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Developmental Studies Hybridoma Bank mhc
Mhc, supplied by Developmental Studies Hybridoma Bank, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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apc256 vio770 anti major histocompatibility complex mhc  (Miltenyi Biotec)
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Miltenyi Biotec apc256 vio770 anti major histocompatibility complex mhc
Apc256 Vio770 Anti Major Histocompatibility Complex Mhc, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/apc256 vio770 anti major histocompatibility complex mhc/product/Miltenyi Biotec
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apc256 vio770 anti major histocompatibility complex mhc - by Bioz Stars, 2026-03
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mouse anti mhc  (Developmental Studies Hybridoma Bank)
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Developmental Studies Hybridoma Bank mouse anti mhc
Mouse Anti Mhc, supplied by Developmental Studies Hybridoma Bank, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/mouse anti mhc/product/Developmental Studies Hybridoma Bank
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mouse anti mhc - by Bioz Stars, 2026-03
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anti myosin heavy chain mhc antibody  (Developmental Studies Hybridoma Bank)
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Developmental Studies Hybridoma Bank anti myosin heavy chain mhc antibody
SMYD2-mediated activation of SARM1 reduces NAD + level to <t>promote</t> <t>C2C12</t> myotube atrophy via increase of mtROS (A and B) The effect of smyd2 RNAi in reducing C2C12 myotubes atrophy was abolished by overexpression of SARM1. In A–7F, smyd2 siRNA (siSMYD2) was co-transfected with/without the overexpression plasmid of sarm1 (OE SARM1) into the differentiated C2C12 myotubes. #1 and #2 were two of siRNAs targeting the distinct coding sequences of smyd2 . The non-targeting siRNA (siNT) was used as control. The transfected myotubes were then treated with or without H 2 O 2 , respectively. (A) The representative images of C2C12 myotubes with <t>MHC</t> staining. Red, MHC protein; Blue, the nuclei stained by DAPI. (B) The analysis of myotube diameter and fusion index. The fusion index was indicated as the value of the number of nuclei present in myotubes divided by the number of total nuclei in MHC + cells. Error bars represent SEM. Myotube diameter: without H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) = 0.0003, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) < 0.0001, ∗∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) < 0.0001; with H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) < 0.0001, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0365; Fusion index: without H 2 O 2 : ∗p (siSMYD2 #1 vs. siNT) = 0.0162, ∗p (siSMYD2 #2 vs. siNT) = 0.0171, ∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0191, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0101; with H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0017, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0449; one-way ANOVA. (C and D) Overexpression of SARM1 attenuated the influences of smyd2 RNAi in up-regulating MHC mRNA level and downregulating the mRNA levels of atrophy-related genes in C2C12 myotubes with/without H 2 O 2 treatments. The mRNA levels of MHC (C), MuRF1 and Atrogin-1 (D) in myotubes were measured by RT-qPCR and normalized to those of control groups without H 2 O 2 treatment. β-actin was used as an internal reference. Error bars represent SEM. n = 3–4 biological replicates. MHC mRNA level: without H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) < 0.0001, ∗∗p (siSMYD2 #2 vs. siNT) = 0.0025, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0003, ∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0025; with H 2 O 2 : ∗∗p (siSMYD2 #1 vs. siNT) = 0.0065, ∗∗p (siSMYD2 #2 vs. siNT) = 0.0069, ∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0246, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0306; MuRF1 mRNA level: without H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) = 0.0001, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0172, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0111; with H 2 O 2 : ∗p (siSMYD2 #1 vs. siNT) = 0.0140, ∗p (siSMYD2 #2 vs. siNT) = 0.0196, ∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0189, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0407; Atrogin-1 mRNA level: without H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) = 0.0006, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0018, ∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0030; with H 2 O 2 : ∗∗p (siSMYD2 #1 vs. siNT) = 0.0031, ∗∗p (siSMYD2 #2 vs. siNT) = 0.0073, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0002; one-way ANOVA. (E) Overexpression of SARM1 attenuated the increased NAD + level of C2C12 myotubes with smyd2 RNAi treatment. The NAD + levels of myotubes were detected with microplate reader and normalized to those of control without H 2 O 2 treatment. Error bars represent SEM. n = 3 biological replicates. ∗p (siSMYD2 #1 vs. siNT) = 0.0100, ∗p (siSMYD2 #2 vs. siNT) = 0.0451, ∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0041, ∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0069; one-way ANOVA. (F) Overexpression of SARM1 alleviated the effect of smyd2 RNAi in decreasing mtROS level in C2C12 myotubes with/without H 2 O 2 treatments. The mtROS and nuclei (Blue) in myotubes were stained with MitoSOX and DAPI, respectively. The stained myotubes were detected by confocal microscopy (the representative images showed on the left), followed by quantitative analysis of fluorescence intensity (on the right). Error bars represent SEM. Without H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) < 0.0001, ∗∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) < 0.0001; with H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) < 0.0001, ∗∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) < 0.0001; one-way ANOVA.
