Ca2+/calmodulin kinase-dependent activation of hypoxia inducible factor 1 transcriptional activity in cells subjected to intermittent hypoxia.
about
Peripheral chemoreception and arterial pressure responses to intermittent hypoxiaUnexpected benefits of intermittent hypoxia: enhanced respiratory and nonrespiratory motor functionImaging tumor hypoxia to advance radiation oncologyHypoxia-inducible factors and hypertension: lessons from sleep apnea syndromeNADPH oxidase subunit 4-mediated reactive oxygen species contribute to cycling hypoxia-promoted tumor progression in glioblastoma multiformeImpact of the phosphatidylinositide 3-kinase signaling pathway on the cardioprotection induced by intermittent hypoxiaHypoxia-inducible factor 1 mediates increased expression of NADPH oxidase-2 in response to intermittent hypoxiaSLEEP DISORDERED BREATHING AND METABOLIC EFFECTS: EVIDENCE FROM ANIMAL MODELSCycling hypoxia and free radicals regulate angiogenesis and radiotherapy responseModulating temporal and spatial oxygenation over adherent cellular culturesExpression and regulation of HIF-1alpha in macrophages under inflammatory conditions; significant reduction of VEGF by CaMKII inhibitorCalcium mediates high glucose-induced HIF-1α and VEGF expression in cultured rat retinal Müller cells through CaMKII-CREB pathway.A novel Ca2+/calmodulin antagonist HBC inhibits angiogenesis and down-regulates hypoxia-inducible factor.Intermittent and sustained hypoxia induce a similar gene expression profile in human aortic endothelial cells.A Transcriptomic Analysis of Physiological Significance of Hypoxia-inducible Factor-1α in Myogenesis and Carbohydrate Metabolism of Genioglossus in MiceExploring the role of mitochondrial UQCRB in angiogenesis using small molecules.CaMKII Inhibitor KN-62 Blunts Tumor Response to Hypoxia by Inhibiting HIF-1α in Hepatoma Cells.Hypoxia-inducible factor 2α (HIF-2α) heterozygous-null mice exhibit exaggerated carotid body sensitivity to hypoxia, breathing instability, and hypertensionA splice variant of the human ion channel TRPM2 modulates neuroblastoma tumor growth through hypoxia-inducible factor (HIF)-1/2α.Hypoxia. 3. Hypoxia and neurotransmitter synthesis.Calcium/calmodulin-dependent protein kinases in the carotid body: an immunohistochemical studyHypoxia. 4. Hypoxia and ion channel functionXanthine oxidase mediates hypoxia-inducible factor-2α degradation by intermittent hypoxia.Endothelial function in obstructive sleep apnea.HIF-1α activation by intermittent hypoxia requires NADPH oxidase stimulation by xanthine oxidaseObstructive sleep apnea and type 2 diabetesSensory plasticity of the carotid body: role of reactive oxygen species and physiological significance.Spinal vascular endothelial growth factor induces phrenic motor facilitation via extracellular signal-regulated kinase and Akt signaling.The growth and aggressive behavior of human osteosarcoma is regulated by a CaMKII-controlled autocrine VEGF signaling mechanismNNC 55-0396, a T-type Ca2+ channel inhibitor, inhibits angiogenesis via suppression of hypoxia-inducible factor-1α signal transduction.Alterations in left ventricular function during intermittent hypoxia: Possible involvement of O-GlcNAc protein and MAPK signaling.Hypoxia-inducible factor 1 transcriptional activity in endothelial cells is required for acute phase cardioprotection induced by ischemic preconditioning.Transcriptional responses to intermittent hypoxiaMetabolic dysfunction in obstructive sleep apnea: A critical examination of underlying mechanismsInflammation induced by increased frequency of intermittent hypoxia is attenuated by tempol administrationCervical spinal erythropoietin induces phrenic motor facilitation via extracellular signal-regulated protein kinase and Akt signaling.The relationship of daytime hypoxemia and nocturnal hypoxia in obstructive sleep apnea syndrome.Cardiovascular morbidity in obstructive sleep apnea: oxidative stress, inflammation, and much more.CaV3.2 T-type Ca2+ channels mediate the augmented calcium influx in carotid body glomus cells by chronic intermittent hypoxia.trans-Resveratrol protects ischemic PC12 Cells by inhibiting the hypoxia associated transcription factors and increasing the levels of antioxidant defense enzymes.
