

Techniques: Enzyme-linked Immunosorbent Assay, Viability Assay, Western Blot, Marker, Staining

Vitamin D supplementation enhances VDR/p53 but not VDR/RXR complex in worsening brain pathology in APP/PS1 AD mice. (a) Mammalian two‐hybrid assays for studies of the interaction of VDR with RXR in neuronal cells exposed to Αβ plus with vitamin D 3 . SH‐SY5Y cells were treated Aβ42 for 6 h and then co‐treated with 10 nM calcitriol for additional 6 h prior to harvesting for mammalian two‐hybrid luciferase assays. (b,c) Western blot analysis of co‐immunoprecipitation of VDR/p53 complex in SH‐SY5Y cells and hippocampal tissues of APP/PS1 mice. (d) Western blot analysis of VDR, p53, and MDM2 in the hippocampal lysates of APP/PS1 mice treated with or without p53 inhibitor. 4.5‐month‐old APP/PS1 mice raised on vitamin D 3 ‐sufficient diets were intraperitoneally injected weekly with 3 mg/kg of p53 inhibitor pifithrin‐α (PFTα) for 7.5 months before harvesting hippocampal tissues for analysis. Densitometrical quantification of VDR, p53, and MDM2 bands were normalized to GAPDH (lower panel). * p < 0.05; ** p < 0.01; *** p < 0.001 by unpaired t ‐test. (e) Western blot analysis of autophagic markers LC3, p62, and ser349 phosphorylated p62 (p62‐S349) in the hippocampal lysates of APP/PS1 mice injected with or without PFTα. Densitometrical quantification of LC3, p62‐S349, and p62 bands were normalized to GAPDH (right panel). (f) Western blot analysis of Αβ and BACE levels in the hippocampal lysates of APP/PS1 mice injected with or without PFTα. Densitometrical quantification of Aβ and BACE bands were normalized to GAPDH (right panel). (g,h) p53 inhibitor amelioration of vitamin D 3 ‐aggravated Aβ aggregation and apoptosis. The Aβ, GFAP, and TUNEL‐positive signals in five consecutive sections per animal ( n = 5) was quantified by ImageJ and presented as the mean ± SD. Scale bars, 50 μm. (i) Cognitive performance assays for the AD mice treated with p53 inhibitor. APP/PS1 mice were given with or without weekly injections of PTFα ( n = 6 mice) starting at the age of 4.5‐month. APP/PS1 mice at 12‐month of age were used for the Morris Water Maze test

Journal: Aging Cell

Article Title: Vitamin D supplementation worsens Alzheimer's progression: Animal model and human cohort studies

doi: 10.1111/acel.13670

Figure Lengend Snippet: Vitamin D supplementation enhances VDR/p53 but not VDR/RXR complex in worsening brain pathology in APP/PS1 AD mice. (a) Mammalian two‐hybrid assays for studies of the interaction of VDR with RXR in neuronal cells exposed to Αβ plus with vitamin D 3 . SH‐SY5Y cells were treated Aβ42 for 6 h and then co‐treated with 10 nM calcitriol for additional 6 h prior to harvesting for mammalian two‐hybrid luciferase assays. (b,c) Western blot analysis of co‐immunoprecipitation of VDR/p53 complex in SH‐SY5Y cells and hippocampal tissues of APP/PS1 mice. (d) Western blot analysis of VDR, p53, and MDM2 in the hippocampal lysates of APP/PS1 mice treated with or without p53 inhibitor. 4.5‐month‐old APP/PS1 mice raised on vitamin D 3 ‐sufficient diets were intraperitoneally injected weekly with 3 mg/kg of p53 inhibitor pifithrin‐α (PFTα) for 7.5 months before harvesting hippocampal tissues for analysis. Densitometrical quantification of VDR, p53, and MDM2 bands were normalized to GAPDH (lower panel). * p < 0.05; ** p < 0.01; *** p < 0.001 by unpaired t ‐test. (e) Western blot analysis of autophagic markers LC3, p62, and ser349 phosphorylated p62 (p62‐S349) in the hippocampal lysates of APP/PS1 mice injected with or without PFTα. Densitometrical quantification of LC3, p62‐S349, and p62 bands were normalized to GAPDH (right panel). (f) Western blot analysis of Αβ and BACE levels in the hippocampal lysates of APP/PS1 mice injected with or without PFTα. Densitometrical quantification of Aβ and BACE bands were normalized to GAPDH (right panel). (g,h) p53 inhibitor amelioration of vitamin D 3 ‐aggravated Aβ aggregation and apoptosis. The Aβ, GFAP, and TUNEL‐positive signals in five consecutive sections per animal ( n = 5) was quantified by ImageJ and presented as the mean ± SD. Scale bars, 50 μm. (i) Cognitive performance assays for the AD mice treated with p53 inhibitor. APP/PS1 mice were given with or without weekly injections of PTFα ( n = 6 mice) starting at the age of 4.5‐month. APP/PS1 mice at 12‐month of age were used for the Morris Water Maze test

Article Snippet: The antibodies used in this study are listed as follows: VDR (C20), Santa Cruz Biotechnology, Cat# sc‐1008; VDR(D6), Santa Cruz, Biotechnology Cat# sc‐1313; GAPDH, GeneTex, Cat# GTX10011; PARP‐1/2 (H‐250), Santa Cruz Biotechnology, Cat# sc‐715; LC3B, Cell Signaling Technology, Cat# 4108; Beta‐Amyloid‐1‐16 antibody, BioLegend, Cat# 803014; β‐Amyloid Antibody, Cell Signaling Technology, Cat# 245; BACE (M‐83), Santa Cruz Biotechnology, Cat# sc‐10748; GFAP (Clone SP78), MybioSourse, Cat# MBS302899; GFAP (GA5), Cell Signaling Technology, Cat# 3670; p53 (DO‐1) Santa Cruz Biotechnology Cat# sc‐12; Cat# sc‐13985; Phospho‐SQSTM1/p62 (Ser349), Cell Signaling Technology, Cat# 95697; SQATM1/p62 (GT1478), Thermo Fisher Scientific, Cat# MA5–27800; TNF‐α (D2D4) XP® Rabbit mAb, Cell Signaling Technology, Cat# 1194; Alexa 488 chicken anti‐rabbit IgG (H + L), Thermo Fisher Scientific, Cat# A‐21441; Alexa 594 chicken anti‐goat IgG (H + L), Thermo Fisher Scientific Cat# A‐2146; Peroxidase‐AffiniPure Goat Anti‐Rabbit IgG (H + L), Jackson ImmunoResearch Labs, Cat# 111‐035‐144; Peroxidase‐AffiniPure Goat Anti‐Mouse IgG (H + L), Jackson ImmunoResearch Labs, Cat# 115‐035‐14; Peroxidase‐AffiniPure Rabbit Anti‐Goat IgG (H + L), Jackson ImmunoResearch Labs, Cat# 305‐035‐003; Mouse anti‐Rabbit light chain; HRP conjugate, Millipore, at# MAB201P; HRP‐conjugated AffiniPure Mouse Anti‐Rabbit IgG Light Chain, Bclonal Cat# AS061.

Techniques: Luciferase, Western Blot, Immunoprecipitation, Injection, TUNEL Assay