Anti Myosin Heavy Chain Mhc Antibody, supplied by Developmental Studies Hybridoma Bank, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/anti myosin heavy chain mhc antibody/product/Developmental Studies Hybridoma Bank
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anti myosin heavy chain mhc antibody - by Bioz Stars, 2026-03
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myosin heavy chain mhc primary antibody  (Developmental Studies Hybridoma Bank)
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Developmental Studies Hybridoma Bank myosin heavy chain mhc primary antibody
SMYD2-mediated activation of SARM1 reduces NAD + level to <t>promote</t> <t>C2C12</t> myotube atrophy via increase of mtROS (A and B) The effect of smyd2 RNAi in reducing C2C12 myotubes atrophy was abolished by overexpression of SARM1. In A–7F, smyd2 siRNA (siSMYD2) was co-transfected with/without the overexpression plasmid of sarm1 (OE SARM1) into the differentiated C2C12 myotubes. #1 and #2 were two of siRNAs targeting the distinct coding sequences of smyd2 . The non-targeting siRNA (siNT) was used as control. The transfected myotubes were then treated with or without H 2 O 2 , respectively. (A) The representative images of C2C12 myotubes with <t>MHC</t> staining. Red, MHC protein; Blue, the nuclei stained by DAPI. (B) The analysis of myotube diameter and fusion index. The fusion index was indicated as the value of the number of nuclei present in myotubes divided by the number of total nuclei in MHC + cells. Error bars represent SEM. Myotube diameter: without H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) = 0.0003, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) < 0.0001, ∗∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) < 0.0001; with H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) < 0.0001, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0365; Fusion index: without H 2 O 2 : ∗p (siSMYD2 #1 vs. siNT) = 0.0162, ∗p (siSMYD2 #2 vs. siNT) = 0.0171, ∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0191, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0101; with H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0017, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0449; one-way ANOVA. (C and D) Overexpression of SARM1 attenuated the influences of smyd2 RNAi in up-regulating MHC mRNA level and downregulating the mRNA levels of atrophy-related genes in C2C12 myotubes with/without H 2 O 2 treatments. The mRNA levels of MHC (C), MuRF1 and Atrogin-1 (D) in myotubes were measured by RT-qPCR and normalized to those of control groups without H 2 O 2 treatment. β-actin was used as an internal reference. Error bars represent SEM. n = 3–4 biological replicates. MHC mRNA level: without H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) < 0.0001, ∗∗p (siSMYD2 #2 vs. siNT) = 0.0025, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0003, ∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0025; with H 2 O 2 : ∗∗p (siSMYD2 #1 vs. siNT) = 0.0065, ∗∗p (siSMYD2 #2 vs. siNT) = 0.0069, ∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0246, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0306; MuRF1 mRNA level: without H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) = 0.0001, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0172, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0111; with H 2 O 2 : ∗p (siSMYD2 #1 vs. siNT) = 0.0140, ∗p (siSMYD2 #2 vs. siNT) = 0.0196, ∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0189, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0407; Atrogin-1 mRNA level: without H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) = 0.0006, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0018, ∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0030; with H 2 O 2 : ∗∗p (siSMYD2 #1 vs. siNT) = 0.0031, ∗∗p (siSMYD2 #2 vs. siNT) = 0.0073, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0002; one-way ANOVA. (E) Overexpression of SARM1 attenuated the increased NAD + level of C2C12 myotubes with smyd2 RNAi treatment. The NAD + levels of myotubes were detected with microplate reader and normalized to those of control without H 2 O 2 treatment. Error bars represent SEM. n = 3 biological replicates. ∗p (siSMYD2 #1 vs. siNT) = 0.0100, ∗p (siSMYD2 #2 vs. siNT) = 0.0451, ∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0041, ∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0069; one-way ANOVA. (F) Overexpression of SARM1 alleviated the effect of smyd2 RNAi in decreasing mtROS level in C2C12 myotubes with/without H 2 O 2 treatments. The mtROS and nuclei (Blue) in myotubes were stained with MitoSOX and DAPI, respectively. The stained myotubes were detected by confocal microscopy (the representative images showed on the left), followed by quantitative analysis of fluorescence intensity (on the right). Error bars represent SEM. Without H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) < 0.0001, ∗∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) < 0.0001; with H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) < 0.0001, ∗∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) < 0.0001; one-way ANOVA.
