LINC-ROR
Contents
Annotated Information
Name
LINC-ROR:long intergenic non-protein coding RNA, regulator of reprogramming
Characteristics
The RoR gene is 2.6 kb in length, located in chromosome 18 (hg19 chr18:54,721,802-54,739,350), consisting of four exons. [1]
Cellular Localization
18q21.31
Function
[[ LINC-ROR can modulate reprogramming of human differentiated cells to induce pluripotent stem cells.[2] RoR can also function as a negative regulator of p53 through interaction with an RNA binding protein, heterogeneous nuclear ribonucleoprotein I. Importantly, a 28-base RoR sequence carrying hnRNP I binding motifs is essential and suffcient for p53 repression. In addition, it can inhibit p53-mediated cell cycle arrest and apoptosis.[1] Linc-RoR functions as an endogenous miRNA sponge for differentiation-related miRNAs. and linc-RoR, miRNAs, and the core TFs can form a regulatory circuit consisting of autoregulatory and dualnegative feedback loops during embryonic stem cell (ESC) self-renewal. This regulatory loop maintains a relative balance in self-renewing human embryonic stem cells (hESCs) to resist slight environmental changes and to elicit a rapid response to strong differentiation signals that promote hESCs differentiation. [3] Linc-RoR modulates miR-145 levels, a sits overexpression diminishes endogenous miR-145 in self-renewing hESCs and drastically delays the increase in miR-145 upon hESC differentiation.[4]
Regulation
RoR-p53 autoregulatory feedback loop where p53 transcriptionally induces RoR expression. [1] Linc-RoR transcription ias mainly controlled by the core TFs Oct4, Sox2, and Nanog.[1]
Diseases
Expression
RoR is highly expressed in embryonic stem cells and iPSCs.[1] In self-renewing human embryonic stem cells (hESCs), linc-RoR is expressed at a high level and removes trace transcribed miRNAs when hESCs are subjected to temporary and slight differentiation agents.[3]
Sequence
Labs working on this lncRNA
- Stem Cell Transplantation Program, Division of Pediatric Hematology and Oncology, Manton Center for Orphan Disease Research, Children's Hospital Boston and Dana Farber Cancer Institute, Boston, Massachusetts, USA.[2]
- Department of Medical Microbiology, Immunology and Cell Biology, Southern Illinois University School of Medicine, Springfield, IL 62794-9621, USA.[1]
- Department of Histology and Embryology, College of Basic Medicine, Second Military Medical University, Shanghai 200433, China.[3]
References
- ↑ 1.0 1.1 1.2 1.3 1.4 1.5 Zhang A, Zhou N, Huang J, Liu Q, Fukuda K, Ma D, Lu Z, Bai C, Watabe K, Mo YY. The human long non-coding RNA-RoR is a p53 repressor in response to DNA damage. Cell Res. 2013 Mar;23(3):340-50.
- ↑ 2.0 2.1 Loewer S, Cabili MN, Guttman M, Loh YH, Thomas K, Park IH, Garber M, Curran M, Onder T, Agarwal S, Manos PD, Datta S, Lander ES, Schlaeger TM, Daley GQ, Rinn JL. Large intergenic non-coding RNA-RoR modulates reprogramming of human induced pluripotent stem cells. Nat Genet. 2010 Dec;42(12):1113-7.
- ↑ 3.0 3.1 3.2 Cite error: Invalid
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