Nucleolar Protein 3 (Apoptosis Repressor with CARD Domain) Proteins (NOL3)

Human Nucleolar Protein 3 (Apoptosis Repressor with CARD Domain) (NOL3) interaction partners

1. Results show that in response to DNA damage, p53 total levels increase proportionally to the strength of the damage; however, p53 tetramers are formed at a constant rate under the control of ARC protein.

2. role of apoptosis repressor with a CARD domain (ARC) in the therapeutic resistance of renal cell carcinoma

3. a novel genetic primary myelofibrosis-like mouse model and identify a tumor suppressor role for NOL3 in the pathogenesis of myeloid malignancies.

4. Increased ARC expression is associated with liver metastasis of colorectal cancer.

5. RUNX3, miR-185 and ARC regulate the sensitivity of gastric cancer cells to chemotherapy.

6. ARC is regulated via BIRC2/MAP3K14 signalling and its overexpression in AML or MSCs can function as a resistant factor to birinapant-induced leukaemia cell death.

7. high expression of ARC plays an important role in the pathogenesis of nasopharyngeal carcinoma and leads to X-radiation and cisplatin resistance in nasopharyngeal carcinoma.

8. ARC is a previously unrecognized inhibitor of apoptosis in beta-cells and that its protective effects are mediated through suppression of the ER stress response pathway.

9. This study utilized unbiased, genome-wide approaches to identify a NOL3 mutation that likely causes Familial cortical myoclonus.

10. HIF-1alpha directly bound to hypoxia-responsive element located at -419 to -414 of ARC gene, which is essential for HIF-1-induced expression.

11. Data show that ARC promotes breast carcinogenesis by driving primary tumor growth, invasion, and metastasis as well as by promoting chemoresistance in invasive cells.

12. ARC, previously unlinked to pulmonary hypertension, is a critical determinant of vascular remodeling in this syndrome.

13. Results suggest that ARC expression levels are highly prognostic in AML and that ARC is a potential therapeutic target in AML.

14. Ras induces ARC in epithelial cancers, and ARC plays a role in the oncogenic actions of Ras

15. These results suggest that the antiapoptotic effect of apoptotic repressor with caspase recruitment domain is, in part, due to inhibition of voltage-gated potassium channels in cardiomyocytes.

16. calcium binding mediates regulation of caspase 8 and cell death by ARC

17. Unexpectedly, ARC was localized almost exclusively to the nuclei of cancer cells, which was unlike the cytoplasmic localization of ARC in non-cancer cells

18. ARC was present in the cytoplasm and nuclei of epithelial cells in invasive ductal carcinoma

19. is downregulated in human failing myocardium

20. nuclear apoptosis repressor with caspase recruitment domain (ARC)is induced in cancer cells and negatively regulates p53

Mouse (Murine) Nucleolar Protein 3 (Apoptosis Repressor with CARD Domain) (NOL3) interaction partners

1. Data suggest that reduced levels of apoptosis repressor with caspase recruitment domain protein (ARC) might correlate with neomycin-induced hair cells (HCs) loss.

2. Although mice lacking Men1 developed insulinomas as expected, elimination of ARC in this context did not significantly alter tumor load. Cellular rates of proliferation and death in these tumors were also not perturbed in the absence of ARC.

3. interaction of ARC with TNF receptor 1 Interferes with recruitment of RIP1, a critical mediator of TNFalpha-induced regulated necrosis.

4. Arc deficiency in dystrophic muscle exacerbates disease pathogenesis due to a Bax-mediated sensitization of mitochondria-dependent death mechanisms

5. ARC is a previously unrecognized inhibitor of apoptosis in beta-cells and that its protective effects are mediated through suppression of the ER stress response pathway.

6. Data show that ARC promotes breast carcinogenesis by driving primary tumor growth, invasion, and metastasis as well as by promoting chemoresistance in invasive cells.

7. ARC, previously unlinked to pulmonary hypertension, is a critical determinant of vascular remodeling in this syndrome.

8. On biomechanical stress induced by aortic banding, ARC-deficient mice developed accelerated cardiomyopathy, which was characterized by reduced contractile function, cardiac enlargement, and myocardial fibrosis

9. catalase, CK2, and ARC constitute an anti-hypertrophic pathway in the heart.

10. endogenous nociceptin differentially modulates diet preference depending on macronutrient content and homeostatic state, independently of the motivating, rewarding or orosensory properties of food, but may involve metabolic or postingestive processes.