mouse anti-pgc-1a antibody Search Results


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Novus Biologicals rabbit anti pgc1a
Rabbit Anti Pgc1a, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Santa Cruz Biotechnology rabbit anti pgc 1a antibody
Figure 4. Elevating <t>PGC-1a</t> Expression in Skeletal Muscle of SOD1G37R Mutant Mice Does Not Alter ALS Disease Course or Pathogenesis (A) Plot of ages (in days) at which disease onset (as determined by the weight peak; at onset, animals do not display any obvious motor phenotype), symptomatic stage (as determined by 10% weight loss from onset, a stage characterized by clear gait abnormalities and tremor) and end-stage (as determined by hindlimb paralysis and inability to right itself) were reached for SOD1G37R (red) and SOD1G37R/MCK-PGC-1a (blue) animals. (B–D) Quantification of innervation at the neuromuscular junction of the gastrocnemius muscle (B), total number of a-motor axons in the lumbar L5 motor root (C), and quantification at disease end-stage of the average number of large cholinergic ventral horn motor neurons per section of lumbar spinal cord from SOD1G37R and SOD1G37R/MCK-PGC-1a animals (D). Data are presented as mean ± SEM. See also Figure S4 for representative sections of the spinal cords used for quantification. (E) Representative micrographs of lumbar spinal cord sections from SOD1G37R and SOD1G37R/MCK-PGC-1a animals at disease end-stage processed for immuno- fluorescence using antibodies detecting activated astrocytes (GFAP) or microglia (IbaI). Dashed outlines correspond to the boundary between gray and white matter.
Rabbit Anti Pgc 1a Antibody, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Santa Cruz Biotechnology pgc 1a antibody
Figure 4. Elevating <t>PGC-1a</t> Expression in Skeletal Muscle of SOD1G37R Mutant Mice Does Not Alter ALS Disease Course or Pathogenesis (A) Plot of ages (in days) at which disease onset (as determined by the weight peak; at onset, animals do not display any obvious motor phenotype), symptomatic stage (as determined by 10% weight loss from onset, a stage characterized by clear gait abnormalities and tremor) and end-stage (as determined by hindlimb paralysis and inability to right itself) were reached for SOD1G37R (red) and SOD1G37R/MCK-PGC-1a (blue) animals. (B–D) Quantification of innervation at the neuromuscular junction of the gastrocnemius muscle (B), total number of a-motor axons in the lumbar L5 motor root (C), and quantification at disease end-stage of the average number of large cholinergic ventral horn motor neurons per section of lumbar spinal cord from SOD1G37R and SOD1G37R/MCK-PGC-1a animals (D). Data are presented as mean ± SEM. See also Figure S4 for representative sections of the spinal cords used for quantification. (E) Representative micrographs of lumbar spinal cord sections from SOD1G37R and SOD1G37R/MCK-PGC-1a animals at disease end-stage processed for immuno- fluorescence using antibodies detecting activated astrocytes (GFAP) or microglia (IbaI). Dashed outlines correspond to the boundary between gray and white matter.
Pgc 1a Antibody, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Proteintech anti pgc1a
Figure 4. Elevating <t>PGC-1a</t> Expression in Skeletal Muscle of SOD1G37R Mutant Mice Does Not Alter ALS Disease Course or Pathogenesis (A) Plot of ages (in days) at which disease onset (as determined by the weight peak; at onset, animals do not display any obvious motor phenotype), symptomatic stage (as determined by 10% weight loss from onset, a stage characterized by clear gait abnormalities and tremor) and end-stage (as determined by hindlimb paralysis and inability to right itself) were reached for SOD1G37R (red) and SOD1G37R/MCK-PGC-1a (blue) animals. (B–D) Quantification of innervation at the neuromuscular junction of the gastrocnemius muscle (B), total number of a-motor axons in the lumbar L5 motor root (C), and quantification at disease end-stage of the average number of large cholinergic ventral horn motor neurons per section of lumbar spinal cord from SOD1G37R and SOD1G37R/MCK-PGC-1a animals (D). Data are presented as mean ± SEM. See also Figure S4 for representative sections of the spinal cords used for quantification. (E) Representative micrographs of lumbar spinal cord sections from SOD1G37R and SOD1G37R/MCK-PGC-1a animals at disease end-stage processed for immuno- fluorescence using antibodies detecting activated astrocytes (GFAP) or microglia (IbaI). Dashed outlines correspond to the boundary between gray and white matter.
