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Related Concept Videos

Experimental RNAi02:15

Experimental RNAi

RNA interference (RNAi) is a cellular mechanism that inhibits gene expression by suppressing its transcription or activating the RNA degradation process. The mechanism was discovered by Andrew Fire and Craig Mello in 1998 in plants. Today, it is observed in almost all eukaryotes, including protozoa, flies, nematodes, insects, parasites, and mammals. This precise cellular mechanism of gene silencing has been developed into a technique that provides an efficient way to identify and determine the...
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MicroRNAs

MicroRNA (miRNA) are short, regulatory RNA transcribed from introns (non-coding regions of a gene) or intergenic regions (stretches of DNA present between genes). Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself, forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA...

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Updated: Jun 27, 2026

Modeling Neural Immune Signaling of Episodic and Chronic Migraine Using Spreading Depression In Vitro
16:13

Modeling Neural Immune Signaling of Episodic and Chronic Migraine Using Spreading Depression In Vitro

Published on: June 13, 2011

Machine Learning-Based Integration Unveils RNA Methylation Regulator-Related Immune-Derived Gene Signatures in

Yiwen Wu1, Jie Qiao2, Yuchun Liu3,4

  • 1Department of Neurosurgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310009, China.

Biomedicines
|June 26, 2026
PubMed
Summary
This summary is machine-generated.

Immune activation in aneurysmal subarachnoid hemorrhage (aSAH) involves RNA methylation. Oncostatin M (OSM) emerged as a key biomarker, suggesting a novel therapeutic target for aSAH-related neuroinflammation.

Keywords:
RNA methylationaneurysmal subarachnoid hemorrhageimmune inflammationmachine learningoncostatin Msingle-cell RNA sequencing

Related Experiment Videos

Last Updated: Jun 27, 2026

Modeling Neural Immune Signaling of Episodic and Chronic Migraine Using Spreading Depression In Vitro
16:13

Modeling Neural Immune Signaling of Episodic and Chronic Migraine Using Spreading Depression In Vitro

Published on: June 13, 2011

Area of Science:

  • Neuroscience
  • Immunology
  • Molecular Biology

Background:

  • Immune-inflammatory activation is central to aneurysmal subarachnoid hemorrhage (aSAH).
  • Epitranscriptomic mechanisms driving this immune response in aSAH are not fully understood.
  • This study investigates RNA methylation's role in aSAH immune dysregulation.

Purpose of the Study:

  • To investigate RNA methylation-associated immune dysregulation in aSAH.
  • To identify potential biomarkers and signaling pathways involved in aSAH.
  • To explore the role of Oncostatin M (OSM) and its associated signaling axis.

Main Methods:

  • Analysis of Gene Expression Omnibus datasets and ImmPort immune genes.
  • Machine learning (XGBoost-LASSO) for biomarker identification and validation.
  • Mendelian randomization, single-cell RNA sequencing, and clinical sample analysis (m6A quantification, qRT-PCR, Western blotting).

Main Results:

  • Eleven RNA methylation regulators were differentially expressed in aSAH.
  • An RNA methylation regulator-related immune-derived gene signature (RMRIGS) centered on Oncostatin M (OSM) effectively discriminated aSAH from controls.
  • OSM showed a protective association with subarachnoid hemorrhage risk, and an OSM-LIFR/GP130 signaling axis was identified in immune cells.

Conclusions:

  • RNA methylation programs are implicated in immune dysregulation following aSAH.
  • The OSM-centered RMRIGS may offer insights into peripheral immune activation and neuroinflammation post-aSAH.
  • The OSM-LIFR/GP130 signaling axis warrants further investigation for its role in aSAH pathogenesis.