Myosin Heavy Chain Mhc Primary Antibody, supplied by Developmental Studies Hybridoma Bank, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/myosin heavy chain mhc primary antibody/product/Developmental Studies Hybridoma Bank
Average 99 stars, based on 1 article reviews
myosin heavy chain mhc primary antibody - by Bioz Stars, 2026-03
99/100 stars
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pe anti mhc 257 ii  (Miltenyi Biotec)
95
Miltenyi Biotec pe anti mhc 257 ii
SMYD2-mediated activation of SARM1 reduces NAD + level to <t>promote</t> <t>C2C12</t> myotube atrophy via increase of mtROS (A and B) The effect of smyd2 RNAi in reducing C2C12 myotubes atrophy was abolished by overexpression of SARM1. In A–7F, smyd2 siRNA (siSMYD2) was co-transfected with/without the overexpression plasmid of sarm1 (OE SARM1) into the differentiated C2C12 myotubes. #1 and #2 were two of siRNAs targeting the distinct coding sequences of smyd2 . The non-targeting siRNA (siNT) was used as control. The transfected myotubes were then treated with or without H 2 O 2 , respectively. (A) The representative images of C2C12 myotubes with <t>MHC</t> staining. Red, MHC protein; Blue, the nuclei stained by DAPI. (B) The analysis of myotube diameter and fusion index. The fusion index was indicated as the value of the number of nuclei present in myotubes divided by the number of total nuclei in MHC + cells. Error bars represent SEM. Myotube diameter: without H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) = 0.0003, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) < 0.0001, ∗∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) < 0.0001; with H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) < 0.0001, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0365; Fusion index: without H 2 O 2 : ∗p (siSMYD2 #1 vs. siNT) = 0.0162, ∗p (siSMYD2 #2 vs. siNT) = 0.0171, ∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0191, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0101; with H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0017, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0449; one-way ANOVA. (C and D) Overexpression of SARM1 attenuated the influences of smyd2 RNAi in up-regulating MHC mRNA level and downregulating the mRNA levels of atrophy-related genes in C2C12 myotubes with/without H 2 O 2 treatments. The mRNA levels of MHC (C), MuRF1 and Atrogin-1 (D) in myotubes were measured by RT-qPCR and normalized to those of control groups without H 2 O 2 treatment. β-actin was used as an internal reference. Error bars represent SEM. n = 3–4 biological replicates. MHC mRNA level: without H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) < 0.0001, ∗∗p (siSMYD2 #2 vs. siNT) = 0.0025, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0003, ∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0025; with H 2 O 2 : ∗∗p (siSMYD2 #1 vs. siNT) = 0.0065, ∗∗p (siSMYD2 #2 vs. siNT) = 0.0069, ∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0246, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0306; MuRF1 mRNA level: without H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) = 0.0001, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0172, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0111; with H 2 O 2 : ∗p (siSMYD2 #1 vs. siNT) = 0.0140, ∗p (siSMYD2 #2 vs. siNT) = 0.0196, ∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0189, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0407; Atrogin-1 mRNA level: without H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) = 0.0006, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0018, ∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0030; with H 2 O 2 : ∗∗p (siSMYD2 #1 vs. siNT) = 0.0031, ∗∗p (siSMYD2 #2 vs. siNT) = 0.0073, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0002; one-way ANOVA. (E) Overexpression of SARM1 attenuated the increased NAD + level of C2C12 myotubes with smyd2 RNAi treatment. The NAD + levels of myotubes were detected with microplate reader and normalized to those of control without H 2 O 2 treatment. Error bars represent SEM. n = 3 biological replicates. ∗p (siSMYD2 #1 vs. siNT) = 0.0100, ∗p (siSMYD2 #2 vs. siNT) = 0.0451, ∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0041, ∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0069; one-way ANOVA. (F) Overexpression of SARM1 alleviated the effect of smyd2 RNAi in decreasing mtROS level in C2C12 myotubes with/without H 2 O 2 treatments. The mtROS and nuclei (Blue) in myotubes were stained with MitoSOX and DAPI, respectively. The stained myotubes were detected by confocal microscopy (the representative images showed on the left), followed by quantitative analysis of fluorescence intensity (on the right). Error bars represent SEM. Without H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) < 0.0001, ∗∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) < 0.0001; with H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) < 0.0001, ∗∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) < 0.0001; one-way ANOVA.
