Arraystar LncPath™ Necroptosis Pathway Microarray simultaneously profiles the expression of the LncRNAs in the Necroptosis signaling pathway and their protein-coding gene targets, to gain comprehensive insights into the underlying regulatory mechanisms of LncRNAs in the Necroptosis signaling pathway.
Necrosis, like apoptosis, can occur in a regulated manner known as "necroptosis" . Necroptosis participates in the pathogenesis of diseases during ischemic injury, neurodegeneration and viral infection, thereby representing an attractive target to avoid unwarranted cell death . Understanding the molecular mechanisms and the pathophysiology of the necroptosis pathway is an important goal of biological research.
The LncPath™ Human Necroptosis Pathway LncRNA Microarray simultaneously profiles the expression of 428 LncRNAs and 106 their protein-coding gene targets related to the necroptosis signaling pathway. The LncPath™ Mouse Necroptosis Pathway LncRNA Microarray simultaneously profiles the expression of 122 LncRNAs and 180 their protein-coding gene targets related to the necroptosis signaling pathway. The LncRNAs whose genes are located at or near the protein-coding genes critical in the necroptosis pathway, and the LncRNAs that have high possibilities of being competing endogenous RNAs (ceRNAs) of the key necroptosis pathway genes, are carefully collected from authoritative databases using rigorous selection processes. By focusing on the LncRNAs most relevant to the necroptosis pathway, the array can achieve much faster and more precise analysis, due to the highly specific yet smaller amount of data to analyze. More importantly, it can establish the expressional relationships between the LncRNAs and their protein-coding gene targets involved in the necroptosis pathway, thereby providing comprehensive insights into the underlying regulatory mechanisms of LncRNAs in the necroptosis pathway.
• Comprehensive and reliable collection of necroptosis pathway focused LncRNAs.
• Simultaneous analysis of LncRNAs and their protein-coding gene targets in the necroptosis pathway.
• Explore and establish expressional relationships and regulatory mechanisms between the LncRNAs and the target pathway genes.
• Faster and more precise pathway-focused analysis.
• Efficient and robust labeling system.
• Innovative probe design.
• Guaranteed performance.
An example showing the detailed information about the LncRNAs and their potential coding gene target
Click the LncRNA accession number listed in databases, you will see the figures showing the detailed information about the LncRNAs and their potential target gene.
Figure 1. The genomic map views of the LncRNA ENST00000563315 and its potential target gene CYLD. From the top to the bottom of the figure 1, the following items are displayed:
Genome view: A chromosome ideogram showing the map position of the LncRNA ENST00000563315 and its potential target gene CYLD(red bar).
Map view ruler: The map coordinates of the human genome assembly hg19 for the map views below.
LncRNA map view: The LncRNAs whose genes located at or near the CYLD gene are presented in the Noncoding panel (shaded green). The LncRNAs are indicated by the transcript IDs, the exons by solid blocks, the introns by thin lines, and the transcription directions by arrows. The exons of LncRNA ENST00000563315 are labeled in red, while the exons of the other LncRNAs are labeled in blue.
Coding gene map view: The coding gene CYLD is presented in the Coding panel (shaded blue). The coding gene is indicated by its canonical transcript ID, the exons by solid blocks, the introns by thin lines, and the transcription direction by arrows.
Figure 2. The relationship between LncRNA ENST00000563315 and its protein coding gene target CYLD. The other neighboring LncRNAs which may regulate CYLD expression are also shown.
Figure 3. The LncRNA uc003hkh.3 may function as a competing endogenous RNA (ceRNA) of the protein coding gene CYLD.
* MuTaMe Score, Mutually Targeted MRE Enrichment Score .
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2.Galluzzi, L. and G. Kroemer (2008) Cell 135 (7): 1161-3.
3.Tay, Y., et al. (2011) Cell 147 (2): 344-57.