Anti Pgc1a, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Cell Signaling Technology Inc resource source identifier rabbit anti-pgc-1a santa cruz sc-13067 rabbit anti-gsk3b cell signaling tech
Figure 4. Elevating <t>PGC-1a</t> Expression in Skeletal Muscle of SOD1G37R Mutant Mice Does Not Alter ALS Disease Course or Pathogenesis (A) Plot of ages (in days) at which disease onset (as determined by the weight peak; at onset, animals do not display any obvious motor phenotype), symptomatic stage (as determined by 10% weight loss from onset, a stage characterized by clear gait abnormalities and tremor) and end-stage (as determined by hindlimb paralysis and inability to right itself) were reached for SOD1G37R (red) and SOD1G37R/MCK-PGC-1a (blue) animals. (B–D) Quantification of innervation at the neuromuscular junction of the gastrocnemius muscle (B), total number of a-motor axons in the lumbar L5 motor root (C), and quantification at disease end-stage of the average number of large cholinergic ventral horn motor neurons per section of lumbar spinal cord from SOD1G37R and SOD1G37R/MCK-PGC-1a animals (D). Data are presented as mean ± SEM. See also Figure S4 for representative sections of the spinal cords used for quantification. (E) Representative micrographs of lumbar spinal cord sections from SOD1G37R and SOD1G37R/MCK-PGC-1a animals at disease end-stage processed for immuno- fluorescence using antibodies detecting activated astrocytes (GFAP) or microglia (IbaI). Dashed outlines correspond to the boundary between gray and white matter.
Resource Source Identifier Rabbit Anti Pgc 1a Santa Cruz Sc 13067 Rabbit Anti Gsk3b Cell Signaling Tech, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Beijing ComWin Biotech Co anti-phospho-ampk (thr172) primary antibodies
Figure 4. Elevating <t>PGC-1a</t> Expression in Skeletal Muscle of SOD1G37R Mutant Mice Does Not Alter ALS Disease Course or Pathogenesis (A) Plot of ages (in days) at which disease onset (as determined by the weight peak; at onset, animals do not display any obvious motor phenotype), symptomatic stage (as determined by 10% weight loss from onset, a stage characterized by clear gait abnormalities and tremor) and end-stage (as determined by hindlimb paralysis and inability to right itself) were reached for SOD1G37R (red) and SOD1G37R/MCK-PGC-1a (blue) animals. (B–D) Quantification of innervation at the neuromuscular junction of the gastrocnemius muscle (B), total number of a-motor axons in the lumbar L5 motor root (C), and quantification at disease end-stage of the average number of large cholinergic ventral horn motor neurons per section of lumbar spinal cord from SOD1G37R and SOD1G37R/MCK-PGC-1a animals (D). Data are presented as mean ± SEM. See also Figure S4 for representative sections of the spinal cords used for quantification. (E) Representative micrographs of lumbar spinal cord sections from SOD1G37R and SOD1G37R/MCK-PGC-1a animals at disease end-stage processed for immuno- fluorescence using antibodies detecting activated astrocytes (GFAP) or microglia (IbaI). Dashed outlines correspond to the boundary between gray and white matter.
