ArticlePloS one2010
Characterization of the activation of protein tyrosine phosphatase, receptor-type, Z polypeptide 1 (PTPRZ1) by hypoxia inducible factor-2 alpha.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 32 citations in OpenAlex.
- Hypoxia-inducible factors: Regulatory functions and status as a therapeutic target in gastric cancer (Review).Oncology letters · 2026Review
- Regulation of Pleiotrophin and PTPRZ1 Expression by Hypoxia to Restrict Hypoxia-Induced Cell Migration.Cancers · 2025Article
- Article
- Hypoxia and hypoxia-inducible factors in Kaposi sarcoma-associated herpesvirus infection and disease pathogenesis.Journal of medical virology · 2023Review
- Protein Tyrosine Phosphatase Receptor Zeta 1 as a Potential Target in Cancer Therapy and Diagnosis.International journal of molecular sciences · 2023Review
- Unearthing of Key Genes Driving the Pathogenesis of Alzheimer's Disease via Bioinformatics.Frontiers in genetics · 2021Article
- Induction of Kaposi's Sarcoma-Associated Herpesvirus-Encoded Thymidine Kinase (ORF21) by X-Box Binding Protein 1.Journal of virology · 2020Article
- The Expression, Functions, Interactions and Prognostic Values of PTPRZ1: A Review and Bioinformatic Analysis.Journal of Cancer · 2019Review
- Allosteric inhibition induces an open WPD-loop: a new avenue towards glioblastoma therapy.RSC advances · 2018Article
- Identification of functional hypoxia inducible factor response elements in the human lysyl oxidase gene promoter.Biochemical and biophysical research communications · 2017Article
- Differential gene network analysis from single cell RNA-seq.Journal of genetics and genomics = Yi chuan xue bao · 2017Article
- HRAS mutation prevalence and associated expression patterns in pheochromocytoma.Genes, chromosomes & cancer · 2016Article
- Expression of receptor protein tyrosine phosphatase ζ is a risk factor for triple negative breast cancer relapse.Biomedical reports · 2016Article
- Induction of Kaposi's Sarcoma-Associated Herpesvirus-Encoded Viral Interleukin-6 by X-Box Binding Protein 1.Journal of virology · 2016Article
- PTN signaling: Components and mechanistic insights in human ovarian cancer.Molecular carcinogenesis · 2015Article
- Hypoxia-inducible factor-mediated induction of WISP-2 contributes to attenuated progression of breast cancer.Hypoxia (Auckland, N.Z.) · 2014Article
- Pleiotrophin gene therapy for peripheral ischemia: evaluation of full-length and truncated gene variants.PloS one · 2013Article
- PTPRZ1 regulates calmodulin phosphorylation and tumor progression in small-cell lung carcinoma.BMC cancer · 2012Article
- N-myc downstream-regulated gene 1/Cap43 may function as tumor suppressor in endometrial cancer.Journal of cancer research and clinical oncology · 2012Article
- Non-canonical HIF-2α function drives autonomous breast cancer cell growth via an AREG-EGFR/ErbB4 autocrine loop.Oncogene · 2012Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundHypoxia inducible factors (HIFs) are the principal means by which cells upregulate genes in response to hypoxia and certain other stresses. There are two major HIFs, HIF-1 and HIF-2. We previously found that certain genes are preferentially activated by HIF-2. One was protein tyrosine phosphatase, receptor-type, Z polypeptide 1 (PTPRZ1). PTPRZ1 is overexpressed in a number of tumors and has been implicated in glioblastoma pathogenesis. METHODOLOGY/PRINCIPAL
findingsTo understand the preferential activation of PTPRZ1 by HIF-2, we studied the PTPRZ1 promoter in HEK293T cells and Hep3B cells. Through deletion and mutational analysis, we identified the principal hypoxia response element. This element bound to both HIF-1 and HIF-2. We further identified a role for ELK1, an E26 transformation-specific (Ets) factor that can bind to HIF-2alpha but not HIF-1alpha, in the HIF-2 responsiveness. Knock-down experiments using siRNA to ELK1 decreased HIF-2 activation by over 50%. Also, a deletion mutation of one of the two Ets binding motifs located near the principal hypoxia response element similarly decreased activation of the PTPRZ1 promoter by HIF-2. Finally, chromatin immunoprecipitation assays showed binding of HIF and ELK1 to the PTPRZ1 promoter region. CONCLUSIONS/SIGNIFICANCE: These results identify HIF-binding and Ets-binding motifs on the PTPRZ1 promoter and provide evidence that preferential activation of PTPRZ1 by HIF-2 results at least in part from cooperative binding of HIF-2 and ELK1 to nearby sites on the PTPRZ1 promoter region. These results may have implications in tumor pathogenesis and in understanding neurobiology, and may help inform the development of novel tumor therapy.
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