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Journal articles on the topic 'EGLN3'

Author: Grafiati

Published: 4 June 2021

Last updated: 5 February 2022

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1

Lieb, Mark E., Keon Menzies, Maria C. Moschella, Rujing Ni, and Mark B. Taubman. "Mammalian EGLN genes have distinct patterns of mRNA expression and regulation." Biochemistry and Cell Biology 80, no. 4 (2002): 421–26. http://dx.doi.org/10.1139/o02-115.

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The mammalian EGLN family contains three paralagous genes (EGLN1, EGLN2, and EGLN3) encoding prolyl hydroxylase isoforms that mediate the oxygen-dependent targeting of the transcription factor hypoxia inducible factor alpha to the proteosome. The rat orthologue of EGLN3 (SM-20) exhibits tissue-restricted expression, is induced by growth factors in cultured vascular smooth muscle, and is up-regulated during myogenesis. To determine if all three EGLN genes are coordinately regulated, we examined their mRNA expression in murine tissues and in cultured cells. We now report that the three murine EG

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2

Villar, Diego, Alicia Vara-Vega, Manuel O. Landázuri, and Luis Del Peso. "Identification of a region on hypoxia-inducible-factor prolyl 4-hydroxylases that determines their specificity for the oxygen degradation domains." Biochemical Journal 408, no. 2 (2007): 231–40. http://dx.doi.org/10.1042/bj20071052.

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HIFs [hypoxia-inducible (transcription) factors] are essential for the induction of an adaptive gene expression programme under low oxygen partial pressure. The activity of these transcription factors is mainly determined by the stability of the HIFα subunit, which is regulated, in an oxygen-dependent manner, by a family of three prolyl 4-hydroxylases [EGLN1–EGLN3 (EGL nine homologues 1–3)]. HIFα contains two, N- and C-terminal, independent ODDs (oxygen-dependent degradation domains), namely NODD and CODD, that, upon hydroxylation by the EGLNs, target HIFα for proteasomal degradation. In vitro

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3

Kornilova, P., L. Potari-Gul, D. Modos, M. Madgwick, W. Haerty, and T. Korcsmaros. "P004 Critical paralog proteins has a cell-type specific rewiring role in Ulcerative Colitis associated signalling processes." Journal of Crohn's and Colitis 15, Supplement_1 (2021): S126—S127. http://dx.doi.org/10.1093/ecco-jcc/jjab076.133.

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Abstract Background Cell functions are regulated by signalling pathways that often cross-talk with each other. These cross-talks are usually cell-type specific and, as we showed earlier, often mediated by so called critical paralog proteins (proteins resulted due to gene duplication but then diverged both in terms of their regulation and their functions). As dysregulation of cell functions is a hallmark of chronic inflammatory diseases, including Ulcerative Colitis (UC), here we investigated the role of such critical paralog proteins in the regulation of some key functions, in UC-associated ce

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4

Pescador, Nuria, Yolanda Cuevas, Salvador Naranjo, et al. "Identification of a functional hypoxia-responsive element that regulates the expression of the egl nine homologue 3 (egln3/phd3) gene." Biochemical Journal 390, no. 1 (2005): 189–97. http://dx.doi.org/10.1042/bj20042121.

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Low oxygen levels induce an adaptive response in cells through the activation of HIFs (hypoxia-inducible factors). These transcription factors are mainly regulated by a group of proline hydroxylases that, in the presence of oxygen, target HIF for degradation. The expression of two such enzymes, EGLN1 [EGL nine homologous protein 1, where EGL stands for egg laying defective (Caenorhabditis elegans gene)] and EGLN3, is induced by hypoxia through a negative feedback loop, and we have demonstrated recently that hypoxic induction of EGLN expression is HIF-dependent. In the present study, we have id

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5

Metzen, Eric. "Enzyme substrate recognition in oxygen sensing: how the HIF trap snaps." Biochemical Journal 408, no. 2 (2007): e5-e6. http://dx.doi.org/10.1042/bj20071306.