Anti Phospho Ampk (Thr172) Primary Antibodies, supplied by Beijing ComWin Biotech Co, 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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Cell Signaling Technology Inc anti pgc 1a
Figure 4. Elevating <t>PGC-1a</t> Expression in Skeletal Muscle of SOD1G37R Mutant Mice Does Not Alter ALS Disease Course or Pathogenesis (A) Plot of ages (in days) at which disease onset (as determined by the weight peak; at onset, animals do not display any obvious motor phenotype), symptomatic stage (as determined by 10% weight loss from onset, a stage characterized by clear gait abnormalities and tremor) and end-stage (as determined by hindlimb paralysis and inability to right itself) were reached for SOD1G37R (red) and SOD1G37R/MCK-PGC-1a (blue) animals. (B–D) Quantification of innervation at the neuromuscular junction of the gastrocnemius muscle (B), total number of a-motor axons in the lumbar L5 motor root (C), and quantification at disease end-stage of the average number of large cholinergic ventral horn motor neurons per section of lumbar spinal cord from SOD1G37R and SOD1G37R/MCK-PGC-1a animals (D). Data are presented as mean ± SEM. See also Figure S4 for representative sections of the spinal cords used for quantification. (E) Representative micrographs of lumbar spinal cord sections from SOD1G37R and SOD1G37R/MCK-PGC-1a animals at disease end-stage processed for immuno- fluorescence using antibodies detecting activated astrocytes (GFAP) or microglia (IbaI). Dashed outlines correspond to the boundary between gray and white matter.
Anti Pgc 1a, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Beijing ComWin Biotech Co anti-ampk
Figure 4. Elevating <t>PGC-1a</t> Expression in Skeletal Muscle of SOD1G37R Mutant Mice Does Not Alter ALS Disease Course or Pathogenesis (A) Plot of ages (in days) at which disease onset (as determined by the weight peak; at onset, animals do not display any obvious motor phenotype), symptomatic stage (as determined by 10% weight loss from onset, a stage characterized by clear gait abnormalities and tremor) and end-stage (as determined by hindlimb paralysis and inability to right itself) were reached for SOD1G37R (red) and SOD1G37R/MCK-PGC-1a (blue) animals. (B–D) Quantification of innervation at the neuromuscular junction of the gastrocnemius muscle (B), total number of a-motor axons in the lumbar L5 motor root (C), and quantification at disease end-stage of the average number of large cholinergic ventral horn motor neurons per section of lumbar spinal cord from SOD1G37R and SOD1G37R/MCK-PGC-1a animals (D). Data are presented as mean ± SEM. See also Figure S4 for representative sections of the spinal cords used for quantification. (E) Representative micrographs of lumbar spinal cord sections from SOD1G37R and SOD1G37R/MCK-PGC-1a animals at disease end-stage processed for immuno- fluorescence using antibodies detecting activated astrocytes (GFAP) or microglia (IbaI). Dashed outlines correspond to the boundary between gray and white matter.
Anti Ampk, supplied by Beijing ComWin Biotech Co, 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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Proteintech anti sert
Figure 4. Elevating <t>PGC-1a</t> Expression in Skeletal Muscle of SOD1G37R Mutant Mice Does Not Alter ALS Disease Course or Pathogenesis (A) Plot of ages (in days) at which disease onset (as determined by the weight peak; at onset, animals do not display any obvious motor phenotype), symptomatic stage (as determined by 10% weight loss from onset, a stage characterized by clear gait abnormalities and tremor) and end-stage (as determined by hindlimb paralysis and inability to right itself) were reached for SOD1G37R (red) and SOD1G37R/MCK-PGC-1a (blue) animals. (B–D) Quantification of innervation at the neuromuscular junction of the gastrocnemius muscle (B), total number of a-motor axons in the lumbar L5 motor root (C), and quantification at disease end-stage of the average number of large cholinergic ventral horn motor neurons per section of lumbar spinal cord from SOD1G37R and SOD1G37R/MCK-PGC-1a animals (D). Data are presented as mean ± SEM. See also Figure S4 for representative sections of the spinal cords used for quantification. (E) Representative micrographs of lumbar spinal cord sections from SOD1G37R and SOD1G37R/MCK-PGC-1a animals at disease end-stage processed for immuno- fluorescence using antibodies detecting activated astrocytes (GFAP) or microglia (IbaI). Dashed outlines correspond to the boundary between gray and white matter.
