scholarly journals NCX1 Is a Novel Target Gene for Hypoxia-Inducible Factor-1 in Ischemic Brain Preconditioning

Stroke ◽  
2011 ◽  
Vol 42 (3) ◽  
pp. 754-763 ◽  
Author(s):  
Valeria Valsecchi ◽  
Giuseppe Pignataro ◽  
Annalisa Del Prete ◽  
Rossana Sirabella ◽  
Carmela Matrone ◽  
...  
Keyword(s):  
Target Gene ◽  
Hypoxia Inducible Factor ◽  
Ischemic Brain ◽  
Hypoxia Inducible Factor 1 ◽  
Novel Target ◽  
Brain Preconditioning

scholarly journals Cathepsin L, a Target of Hypoxia-Inducible Factor-1-α, Is Involved in Melanosome Degradation in Melanocytes

2021 ◽  
Vol 22 (16) ◽  
pp. 8596
Author(s):  
Ji Young Kim ◽  
Eun Jung Lee ◽  
Yuri Ahn ◽  
Sujin Park ◽  
Yu Jeong Bae ◽  
...  
Keyword(s):  
Target Gene ◽  
Target Genes ◽  
Cathepsin L ◽  
Hypoxia Inducible Factor ◽  
Luciferase Reporter ◽  
Lysosomal Activity ◽  
Hypoxia Inducible Factor 1 ◽  
Lysosomal Protease ◽  
Hypoxic Conditions ◽  
Novel Target

Hypoxic conditions induce the activation of hypoxia-inducible factor-1α (HIF-1α) to restore the supply of oxygen to tissues and cells. Activated HIF-1α translocates into the nucleus and binds to hypoxia response elements to promote the transcription of target genes. Cathepsin L (CTSL) is a lysosomal protease that degrades cellular proteins via the endolysosomal pathway. In this study, we attempted to determine if CTSL is a hypoxia responsive target gene of HIF-1α, and decipher its role in melanocytes in association with the autophagic pathway. The results of our luciferase reporter assay showed that the expression of CTSL is transcriptionally activated through the binding of HIF1-α at its promoter. Under autophagy-inducing starvation conditions, HIF-1α and CTSL expression is highly upregulated in melan-a cells. The mature form of CTSL is closely involved in melanosome degradation through lysosomal activity upon autophagosome–lysosome fusion. The inhibition of conversion of pro-CTSL to mature CTSL leads to the accumulation of gp100 and tyrosinase in addition to microtubule-associated protein 1 light chain 3 (LC3) II, due to decreased lysosomal activity in the autophagic pathway. In conclusion, we have identified that CTSL, a novel target of HIF-1α, participates in melanosome degradation in melanocytes through lysosomal activity during autophagosome–lysosome fusion.

Hypoxia inducible factor-1: a novel target for cancer therapy

2005 ◽  
Vol 16 (9) ◽  
pp. 901-909 ◽  
Author(s):  
Vladimir E. Belozerov ◽  
Erwin G. Van Meir
Keyword(s):  
Cancer Therapy ◽  
Hypoxia Inducible Factor ◽  
Hypoxia Inducible Factor 1 ◽  
Novel Target

Abstract WMP70: HIF-1alpha Sumoylation Provides Neuroprotection in Ischemic Stroke

Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
Jingqi Yan ◽  
Honglian Shi
Keyword(s):  
Therapeutic Target ◽  
Hypoxia Inducible Factor ◽  
Artery Occlusion ◽  
Neuron Death ◽  
Ischemic Brain ◽  
Hypoxia Inducible Factor 1 ◽  
Induced Neuron ◽  
Cerebral Artery Occlusion ◽  
First Time

Hypoxia-inducible factor 1 (HIF-1) is a transcriptional factor that regulates the cellular adaptive response to hypoxia and has been suggested as a potent therapeutic target in stroke. To find new post-transpational modification pathways of HIF-1 in ischemic brain, we determined SUMOylation of HIF-1α protein in ischemic brain of a rat middle cerebral artery occlusion (MCAO) stroke model. The results demonstrated that SUMOylation of HIF-1α by SUMO1 was increased in the ischemic brain. Immunostaining images showed that HIF-1α co-localized with SUMO1 in the neuron nucleus of the ischemic brain. Inhibition of HIF-1α SUMOylation by Ubc9 siRNA reduced HIF-1α protein level in primary neurons during hypoxia. Furthermore, ischemia-induced neuron death was increased by the Ubc9 siRNA. The results, for the first time, demonstrate that HIF-1α is directly SUMOylated in the ischemic brain. HIF-1α SUMOylation is important for HIF-1α stability and neuron survival during ischemia. These results complement the knowledge about HIF-1 regulation in ischemic brain and shed new light on the role of HIF-1 as a stroke therapeutic target.

Control of HIF-1α Levels Potentially Promotes the Tissue Repair in Various Conditions Through Target Gene Expression

2021 ◽  
Vol 6 (1) ◽  
pp. 1266-1274
Author(s):  
Riyadh Firdaus ◽  
Ani Retno Prijanti
Keyword(s):  
Tissue Repair ◽  
Target Gene ◽  
Hypoxia Inducible Factor ◽  
The Body ◽  
Beta Subunits ◽  
Oxygen Balance ◽  
Hypoxia Inducible Factor 1 ◽  
Systemic Hypoxia ◽  
Adaptation Response ◽  
Tumor Growth And Metastasis

Hypoxia inducible factor-1 (HIF-1) is a transcription factor that plays an important role in maintaining oxygen balance at both the cellular and systemic levels, and is associated with various controls in the body. HIF-1 is a heterodimer of alpha and beta subunits. Alpha subunits are mostly dependent on oxygen levels in the body. In many cancers, excessive HIF-1α is thought to be involved in the promotion of tumor growth and metastasis. In addition, in the induction of systemic hypoxia, there is an increase of HIF-1α in the heart, brain, and even the kidneys as an adaptation response to hypoxia. Several studies regarding HIF-1a expression in traumatic brain injury, found that HIF-1a increased immediately after TBI, and decreased significantly after 24 hours. This can be used as a basis for further research on HIF-1a control as an effort to stop tissue damage or even help tissue repair.

Hypoxia‐inducible protein 2 is a novel lipid droplet protein and a specific target gene of hypoxia‐inducible factor‐1

2010 ◽  
Vol 24 (11) ◽  
pp. 4443-4458 ◽  
Author(s):  
Tina Gimm ◽  
Melanie Wiese ◽  
Barbara Teschemacher ◽  
Anke Deggerich ◽  
Johannes Schödel ◽  
...  
Keyword(s):  
Lipid Droplet ◽  
Target Gene ◽  
Hypoxia Inducible Factor ◽  
Specific Target ◽  
Hypoxia Inducible Factor 1 ◽  
Specific Target Gene ◽  
Inducible Protein ◽  
Lipid Droplet Protein
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