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The transcriptional activator HIF (hypoxia-inducible factor) is a focal point of biomedical research because many situations in physiology and in pathology coincide with hypoxia. The effects of HIF activation may be a facet of normal growth, as in embryonic development, they may counterbalance a disease, as seen in the stimulation of erythropoiesis in anaemia, and they may be part of the pathological processes, as exemplified by tumour angiogenesis. The oxygen-sensitive α-subunits of HIF are primarily regulated by the enzymatic hydroxylation that induces rapid proteasomal degradation. The HIFα

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6

Shah, Reshma, Eleftheria Hatzimichael, Nelofer Syed, Konstantinos L. Bourantas, and Tim Crook. "Epigenetic Profiling Identifies EGLN3 as a Frequent Target for Transcriptional Silencing in Plasma Cell Neoplasias." Blood 110, no. 11 (2007): 2132. http://dx.doi.org/10.1182/blood.v110.11.2132.2132.

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Abstract Background: Multiple myeloma (MM) results from an excess of monoclonal plasma cells in the bone marrow. MM cells are interleukin (IL)-6 and stromal cell dependent. Although the molecular signature of MM cells has been identified, the signature of the stromal component of the BM microenviroment is not yet fully determined and holds important clues to the understanding of disease pathobiology and progression. It has been suggested that bone marrow hypoxia is lessened during myeloma progression and that myeloma-associated angiogenesis is functional. Hypoxia-inducible factor 1 (HIF-1) is

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7

Timoshkina, Natalya N., Oleg I. Kit, Anton Pushkin, et al. "Comparative gene expression analysis in gliomas with different IDH1/2 status." Journal of Clinical Oncology 37, no. 15_suppl (2019): e13008-e13008. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.e13008.

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e13008 Background: The new 2016 WHO classification of tumors of the central nervous system takes into consideration mutational status of IDH genes. Research of molecular changes in gliomas remain to be an actual issue. We analyzed the gene expression of some significant pathways in gliomas. Methods: 27 patients (12 females, 15 males) aged from 27 to 76 years with verified brain tumors (glioblastomas (G4) – 67%, anaplastic astrocytomas and oligoastrocytomas (G3) – 11%, astrocytomas (G2) – 22%) were investigated. 7 mutations in the IDH1 gene and 5 ones in IDH2 in fresh frozen tumor tissues were

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8

Fan, Sijia, Jing Wang, Guangqing Yu, et al. "TET is targeted for proteasomal degradation by the PHD-pVHL pathway to reduce DNA hydroxymethylation." Journal of Biological Chemistry 295, no. 48 (2020): 16299–313. http://dx.doi.org/10.1074/jbc.ra120.014538.

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Hypoxia-inducible factors are heterodimeric transcription factors that play a crucial role in a cell's ability to adapt to low oxygen. The von Hippel-Lindau tumor suppressor (pVHL) acts as a master regulator of HIF activity, and its targeting of prolyl hydroxylated HIF-α for proteasomal degradation under normoxia is thought to be a major mechanism for pVHL tumor suppression and cellular response to oxygen. Whether pVHL regulates other targets through a similar mechanism is largely unknown. Here, we identify TET2/3 as novel targets of pVHL. pVHL induces proteasomal degradation of TET2/3, result

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9

Losman, Julie-Aurore, Sungwoo Lee, Peppi Koivunen, Ryan E. Looper та William G. Kaelin. "Enantiomer-Specific Transformation by 2HG Is Linked to Opposing Effects on α-Ketoglutarate-Dependent Dioxygenases". Blood 118, № 21 (2011): LBA—4—LBA—4. http://dx.doi.org/10.1182/blood.v118.21.lba-4.bld0076_p2_lba-4.

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Abstract LBA-4 Somatic mutations in IDH1 and IDH2 occur frequently in clonal myeloid disorders and result in the neomorphic ability of IDH to convert α-ketoglutarate (2-OG) to the R-enantiomer of 2-hydroxyglutarate (R-2HG) (Dang, et al Nature 462: 739, 2009). 2OG is an essential cofactor for many metabolic enzymes, including the TET family of 5-methylcytosine hydroxylases and the EglN family of prolyl-4-hydroxylases, and 2HG has been shown to inhibit several 2OG-dependent dioxygenases in vitro, including TET2 (Xu, et al Cancer Cell 19: 17, 2011; Figueroa, et al Cancer Cell 18: 1, 2010). We rec

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Losman, Julie-Aurore, Sungwoo Lee, Peppi Koivunen, Ryan E. Looper та William G. Kaelin. "Enantiomer-Specific Transformation by 2HG Is Linked to Opposing Effects on α-Ketoglutarate-Dependent Dioxygenases". Blood 118, № 21 (2011): LBA—4—LBA—4. http://dx.doi.org/10.1182/blood.v118.21.lba-4.lba-4.