P2860
Q26996367-ABD06054-23A4-4D10-B487-B9C8FCAE5204Q27000674-DBA53966-69C3-43DC-AC15-7855511B377DQ27007862-E0DA17B5-BB1F-44D9-9AE7-9E4C18C70CFEQ27026931-8F9D6375-F8A0-4A5E-9FF9-F116173906FBQ28477083-1FBCB218-318C-4955-B6A1-5DD154B82074Q28534096-152E9273-25E9-4850-813D-68DB1A50AEECQ28582257-9F641E2A-AEF6-4549-A52F-2024C1E680E6Q30494316-9A2447F3-B2FD-4C80-A2D0-56619E937B92Q30573416-A8A70846-3AF3-4CC8-8345-797D5C29BE49Q33499690-2F72BBCD-7345-4B9C-8C64-C2ACFF0224FCQ33547668-063110ED-A313-4D41-B8C9-ECB3EDC6A9D3Q33571261-090A9900-F668-4E10-986A-D163DAD4A32EQ33606606-B300052E-814B-40C5-BD36-AF368229A747Q33847657-1922D2E1-F9DC-4F0D-9A57-E4F95D633008Q33864729-D9C67927-5BF4-401A-912C-43D6B6BF4D9BQ34332044-583046B5-8B3E-4CE9-A925-02DB30504806Q34382055-3B3B3C6B-1B3F-4402-90D1-5E988CB6249AQ34582873-2949F6B6-B208-4995-B612-B25B271089D1Q34774611-82FE6AD6-5C4E-4F89-A76A-4002ECFD4FCFQ34782170-E4FAD99B-9DD7-490C-BC00-CFD80A1110DCQ34958328-4F9BD54A-B899-4B00-AAE0-CFF241E8FAE4Q34979263-FE758EB6-3AAB-448A-B130-FAD2E43CC690Q35016826-D71C6480-620B-4C58-80D8-F64DD095C1DAQ35086889-A2CDF041-BE14-4FBB-88A1-3B4EAD15E099Q35159133-3D0A3D4E-CD11-4DF2-99F6-6933AEE9C751Q35179113-D82AEFD4-7B3D-4D6D-A1F3-650B2E06FEB9Q35206888-1C627799-C230-49CC-A977-AA187441DE26Q35212423-0CDB1208-F6BD-474F-AA2C-8BC071C983F9Q35362682-C3B00D4B-07C7-482C-83B0-09AD217262CFQ35486167-5B729726-3C94-446A-9711-63162844FFCEQ35827630-F3ECF890-839D-40D4-84E0-F4338B1D55DFQ36068993-0FFE9063-D455-4265-A2F6-C59308B571D4Q36079641-7E31C8D3-E5BB-45CE-8A25-C095F072DA1AQ36093354-321E6B9A-05D1-43C4-994A-50FD7B189E88Q36322301-93FDC0CF-C38D-4FF3-AC8D-70F9794A1385Q36422327-46D51F7E-5DC4-4333-AF07-5DB251F8247AQ36427090-6CEA41C0-8470-4CF2-AFEC-30C99359A8DEQ36482623-9C7CAFB2-2FEB-4C76-92C8-31134EEB00BFQ36598059-5A6462B5-15ED-4882-87D0-F8476BF27485Q36638599-7A031A3B-DCED-48A7-A595-050520C82B55
P2860
Ca2+/calmodulin kinase-dependent activation of hypoxia inducible factor 1 transcriptional activity in cells subjected to intermittent hypoxia.
description
2004 nî lūn-bûn
@nan
2004年の論文
@ja
2004年学术文章
@wuu
2004年学术文章
@zh
2004年学术文章
@zh-cn
2004年学术文章
@zh-hans
2004年学术文章
@zh-my
2004年学术文章
@zh-sg
2004年學術文章
@yue
2004年學術文章
@zh-hant
name
Ca2+/calmodulin kinase-depende ...... ected to intermittent hypoxia.
@en
Ca2+/calmodulin kinase-depende ...... ected to intermittent hypoxia.
@nl
type
label
Ca2+/calmodulin kinase-depende ...... ected to intermittent hypoxia.
@en
Ca2+/calmodulin kinase-depende ...... ected to intermittent hypoxia.
@nl
prefLabel
Ca2+/calmodulin kinase-depende ...... ected to intermittent hypoxia.
@en
Ca2+/calmodulin kinase-depende ...... ected to intermittent hypoxia.
@nl
P2093
P2860
P356
P1476
Ca2+/calmodulin kinase-depende ...... ected to intermittent hypoxia.
@en
P2093
C Raman Bhasker
Guoxiang Yuan
Jayasri Nanduri
Nanduri R Prabhakar
P2860
P304
P356
10.1074/JBC.M407706200
P407
P577
2004-11-29T00:00:00Z