mrna probes for ythdc2 and slc7a11 (Shanghai GenePharma)

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Shanghai GenePharma mrna probes for ythdc2 and slc7a11

Zinc finger protein 36 (Zfp36) through the <t>Ythdc2/SLC7A11/glutathione</t> (GSH)‐dependent ferroptosis pathway improve cardiac hypertrophy. (A‒H) The mRNA and protein expression levels of SLC7A11 ( n = 4‒5). (I) RNA immunoprecipitation (RIP)‐PCR analysed the m 6 A modification of SLC7A11 mRNA ( n = 3). (J) RNA‐pull down verified Ythdc2 bond to SLC7A11 mRNA ( n = 3). (K) RIP analysed the binding relation between Ythdc2 and SLC7A11 mRNA ( n = 3). (L) Co‐localisation of Ythdc2 and SLC7A11 mRNA in cardiomyocyte. (M) Real‐time PCR analysed the mRNA expression levels of SLC7A11 treated with or not Act D in over‐expression or knockdown Ythdc2 ( n = 3‒4). (N‒Q) Protein expression levels of SLC7A11 in mice hearts ( n = 4‒6). (R and S) GSH was negatively regulated by Ythdc2 in cardiac hypertrophy ( n = 3). (T‒U) Zfp36 regulates GSH level by Ythdc2 ( n = 3‒4). Statistical analysis was performed with Student's t ‐test or one‐way analysis of variance (ANOVA). Results presented as mean ± standard deviation (SD). * p < .05; ** p < .01.

Mrna Probes For Ythdc2 And Slc7a11, supplied by Shanghai GenePharma, 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/ythdc2/ythdc2+sirna++sense++gaguccaguuuagagaatt++anti+sense++uucuuaaacuggacutt/pmc11859123-282-6-9
Average 90 stars, based on 1 article reviews

mrna probes for ythdc2 and slc7a11 - by Bioz Stars, 2026-11

90/100 stars

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1) Product Images from "Targeting Zfp36 to combat cardiac hypertrophy: Insights into ferroptosis pathways"

Article Title: Targeting Zfp36 to combat cardiac hypertrophy: Insights into ferroptosis pathways

Journal: Clinical and Translational Medicine

doi: 10.1002/ctm2.70247

Zinc finger protein 36 (Zfp36) through the Ythdc2/SLC7A11/glutathione (GSH)‐dependent ferroptosis pathway improve cardiac hypertrophy. (A‒H) The mRNA and protein expression levels of SLC7A11 ( n = 4‒5). (I) RNA immunoprecipitation (RIP)‐PCR analysed the m 6 A modification of SLC7A11 mRNA ( n = 3). (J) RNA‐pull down verified Ythdc2 bond to SLC7A11 mRNA ( n = 3). (K) RIP analysed the binding relation between Ythdc2 and SLC7A11 mRNA ( n = 3). (L) Co‐localisation of Ythdc2 and SLC7A11 mRNA in cardiomyocyte. (M) Real‐time PCR analysed the mRNA expression levels of SLC7A11 treated with or not Act D in over‐expression or knockdown Ythdc2 ( n = 3‒4). (N‒Q) Protein expression levels of SLC7A11 in mice hearts ( n = 4‒6). (R and S) GSH was negatively regulated by Ythdc2 in cardiac hypertrophy ( n = 3). (T‒U) Zfp36 regulates GSH level by Ythdc2 ( n = 3‒4). Statistical analysis was performed with Student's t ‐test or one‐way analysis of variance (ANOVA). Results presented as mean ± standard deviation (SD). * p < .05; ** p < .01.

Figure Legend Snippet: Zinc finger protein 36 (Zfp36) through the Ythdc2/SLC7A11/glutathione (GSH)‐dependent ferroptosis pathway improve cardiac hypertrophy. (A‒H) The mRNA and protein expression levels of SLC7A11 ( n = 4‒5). (I) RNA immunoprecipitation (RIP)‐PCR analysed the m 6 A modification of SLC7A11 mRNA ( n = 3). (J) RNA‐pull down verified Ythdc2 bond to SLC7A11 mRNA ( n = 3). (K) RIP analysed the binding relation between Ythdc2 and SLC7A11 mRNA ( n = 3). (L) Co‐localisation of Ythdc2 and SLC7A11 mRNA in cardiomyocyte. (M) Real‐time PCR analysed the mRNA expression levels of SLC7A11 treated with or not Act D in over‐expression or knockdown Ythdc2 ( n = 3‒4). (N‒Q) Protein expression levels of SLC7A11 in mice hearts ( n = 4‒6). (R and S) GSH was negatively regulated by Ythdc2 in cardiac hypertrophy ( n = 3). (T‒U) Zfp36 regulates GSH level by Ythdc2 ( n = 3‒4). Statistical analysis was performed with Student's t ‐test or one‐way analysis of variance (ANOVA). Results presented as mean ± standard deviation (SD). * p < .05; ** p < .01.

Techniques Used: Expressing, RNA Immunoprecipitation, Modification, Binding Assay, Real-time Polymerase Chain Reaction, Over Expression, Knockdown, Standard Deviation

Expressing:

Article Title: FTO Knockdown-Mediated Maturation of miR-383-5p Inhibits Malignant Advancement of Pancreatic Cancer by Targeting ITGA3.
Article Snippet: m6A demethylase FTO is confirmed to be involved in pancreatic cancer progression.. FTO regulates miRNA processing.. To investigate the regulatory effect of FTO on miR-383-5p and its role in pancreatic cancer.

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mrna probes for ythdc2 and slc7a11 (Shanghai GenePharma)

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Expressing:

RNA Immunoprecipitation:

Modification:

Binding Assay:

Real-time Polymerase Chain Reaction:

Over Expression:

Knockdown:

Standard Deviation:

Incubation:

Control:

Aqueous Normal-phase Chromatography:

SYBR Green Assay:

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