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 (show TP53 Proteins) total levels increase proportionally to the strength of the damage; however, p53 (show TP53 Proteins) 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 (show MOK Proteins)

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 (show RUNX3 Proteins), miR (show MLXIP Proteins)-185 and ARC regulate the sensitivity of gastric cancer cells to chemotherapy.

6. ARC is regulated via BIRC2 (show BIRC2 Proteins)/MAP3K14 (show MAP3K14 Proteins) signalling and its overexpression in AML (show RUNX1 Proteins) 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 (show HIF1A Proteins) directly bound to hypoxia-responsive element located at -419 to -414 of ARC gene, which is essential for HIF-1 (show HIF1A Proteins)-induced expression.

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 (show HLCS Proteins)) 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 (show TNF Proteins) receptor 1 Interferes with recruitment of RIP1 (show RALBP1 Proteins), a critical mediator of TNFalpha (show TNF Proteins)-induced regulated necrosis.

4. Arc deficiency in dystrophic muscle exacerbates disease pathogenesis due to a Bax (show BAX Proteins)-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 (show CAT Proteins), CK2 (show CSNK2A1 Proteins), 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.