Pe Anti Mhc 257 Ii, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/pe anti mhc 257 ii/product/Miltenyi Biotec
Average 95 stars, based on 1 article reviews
pe anti mhc 257 ii - by Bioz Stars, 2026-03
95/100 stars
  Buy from Supplier
pe anti mhc257 ii  (Miltenyi Biotec)
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Miltenyi Biotec pe anti mhc257 ii
SMYD2-mediated activation of SARM1 reduces NAD + level to <t>promote</t> <t>C2C12</t> myotube atrophy via increase of mtROS (A and B) The effect of smyd2 RNAi in reducing C2C12 myotubes atrophy was abolished by overexpression of SARM1. In A–7F, smyd2 siRNA (siSMYD2) was co-transfected with/without the overexpression plasmid of sarm1 (OE SARM1) into the differentiated C2C12 myotubes. #1 and #2 were two of siRNAs targeting the distinct coding sequences of smyd2 . The non-targeting siRNA (siNT) was used as control. The transfected myotubes were then treated with or without H 2 O 2 , respectively. (A) The representative images of C2C12 myotubes with <t>MHC</t> staining. Red, MHC protein; Blue, the nuclei stained by DAPI. (B) The analysis of myotube diameter and fusion index. The fusion index was indicated as the value of the number of nuclei present in myotubes divided by the number of total nuclei in MHC + cells. Error bars represent SEM. Myotube diameter: without H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) = 0.0003, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) < 0.0001, ∗∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) < 0.0001; with H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) < 0.0001, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0365; Fusion index: without H 2 O 2 : ∗p (siSMYD2 #1 vs. siNT) = 0.0162, ∗p (siSMYD2 #2 vs. siNT) = 0.0171, ∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0191, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0101; with H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0017, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0449; one-way ANOVA. (C and D) Overexpression of SARM1 attenuated the influences of smyd2 RNAi in up-regulating MHC mRNA level and downregulating the mRNA levels of atrophy-related genes in C2C12 myotubes with/without H 2 O 2 treatments. The mRNA levels of MHC (C), MuRF1 and Atrogin-1 (D) in myotubes were measured by RT-qPCR and normalized to those of control groups without H 2 O 2 treatment. β-actin was used as an internal reference. Error bars represent SEM. n = 3–4 biological replicates. MHC mRNA level: without H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) < 0.0001, ∗∗p (siSMYD2 #2 vs. siNT) = 0.0025, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0003, ∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0025; with H 2 O 2 : ∗∗p (siSMYD2 #1 vs. siNT) = 0.0065, ∗∗p (siSMYD2 #2 vs. siNT) = 0.0069, ∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0246, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0306; MuRF1 mRNA level: without H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) = 0.0001, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0172, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0111; with H 2 O 2 : ∗p (siSMYD2 #1 vs. siNT) = 0.0140, ∗p (siSMYD2 #2 vs. siNT) = 0.0196, ∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0189, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0407; Atrogin-1 mRNA level: without H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) = 0.0006, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0018, ∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0030; with H 2 O 2 : ∗∗p (siSMYD2 #1 vs. siNT) = 0.0031, ∗∗p (siSMYD2 #2 vs. siNT) = 0.0073, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0002; one-way ANOVA. (E) Overexpression of SARM1 attenuated the increased NAD + level of C2C12 myotubes with smyd2 RNAi treatment. The NAD + levels of myotubes were detected with microplate reader and normalized to those of control without H 2 O 2 treatment. Error bars represent SEM. n = 3 biological replicates. ∗p (siSMYD2 #1 vs. siNT) = 0.0100, ∗p (siSMYD2 #2 vs. siNT) = 0.0451, ∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0041, ∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0069; one-way ANOVA. (F) Overexpression of SARM1 alleviated the effect of smyd2 RNAi in decreasing mtROS level in C2C12 myotubes with/without H 2 O 2 treatments. The mtROS and nuclei (Blue) in myotubes were stained with MitoSOX and DAPI, respectively. The stained myotubes were detected by confocal microscopy (the representative images showed on the left), followed by quantitative analysis of fluorescence intensity (on the right). Error bars represent SEM. Without H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) < 0.0001, ∗∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) < 0.0001; with H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) < 0.0001, ∗∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) < 0.0001; one-way ANOVA.