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Abstract Abstract LBA-4 Somatic mutations in IDH1 and IDH2 occur frequently in clonal myeloid disorders and result in the neomorphic ability of IDH to convert α-ketoglutarate (2-OG) to the R-enantiomer of 2-hydroxyglutarate (R-2HG) (Dang, et al Nature 462: 739, 2009). 2OG is an essential cofactor for many metabolic enzymes, including the TET family of 5-methylcytosine hydroxylases and the EglN family of prolyl-4-hydroxylases, and 2HG has been shown to inhibit several 2OG-dependent dioxygenases in vitro, including TET2 (Xu, et al Cancer Cell 19: 17, 2011; Figueroa, et al Cancer Cell 18: 1, 2010

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11

Kelly, Tara, Hanne Johnsen, Erik Burgerhout, et al. "Low Oxygen Stress During Early Development Influences Regulation of Hypoxia-Response Genes in Farmed Atlantic Salmon (Salmo salar)." G3 Genes|Genomes|Genetics 10, no. 9 (2020): 3179–88. http://dx.doi.org/10.1534/g3.120.401459.

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Abstract Survival and growth of developing salmonids are negatively affected by low oxygen levels within gravel nests in natural streams, and hypoxic stress is often experienced by farmed Atlantic salmon (Salmo salar) within hatcheries. Exposure to hypoxia during early development may have long-lasting effects by altering epigenetic marks and gene expression in oxygen regulatory pathways. Here, we examine the transcriptomic response to low dissolved oxygen (DO) in post-hatch salmon reared continuously in 30%, 60% or 100% DO from fertilization until start of feeding. RNA sequencing revealed mul

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12

Gesang, Luobu, Lamu Gusang, Ciren Dawa, Gawa Gesang, and Kang Li. "Whole-Genome Sequencing Identifies the Egl Nine Homologue 3 (egln3/phd3) and Protein Phosphatase 1 Regulatory Inhibitor Subunit 2 (PPP1R2P1) Associated with High-Altitude Polycythemia in Tibetans at High Altitude." Disease Markers 2019 (November 7, 2019): 1–8. http://dx.doi.org/10.1155/2019/5946461.

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Background. The hypoxic conditions at high altitudes are great threats to survival, causing pressure for adaptation. More and more high-altitude denizens are not adapted with the condition known as high-altitude polycythemia (HAPC) that featured excessive erythrocytosis. As a high-altitude sickness, the etiology of HAPC is still unclear. Methods. In this study, we reported the whole-genome sequencing-based study of 10 native Tibetans with HAPC and 10 control subjects followed by genotyping of selected 21 variants from discovered single nucleotide variants (SNVs) in an independent cohort (232 c

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13

Fong, Louise Y., Cristian Taccioli, Alexey Palamarchuk, et al. "Abrogation of esophageal carcinoma development in miR-31 knockout rats." Proceedings of the National Academy of Sciences 117, no. 11 (2020): 6075–85. http://dx.doi.org/10.1073/pnas.1920333117.

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MicroRNA-31 (miR-31) is overexpressed in esophageal squamous cell carcinoma (ESCC), a deadly disease associated with dietary Zn deficiency and inflammation. In a Zn deficiency-promoted rat ESCC model with miR-31 up-regulation, cancer-associated inflammation, and a high ESCC burden followingN-nitrosomethylbenzylamine (NMBA) exposure, systemic antimiR-31 delivery reduced ESCC incidence from 85 to 45% (P= 0.038) and miR-31 gene knockout abrogated development of ESCC (P= 1 × 10−6). Transcriptomics, genome sequencing, and metabolomics analyses in these Zn-deficient rats revealed the molecular basis

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14

Li, Shuijie, Javier Rodriguez, Wenyu Li, et al. "EglN3 hydroxylase stabilizes BIM-EL linking VHL type 2C mutations to pheochromocytoma pathogenesis and chemotherapy resistance." Proceedings of the National Academy of Sciences 116, no. 34 (2019): 16997–7006. http://dx.doi.org/10.1073/pnas.1900748116.