Anti Sert, supplied by Proteintech, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Bioss 8-ohdg polyclonal antibody
Figure 4. Elevating <t>PGC-1a</t> Expression in Skeletal Muscle of SOD1G37R Mutant Mice Does Not Alter ALS Disease Course or Pathogenesis (A) Plot of ages (in days) at which disease onset (as determined by the weight peak; at onset, animals do not display any obvious motor phenotype), symptomatic stage (as determined by 10% weight loss from onset, a stage characterized by clear gait abnormalities and tremor) and end-stage (as determined by hindlimb paralysis and inability to right itself) were reached for SOD1G37R (red) and SOD1G37R/MCK-PGC-1a (blue) animals. (B–D) Quantification of innervation at the neuromuscular junction of the gastrocnemius muscle (B), total number of a-motor axons in the lumbar L5 motor root (C), and quantification at disease end-stage of the average number of large cholinergic ventral horn motor neurons per section of lumbar spinal cord from SOD1G37R and SOD1G37R/MCK-PGC-1a animals (D). Data are presented as mean ± SEM. See also Figure S4 for representative sections of the spinal cords used for quantification. (E) Representative micrographs of lumbar spinal cord sections from SOD1G37R and SOD1G37R/MCK-PGC-1a animals at disease end-stage processed for immuno- fluorescence using antibodies detecting activated astrocytes (GFAP) or microglia (IbaI). Dashed outlines correspond to the boundary between gray and white matter.
8 Ohdg Polyclonal Antibody, supplied by Bioss, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Bioss cdc2/cdk1 polyclonal antibody
Figure 4. Elevating <t>PGC-1a</t> Expression in Skeletal Muscle of SOD1G37R Mutant Mice Does Not Alter ALS Disease Course or Pathogenesis (A) Plot of ages (in days) at which disease onset (as determined by the weight peak; at onset, animals do not display any obvious motor phenotype), symptomatic stage (as determined by 10% weight loss from onset, a stage characterized by clear gait abnormalities and tremor) and end-stage (as determined by hindlimb paralysis and inability to right itself) were reached for SOD1G37R (red) and SOD1G37R/MCK-PGC-1a (blue) animals. (B–D) Quantification of innervation at the neuromuscular junction of the gastrocnemius muscle (B), total number of a-motor axons in the lumbar L5 motor root (C), and quantification at disease end-stage of the average number of large cholinergic ventral horn motor neurons per section of lumbar spinal cord from SOD1G37R and SOD1G37R/MCK-PGC-1a animals (D). Data are presented as mean ± SEM. See also Figure S4 for representative sections of the spinal cords used for quantification. (E) Representative micrographs of lumbar spinal cord sections from SOD1G37R and SOD1G37R/MCK-PGC-1a animals at disease end-stage processed for immuno- fluorescence using antibodies detecting activated astrocytes (GFAP) or microglia (IbaI). Dashed outlines correspond to the boundary between gray and white matter.
Cdc2/Cdk1 Polyclonal Antibody, supplied by Bioss, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Bioss cd16 polyclonal antibody
Figure 4. Elevating <t>PGC-1a</t> Expression in Skeletal Muscle of SOD1G37R Mutant Mice Does Not Alter ALS Disease Course or Pathogenesis (A) Plot of ages (in days) at which disease onset (as determined by the weight peak; at onset, animals do not display any obvious motor phenotype), symptomatic stage (as determined by 10% weight loss from onset, a stage characterized by clear gait abnormalities and tremor) and end-stage (as determined by hindlimb paralysis and inability to right itself) were reached for SOD1G37R (red) and SOD1G37R/MCK-PGC-1a (blue) animals. (B–D) Quantification of innervation at the neuromuscular junction of the gastrocnemius muscle (B), total number of a-motor axons in the lumbar L5 motor root (C), and quantification at disease end-stage of the average number of large cholinergic ventral horn motor neurons per section of lumbar spinal cord from SOD1G37R and SOD1G37R/MCK-PGC-1a animals (D). Data are presented as mean ± SEM. See also Figure S4 for representative sections of the spinal cords used for quantification. (E) Representative micrographs of lumbar spinal cord sections from SOD1G37R and SOD1G37R/MCK-PGC-1a animals at disease end-stage processed for immuno- fluorescence using antibodies detecting activated astrocytes (GFAP) or microglia (IbaI). Dashed outlines correspond to the boundary between gray and white matter.