Pe Anti Mhc257 Ii, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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SMYD2-mediated activation of SARM1 reduces NAD + level to <t>promote</t> <t>C2C12</t> myotube atrophy via increase of mtROS (A and B) The effect of smyd2 RNAi in reducing C2C12 myotubes atrophy was abolished by overexpression of SARM1. In A–7F, smyd2 siRNA (siSMYD2) was co-transfected with/without the overexpression plasmid of sarm1 (OE SARM1) into the differentiated C2C12 myotubes. #1 and #2 were two of siRNAs targeting the distinct coding sequences of smyd2 . The non-targeting siRNA (siNT) was used as control. The transfected myotubes were then treated with or without H 2 O 2 , respectively. (A) The representative images of C2C12 myotubes with <t>MHC</t> staining. Red, MHC protein; Blue, the nuclei stained by DAPI. (B) The analysis of myotube diameter and fusion index. The fusion index was indicated as the value of the number of nuclei present in myotubes divided by the number of total nuclei in MHC + cells. Error bars represent SEM. Myotube diameter: without H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) = 0.0003, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) < 0.0001, ∗∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) < 0.0001; with H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) < 0.0001, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0365; Fusion index: without H 2 O 2 : ∗p (siSMYD2 #1 vs. siNT) = 0.0162, ∗p (siSMYD2 #2 vs. siNT) = 0.0171, ∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0191, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0101; with H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0017, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0449; one-way ANOVA. (C and D) Overexpression of SARM1 attenuated the influences of smyd2 RNAi in up-regulating MHC mRNA level and downregulating the mRNA levels of atrophy-related genes in C2C12 myotubes with/without H 2 O 2 treatments. The mRNA levels of MHC (C), MuRF1 and Atrogin-1 (D) in myotubes were measured by RT-qPCR and normalized to those of control groups without H 2 O 2 treatment. β-actin was used as an internal reference. Error bars represent SEM. n = 3–4 biological replicates. MHC mRNA level: without H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) < 0.0001, ∗∗p (siSMYD2 #2 vs. siNT) = 0.0025, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0003, ∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0025; with H 2 O 2 : ∗∗p (siSMYD2 #1 vs. siNT) = 0.0065, ∗∗p (siSMYD2 #2 vs. siNT) = 0.0069, ∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0246, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0306; MuRF1 mRNA level: without H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) = 0.0001, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0172, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0111; with H 2 O 2 : ∗p (siSMYD2 #1 vs. siNT) = 0.0140, ∗p (siSMYD2 #2 vs. siNT) = 0.0196, ∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0189, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0407; Atrogin-1 mRNA level: without H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) = 0.0006, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0018, ∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0030; with H 2 O 2 : ∗∗p (siSMYD2 #1 vs. siNT) = 0.0031, ∗∗p (siSMYD2 #2 vs. siNT) = 0.0073, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0002; one-way ANOVA. (E) Overexpression of SARM1 attenuated the increased NAD + level of C2C12 myotubes with smyd2 RNAi treatment. The NAD + levels of myotubes were detected with microplate reader and normalized to those of control without H 2 O 2 treatment. Error bars represent SEM. n = 3 biological replicates. ∗p (siSMYD2 #1 vs. siNT) = 0.0100, ∗p (siSMYD2 #2 vs. siNT) = 0.0451, ∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0041, ∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0069; one-way ANOVA. (F) Overexpression of SARM1 alleviated the effect of smyd2 RNAi in decreasing mtROS level in C2C12 myotubes with/without H 2 O 2 treatments. The mtROS and nuclei (Blue) in myotubes were stained with MitoSOX and DAPI, respectively. The stained myotubes were detected by confocal microscopy (the representative images showed on the left), followed by quantitative analysis of fluorescence intensity (on the right). Error bars represent SEM. Without H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) < 0.0001, ∗∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) < 0.0001; with H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) < 0.0001, ∗∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) < 0.0001; one-way ANOVA.
