anti-RORA (RORA) 抗体产品概述

Human RAR-Related Orphan Receptor A (RORA) interaction partners

1. The expression of RORalpha in salivary glands was significantly increased in patients with primary Sjogren's syndrome.

2. Taken together, these studies indicate that LSD1-mediated RORalpha2 transcriptional activity is important to promote tumor cell migration in human breast cancer as well as breast cancer cell lines.

3. the RORA rs11071559C>T polymorphism was associated with an elevated susceptibility to pediatric asthma in the Chinese Zhuang population

4. RORalpha controls inflammatory state of human macrophages.

5. study identified three significant SNPs (RORA rs782917 G > A, RORA rs17204952 C > T and DNMT1 rs7253062 G > A) as potential predictors of cutaneous melanoma specific survival

6. three copy-number variant deletions (two de novo and one dominantly inherited in three generations), one de novo disrupting duplication, and nine de novo point mutations (three truncating, one canonical splice site, and five missense mutations) involving RORA, are reported.

7. We have identified RORalpha as a regulator of Treg genes responsible for suppressing allergic skin inflammation and also documented higher expression of RORalpha in skin-resident Tregs than in peripheral blood circulating Tregs in humans, suggesting that RORalpha and the TL1A-DR3 circuit could be therapeutically targeted in atopic dermatitis.

8. RORA downregulation may be a potential indicator of positive response to interferon beta treatment of multiple sclerosis patients

9. In the present study we have detected an association between rs4774388 genotype and breast cancer risk in a population of Iranian breast cancer patients.

10. rs4774388-TT genotype was significantly higher in patients compared with controls and was associated with autism spectrum disorder risk in dominant inheritance model

11. human melanoma development and aggressiveness is associated with decreased expression of RORalpha and RORgamma, suggesting that RORs could be important in melanoma progression and host responses against the tumor

12. CYP11A1- derived hydroxyvitamin D derivatives as "inverse" agonists on ROR-alpha and ROR-gamma.

13. The expression RORalpha is significantly elevated under hypoxic conditions in keratinocytes in an HIF-1alpha dependent manner.

14. RORgammat and RORalpha have overlapping roles in human Th17 cell differentiation through regulation of a defined common set of Th17 genes

15. Retinoid-related orphan receptor alpha-regulated development of the mouse cerebellum has a distinct critical period for (1) lengthening Purkinje cell (PC) primary dendrite stems and the eventual increase in the thickness of the molecular layer and (2) the establishment of mGluR signaling and associated removal of surplus climbing fibers from PCs.

16. findings strongly suggest that CLDND1 is a direct RORalpha target

17. TRIB3 promotes acute promyelocytic leukemia progression through stabilization of the oncoprotein PML-RARalpha and inhibition of p53-mediated senescence.

18. Retinoid-related orphan receptor alpha (RORalpha) reduction occurs in gastric cancer leading to the survival of tumor cells, which is attenuated by AMP-activated protein kinase (AMPK), therefore, both RORalpha and AMPK are potential targets for the intervention and therapy in gastric carcinoma.

19. the RAR-related orphan receptor-a gene (RORA) and the Peroxisome Proliferator-Activated Receptor Gamma, Coactivator 1 Alpha gene (PPARGC1A or PGC-1alpha) were significantly associated with the Li response. Our results suggest genetic associations between Li response and these two close biological partners: PPARGC1A and RORA involved in circadian rhythms and bioenergetics processes in Li response

20. The present study is to determine if any relation exists between RORA rs11639084 and rs4774388 gene polymorphisms on the individual susceptibility of multiple sclerosis.

Zebrafish RAR-Related Orphan Receptor A (RORA) interaction partners

1. study reports cloning and expression pattern of zebrafish ROR alpha orthologues rora1 and rora2; both rora1 and rora2 are spatially expressed in the retina and tectum; expression of rora2 was further observed in the cerebellum

Mouse (Murine) RAR-Related Orphan Receptor A (RORA) interaction partners

1. results indicate that osteoarthritis is a disease associated with metabolic disorders and suggest that targeting the CH25H-CYP7B1-RORalpha axis of cholesterol metabolism may provide a therapeutic avenue for treating osteoarthritis.

2. Our study showed the pivotal role of RORalpha as an inhibitor of the thermogenic program in white adipose tissue

3. We have identified RORalpha as a regulator of Treg genes responsible for suppressing allergic skin inflammation and also documented higher expression of RORalpha in skin-resident Tregs than in peripheral blood circulating Tregs in humans, suggesting that RORalpha and the TL1A-DR3 circuit could be therapeutically targeted in atopic dermatitis.

4. These findings demonstrated for the first time that nuclear receptor RORalpha deficiency aggravated HFD-induced myocardial dysfunction at least in part by impairing mitochondrial biogenesis in association with disrupting AMPK-PGC1alpha signaling.

5. RORalpha/gamma controls circadian expression of Insig2, which keeps feeding-induced SREBP1c activation under check

6. RORalpha induces KLF4 mediated Kupffer cells polarization and protects against NASH.

7. RORalpha/gamma are important therapeutic targets for cutaneous inflammation; RORa and RORg have roles in inflammation in mouse models of atopic dermatitis and acute irritant dermititis

8. Data demonstrated that the circadian rhythm of testosterone synthesis in TM3 cells was disturbed following Fen treatment as evidenced by changes in the circadian rhythmicity of core clock genes (Bmal1, Rev-erbalpha, Roralpha).

9. RORalpha inhibits PPARgamma-mediated transcriptional activity by interacting with HDAC3 and competing for the promoters of lipogenic genes.

10. The expression RORalpha is significantly elevated under hypoxic conditions in keratinocytes in an HIF-1alpha dependent manner.

11. that retinoic acid receptor-related orphan receptor alpha is a novel transcriptional regulator of SEMA3E-mediated neurovascular coupling in pathological retinal angiogenesis

12. The deficiency of LXRalpha decreased glucose uptake after MI, resulting in a metabolic shift that suppressed glucose metabolism, which was in association with adverse cardiac remodeling.

13. Data suggest that inflammatory response in macrophages, white adipocytes, and white adipose tissue in obese mice, includes up-regulation of expression of Rora; in adipose tissue, overexpression of Rora or treatment with Rora agonist enhances expression of cytokines, promotes macrophage infiltration, up-regulates expression of genes involved in ER stress response, and enhances signaling seen in unfolded protein response.

14. these findings reveal that RORalpha regulates macrophage M2 polarization via activation of AMPKalpha

15. RORalpha-dependent type 2 innate lymphoid cells are required and sufficient for type 2 cytokine expression and mucous metaplasia in immature mice.

16. pharmacological activation of RORalpha by melatonin and SR1078 (a synthetic agonist) showed beneficial effects against diabetic cardiomyopathy, while the RORalpha inhibitor SR3335 significantly exacerbated cardiac impairments in diabetic mice.

17. study provides the first direct evidence that the nuclear melatonin receptor RORalpha is a novel endogenous protective receptor against MI/R injury and an important mediator of melatonin-exerted cardioprotection; melatonin-RORalpha axis signaling thus appears important in protection against ischemic heart injury.

18. RORalpha regulates pathologic retinal angiogenesis by modulating SOCS3-dependent inflammation

19. This study showed that spontaneous Rora mutations causing cerebellar pathology are impaired in motor functions during the neonatal period.

20. the inhibition of NF-kappaB by melatonin, but not that of NLRP3, was blunted in RORalpha (sg/sg) mice, indicating that functional RORalpha transcription factor is necessary for the initiation of the innate immune response against inflammation.