LncRNA Information | ||||||
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ID | EL0282 | Name | CCDC26 | Aliases | RAM | |
Species | Homo sapiens | Chromosome | 8 | Start site | 129351691 | |
End site | 129680239 | Chain | minus | Exon NO. | 6 | |
Assembly | Ensembl Release 89 | Class | lincRNA | NCBI accession | NR_130917, NR_130918, NR_130919, NR_130920 | |
Ensembl | ENSG00000229140 | Sequence |
Disease | |||||||||
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Disease | Method | Sample | Expression pattern | Dysfunction type | Description | PMID | Source | ||
acute myeloid leukemia | microarray, qPCR, Western blot etc. | cell lines (HL-60, K562 etc.) | up-regulated | interaction | We found that CCDC26 transcripts were abundant in the nuclear fraction of K562 human myeloid leukemia cells. We suggest that CCDC26 controls growth of myeloid leukemia cells through regulation of KIT expression.A KIT inhibitor might be an effective treatment against the forms of AML in which CCDC26 is altered. | 25928165 | Lnc2Cancer | ||
glioma | N/A | N/A | N/A | mutation | In the pooled analysis, the odds ratio for low-grade glioma associated with rs55705857 was 4.3 (P = 2.31 脳 10(-94)). rs55705857 maps to a highly evolutionarily conserved sequence within the long non-coding RNA CCDC26 raising the possibility of direct functionality. | 23399484 | LncRNADisease | ||
Interaction | |||||||||
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Interaction target | Level of interaction | Type of interaction | Description | PMID | Source | ||||
KIT | RNA-DNA | regulation | We suggest that CCDC26 controls growth of myeloid leukemia cells through regulation of KIT expression. A KIT inhibitor might be an effective treatment against the forms of AML in which CCDC26 is altered. | 25928165 | |||||