Apc 256 Vio770 Anti Major Histocompatibility Complex Mhc, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


SMYD2-mediated activation of SARM1 reduces NAD + level to promote C2C12 myotube atrophy via increase of mtROS (A and B) The effect of smyd2 RNAi in reducing C2C12 myotubes atrophy was abolished by overexpression of SARM1. In A–7F, smyd2 siRNA (siSMYD2) was co-transfected with/without the overexpression plasmid of sarm1 (OE SARM1) into the differentiated C2C12 myotubes. #1 and #2 were two of siRNAs targeting the distinct coding sequences of smyd2 . The non-targeting siRNA (siNT) was used as control. The transfected myotubes were then treated with or without H 2 O 2 , respectively. (A) The representative images of C2C12 myotubes with MHC staining. Red, MHC protein; Blue, the nuclei stained by DAPI. (B) The analysis of myotube diameter and fusion index. The fusion index was indicated as the value of the number of nuclei present in myotubes divided by the number of total nuclei in MHC + cells. Error bars represent SEM. Myotube diameter: without H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) = 0.0003, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) < 0.0001, ∗∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) < 0.0001; with H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) < 0.0001, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0365; Fusion index: without H 2 O 2 : ∗p (siSMYD2 #1 vs. siNT) = 0.0162, ∗p (siSMYD2 #2 vs. siNT) = 0.0171, ∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0191, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0101; with H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0017, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0449; one-way ANOVA. (C and D) Overexpression of SARM1 attenuated the influences of smyd2 RNAi in up-regulating MHC mRNA level and downregulating the mRNA levels of atrophy-related genes in C2C12 myotubes with/without H 2 O 2 treatments. The mRNA levels of MHC (C), MuRF1 and Atrogin-1 (D) in myotubes were measured by RT-qPCR and normalized to those of control groups without H 2 O 2 treatment. β-actin was used as an internal reference. Error bars represent SEM. n = 3–4 biological replicates. MHC mRNA level: without H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) < 0.0001, ∗∗p (siSMYD2 #2 vs. siNT) = 0.0025, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0003, ∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0025; with H 2 O 2 : ∗∗p (siSMYD2 #1 vs. siNT) = 0.0065, ∗∗p (siSMYD2 #2 vs. siNT) = 0.0069, ∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0246, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0306; MuRF1 mRNA level: without H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) = 0.0001, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0172, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0111; with H 2 O 2 : ∗p (siSMYD2 #1 vs. siNT) = 0.0140, ∗p (siSMYD2 #2 vs. siNT) = 0.0196, ∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0189, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0407; Atrogin-1 mRNA level: without H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) = 0.0006, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0018, ∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0030; with H 2 O 2 : ∗∗p (siSMYD2 #1 vs. siNT) = 0.0031, ∗∗p (siSMYD2 #2 vs. siNT) = 0.0073, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0002; one-way ANOVA. (E) Overexpression of SARM1 attenuated the increased NAD + level of C2C12 myotubes with smyd2 RNAi treatment. The NAD + levels of myotubes were detected with microplate reader and normalized to those of control without H 2 O 2 treatment. Error bars represent SEM. n = 3 biological replicates. ∗p (siSMYD2 #1 vs. siNT) = 0.0100, ∗p (siSMYD2 #2 vs. siNT) = 0.0451, ∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0041, ∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0069; one-way ANOVA. (F) Overexpression of SARM1 alleviated the effect of smyd2 RNAi in decreasing mtROS level in C2C12 myotubes with/without H 2 O 2 treatments. The mtROS and nuclei (Blue) in myotubes were stained with MitoSOX and DAPI, respectively. The stained myotubes were detected by confocal microscopy (the representative images showed on the left), followed by quantitative analysis of fluorescence intensity (on the right). Error bars represent SEM. Without H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) < 0.0001, ∗∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) < 0.0001; with H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) < 0.0001, ∗∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) < 0.0001; one-way ANOVA.

