Ask about this productRelated genes to: ROR1 antibody
- Gene:
- ROR1 NIH gene
- Name:
- receptor tyrosine kinase like orphan receptor 1
- Previous symbol:
- NTRKR1
- Synonyms:
- -
- Chromosome:
- 1p31.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-02-29
- Date modifiied:
- 2016-06-28
- Gene:
- RORA NIH gene
- Name:
- RAR related orphan receptor A
- Previous symbol:
- -
- Synonyms:
- RZRA, ROR1, ROR2, ROR3, NR1F1
- Chromosome:
- 15q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-04-13
- Date modifiied:
- 2016-10-05
Related products to: ROR1 antibody
Related articles to: ROR1 antibody
- Dendritic differentiation involves both regressive and growth events. The mechanisms controlling the regressive events are poorly understood. This study is aimed at determining the role of the nuclear receptor retinoid-related orphan receptor alpha (RORalpha) in Purkinje cell (PC) dendritic differentiation in organotypic cultures. As observed in vivo, in these cultures, fusiform PCs with embryonic bipolar shape undergo regression before the outgrowth of the ultimate dendritic tree. We show that lentiviral-mediated hRORalpha1 overexpression in fusiform PCs leads to a cell-autonomous accelerated progression of dendritic differentiation. In addition, RORalpha is necessary for the PC regressive events: whereas staggerer RORalpha-deficient PCs remain in the embryonic fusiform stage, replacement of hRORalpha1 restores normal dendritogenesis. These results demonstrate that RORalpha expression in fusiform PCs is crucial for the dendritic regression and progression of the following step of extension of dendritic processes. However, it does not seem to participate to the last stage of dendritic growth. This study identifies RORalpha as a nuclear receptor crucial for the control of dendritic remodeling during development. - Source: PubMed
Boukhtouche FatihaJanmaat SonjaVodjdani GuilanGautheron VanessaMallet JacquesDusart IsabelleMariani Jean - The newly identified apolipoprotein A5 (APOA5), selectively expressed in the liver, is a crucial determinant of plasma triglyceride levels. Because elevated plasma triglyceride concentrations constitute an independent risk factor for cardiovascular diseases, it is important to understand how the expression of this gene is regulated. In the present study, we identified the retinoic acid receptor-related orphan receptor-alpha (RORalpha) as a regulator of human APOA5 gene expression. - Source: PubMed
Publication date: 2005/03/24
Genoux AnneliseDehondt HélèneHelleboid-Chapman AudreyDuhem ChristianHum Dean WMartin GenevièvePennacchio Len AStaels BartFruchart-Najib JamilaFruchart Jean-Charles - We characterized the expression levels of the retinoid Z receptor alpha (RZR alpha), RORalpha mRNA isoforms (RORalpha1, RORalpha2, and RORalpha3), and both melatonin receptor MT1 and hydroxindole-O-methyltransferase (HIOMT) genes. For this purpose, the following human peripheral blood mononuclear cells populations were isolated: monocytes (CD14+ cells), B lymphocytes (CD19+ cells), T helper lymphocytes (CD14(-) CD4+), cytotoxic T lymphocytes (CD56(-) CD8+ cells), and natural killer (NK) lymphocytes (CD56+ cells). PBMCs subsets were obtained by Dynabeads M-450 (Dynal) isolation procedure. We observed a strong gene expression signal for RZRalpha in all subpopulations studied, whereas both RORalpha1 and RORalpha2 transcripts were amplified only in CD8+ cells. Specific signal for RORalpha2 was obtained in all subpopulations studied, but we were not able to detect the RORalpha3 mRNA transcript in human immune cells studied. A weaker signal (especially in CD19+ cells) was also detected in all subsets of cells for the MT1 gene. With regard to HIOMT, a strong signal was achieved among all but one subpopulation of cells; the only exception was CD14+ cells. Thus, in addition to its classical function in the nervous and endocrine system, melatonin could act directly as a paracrine and/or autocrine agent in the human immune system. - Source: PubMed
Pozo DavidGarcía-Mauriño SofíaGuerrero Juan MCalvo Juan R - Hypoxia plays a key role in the pathophysiology of many disease states, and expression of the retinoic acid receptor-related orphan receptor alpha (RORalpha) gene increases under hypoxia. We investigated the mechanism for this transient hypoxia-induced increase in RORalpha expression. Reverse transcription-coupled PCR analysis revealed that the steady-state level of mRNA for the RORalpha4 isoform, but not the RORalpha1 isoform, increased in HepG2 cells after 3 h of hypoxia. Transient transfection studies showed that the hypoxia-induced increase in RORalpha4 mRNA occurs at the transcriptional level and is dependent on a hypoxia-responsive element (HRE) located downstream of the promoter. A dominant-negative mutant of hypoxia-inducible factor-1alpha (HIF-1alpha) abrogates the transcription activated by hypoxia as well as the transcription activated by exogenously expressed HIF-1alpha, demonstrating the direct involvement of HIF-1alpha in the transcriptional activation. However, HIF-1 alone was not sufficient to activate transcription in hypoxic conditions but, rather, required Sp1/Sp3, which binds to a cluster of GC-rich sequences adjacent to the HRE. Deletion of one or more of these GC boxes reduced or eliminated the HIF-1-dependent transcription. Together, these results suggest that the hypoxia-responsive region of the RORalpha4 promoter is composed of the HRE and GC-rich sequences and that the transcriptional activation under hypoxia is conferred through the cooperation of HIF-1 with Sp1/Sp3. - Source: PubMed
Publication date: 2004/01/23
Miki NaokiIkuta MegumiMatsui Takashi - Retinoic acid receptor-related orphan receptor-alpha (RORalpha) is a nuclear orphan receptor. Adenovirus-mediated overexpression of RORalpha1 and RORalpha4 suppressed tumor necrosis factor-alpha (TNF-alpha)-induced expression of vascular cell adhesion molecule-1 (VCAM-1) and intracellular adhesion molecule-1 (ICAM-1) in human umbilical vein endothelial cells. Overexpression of RORalpha1 and RORalpha4 also suppressed TNF-alpha-stimulated translocation of p50 and p65 to the nucleus. In contrast, dominant-negative deletion mutants of RORalpha1 and RORalpha4 failed to suppress the induction of VCAM-1 and ICAM-1 and translocations of p50 and p65. These results suggest that RORalpha1 and RORalpha4 regulate the inflammatory responses via inhibition of the nuclear factor-kappaB signaling pathway in endothelial cells. - Source: PubMed
Migita HideyukiSatozawa NoboruLin Jiing-HueyMorser JohnKawai Kohichi