Cd16 Polyclonal Antibody, supplied by Bioss, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Figure 4. Elevating PGC-1a Expression in Skeletal Muscle of SOD1G37R Mutant Mice Does Not Alter ALS Disease Course or Pathogenesis (A) Plot of ages (in days) at which disease onset (as determined by the weight peak; at onset, animals do not display any obvious motor phenotype), symptomatic stage (as determined by 10% weight loss from onset, a stage characterized by clear gait abnormalities and tremor) and end-stage (as determined by hindlimb paralysis and inability to right itself) were reached for SOD1G37R (red) and SOD1G37R/MCK-PGC-1a (blue) animals. (B–D) Quantification of innervation at the neuromuscular junction of the gastrocnemius muscle (B), total number of a-motor axons in the lumbar L5 motor root (C), and quantification at disease end-stage of the average number of large cholinergic ventral horn motor neurons per section of lumbar spinal cord from SOD1G37R and SOD1G37R/MCK-PGC-1a animals (D). Data are presented as mean ± SEM. See also Figure S4 for representative sections of the spinal cords used for quantification. (E) Representative micrographs of lumbar spinal cord sections from SOD1G37R and SOD1G37R/MCK-PGC-1a animals at disease end-stage processed for immuno- fluorescence using antibodies detecting activated astrocytes (GFAP) or microglia (IbaI). Dashed outlines correspond to the boundary between gray and white matter.

Journal: Cell metabolism

Article Title: Elevated PGC-1α activity sustains mitochondrial biogenesis and muscle function without extending survival in a mouse model of inherited ALS.

doi: 10.1016/j.cmet.2012.03.019

Figure Lengend Snippet: Figure 4. Elevating PGC-1a Expression in Skeletal Muscle of SOD1G37R Mutant Mice Does Not Alter ALS Disease Course or Pathogenesis (A) Plot of ages (in days) at which disease onset (as determined by the weight peak; at onset, animals do not display any obvious motor phenotype), symptomatic stage (as determined by 10% weight loss from onset, a stage characterized by clear gait abnormalities and tremor) and end-stage (as determined by hindlimb paralysis and inability to right itself) were reached for SOD1G37R (red) and SOD1G37R/MCK-PGC-1a (blue) animals. (B–D) Quantification of innervation at the neuromuscular junction of the gastrocnemius muscle (B), total number of a-motor axons in the lumbar L5 motor root (C), and quantification at disease end-stage of the average number of large cholinergic ventral horn motor neurons per section of lumbar spinal cord from SOD1G37R and SOD1G37R/MCK-PGC-1a animals (D). Data are presented as mean ± SEM. See also Figure S4 for representative sections of the spinal cords used for quantification. (E) Representative micrographs of lumbar spinal cord sections from SOD1G37R and SOD1G37R/MCK-PGC-1a animals at disease end-stage processed for immuno- fluorescence using antibodies detecting activated astrocytes (GFAP) or microglia (IbaI). Dashed outlines correspond to the boundary between gray and white matter.

Article Snippet: Immunoblotting PGC-1a was immunoprecipitated using a rabbit anti-PGC-1a antibody (Santa Cruz; H300) from the gastrocnemius muscle of nontransgenic and MCK-PGC-1a mice.

Techniques: Expressing, Mutagenesis