Journal: iScience

Article Title: Histone methyltransferase SET-18/SMYD2-mediated activation of NADase TIR-1d/SARM1 increases mtROS to promote aging

doi: 10.1016/j.isci.2026.114649

Figure Lengend Snippet: SMYD2-mediated activation of SARM1 reduces NAD + level to promote C2C12 myotube atrophy via increase of mtROS (A and B) The effect of smyd2 RNAi in reducing C2C12 myotubes atrophy was abolished by overexpression of SARM1. In A–7F, smyd2 siRNA (siSMYD2) was co-transfected with/without the overexpression plasmid of sarm1 (OE SARM1) into the differentiated C2C12 myotubes. #1 and #2 were two of siRNAs targeting the distinct coding sequences of smyd2 . The non-targeting siRNA (siNT) was used as control. The transfected myotubes were then treated with or without H 2 O 2 , respectively. (A) The representative images of C2C12 myotubes with MHC staining. Red, MHC protein; Blue, the nuclei stained by DAPI. (B) The analysis of myotube diameter and fusion index. The fusion index was indicated as the value of the number of nuclei present in myotubes divided by the number of total nuclei in MHC + cells. Error bars represent SEM. Myotube diameter: without H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) = 0.0003, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) < 0.0001, ∗∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) < 0.0001; with H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) < 0.0001, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0365; Fusion index: without H 2 O 2 : ∗p (siSMYD2 #1 vs. siNT) = 0.0162, ∗p (siSMYD2 #2 vs. siNT) = 0.0171, ∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0191, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0101; with H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0017, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0449; one-way ANOVA. (C and D) Overexpression of SARM1 attenuated the influences of smyd2 RNAi in up-regulating MHC mRNA level and downregulating the mRNA levels of atrophy-related genes in C2C12 myotubes with/without H 2 O 2 treatments. The mRNA levels of MHC (C), MuRF1 and Atrogin-1 (D) in myotubes were measured by RT-qPCR and normalized to those of control groups without H 2 O 2 treatment. β-actin was used as an internal reference. Error bars represent SEM. n = 3–4 biological replicates. MHC mRNA level: without H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) < 0.0001, ∗∗p (siSMYD2 #2 vs. siNT) = 0.0025, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0003, ∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0025; with H 2 O 2 : ∗∗p (siSMYD2 #1 vs. siNT) = 0.0065, ∗∗p (siSMYD2 #2 vs. siNT) = 0.0069, ∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0246, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0306; MuRF1 mRNA level: without H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) = 0.0001, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0172, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0111; with H 2 O 2 : ∗p (siSMYD2 #1 vs. siNT) = 0.0140, ∗p (siSMYD2 #2 vs. siNT) = 0.0196, ∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0189, ∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0407; Atrogin-1 mRNA level: without H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) = 0.0006, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0018, ∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0030; with H 2 O 2 : ∗∗p (siSMYD2 #1 vs. siNT) = 0.0031, ∗∗p (siSMYD2 #2 vs. siNT) = 0.0073, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0002; one-way ANOVA. (E) Overexpression of SARM1 attenuated the increased NAD + level of C2C12 myotubes with smyd2 RNAi treatment. The NAD + levels of myotubes were detected with microplate reader and normalized to those of control without H 2 O 2 treatment. Error bars represent SEM. n = 3 biological replicates. ∗p (siSMYD2 #1 vs. siNT) = 0.0100, ∗p (siSMYD2 #2 vs. siNT) = 0.0451, ∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) = 0.0041, ∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) = 0.0069; one-way ANOVA. (F) Overexpression of SARM1 alleviated the effect of smyd2 RNAi in decreasing mtROS level in C2C12 myotubes with/without H 2 O 2 treatments. The mtROS and nuclei (Blue) in myotubes were stained with MitoSOX and DAPI, respectively. The stained myotubes were detected by confocal microscopy (the representative images showed on the left), followed by quantitative analysis of fluorescence intensity (on the right). Error bars represent SEM. Without H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) < 0.0001, ∗∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) < 0.0001; with H 2 O 2 : ∗∗∗p (siSMYD2 #1 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #2 vs. siNT) < 0.0001, ∗∗∗p (siSMYD2 #1+OE SARM1 vs. siSMYD2 #1) < 0.0001, ∗∗∗p (siSMYD2 #2+OE SARM1 vs. siSMYD2 #2) < 0.0001; one-way ANOVA.

Article Snippet: The C2C12 myotubes were incubated with anti-myosin heavy chain (MHC) antibody (MF20, DSHB) followed by fluorescent secondary antibody (C2181, Sigma Chemical) to identify MHC expression.

Techniques: Activation Assay, Over Expression, Transfection, Plasmid Preparation, Control, Staining, Quantitative RT-PCR, Confocal Microscopy, Fluorescence