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Despite the discovery of the oxygen-sensitive regulation of HIFα by the von Hippel–Lindau (VHL) protein, the mechanisms underlying the complex genotype/phenotype correlations in VHL disease remain unknown. Some germline VHL mutations cause familial pheochromocytoma and encode proteins that preserve their ability to down-regulate HIFα. While type 1, 2A, and 2B VHL mutants are defective in regulating HIFα, type 2C mutants encode proteins that preserve their ability to down-regulate HIFα. Here, we identified an oxygen-sensitive function of VHL that is abolished by VHL type 2C mutations. We found

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15

Sciorra, Vicki A., Michael A. Sanchez, Akemi Kunibe, and Andrew E. Wurmser. "Suppression of Glioma Progression by Egln3." PLoS ONE 7, no. 8 (2012): e40053. http://dx.doi.org/10.1371/journal.pone.0040053.

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16

Hatzimichael, Eleftheria, Aggeliki Dasoula, Reshma Shah, et al. "The prolyl-hydroxylase EGLN3 and not EGLN1 is inactivated by methylation in plasma cell neoplasia." European Journal of Haematology 84, no. 1 (2010): 47–51. http://dx.doi.org/10.1111/j.1600-0609.2009.01344.x.

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17

Pushkin, Anton A., Ilya A. Alliluev, Eduard E. Rostorguev, et al. "Differential expression of KDM1A and SMAD7 genes in gliomas depending on the tumor grade." Journal of Clinical Oncology 38, no. 15_suppl (2020): e14549-e14549. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e14549.

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e14549 Background: Gliomas are the most common type of primary brain tumors characterized by pronounced proliferation and aggressive infiltration. The purpose of the study was to analyze the expression of genes participating in the EGFR, TGF-B, HH/GLI, NOTCH and HIF1-alpha signaling pathways, transcription factors HBP1, MSI1/2 and demethylating agents in samples of various glioma types. Methods: The study included paired samples (tumor and physiologically unchanged neural tissue) obtained from 75 patients with histologically verified glial tumors of various grades (G2 - 21, G3 - 11, G4 - 43 pa

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18

Apanovich, Natalya, Maria Peters, Pavel Apanovich, et al. "The Genes—Candidates for Prognostic Markers of Metastasis by Expression Level in Clear Cell Renal Cell Cancer." Diagnostics 10, no. 1 (2020): 30. http://dx.doi.org/10.3390/diagnostics10010030.

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The molecular prognostic markers of metastasis are important for personalized approaches to clear cell renal cell carcinoma (ccRCC) treatment but markers for practical use are still missing. To address this gap we studied the expression of ten genes—CA9, NDUFA4L2, VWF, IGFBP3, BHLHE41, EGLN3, SAA1, CSF1R, C1QA, and FN1—through RT-PCR, in 56 ccRCC patients without metastases and with metastases. All of these, excluding CSF1R, showed differential and increased (besides SAA1) expression in non-metastasis tumors. The gene expression levels in metastasis tumors were decreased, besides CSF1R, FN1 (n

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19

Fu, Jian. "Catalytic-independent inhibition of cIAP1-mediated RIP1 ubiquitination by EGLN3." Cellular Signalling 28, no. 2 (2016): 72–80. http://dx.doi.org/10.1016/j.cellsig.2015.11.011.

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20

Fu, Jian, Keon Menzies, Robert S. Freeman, and Mark B. Taubman. "EGLN3 Prolyl Hydroxylase Regulates Skeletal Muscle Differentiation and Myogenin Protein Stability." Journal of Biological Chemistry 282, no. 17 (2007): 12410–18. http://dx.doi.org/10.1074/jbc.m608748200.

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21

Xie, L., K. Xiao, E. J. Whalen, et al. "Oxygen-Regulated 2-Adrenergic Receptor Hydroxylation by EGLN3 and Ubiquitylation by pVHL." Science Signaling 2, no. 78 (2009): ra33. http://dx.doi.org/10.1126/scisignal.2000444.

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22

Frank, Derk, Johanne Gantenberg, Inka Boomgaarden, et al. "MicroRNA-20a inhibits stress-induced cardiomyocyte apoptosis involving its novel target Egln3/PHD3." Journal of Molecular and Cellular Cardiology 52, no. 3 (2012): 711–17. http://dx.doi.org/10.1016/j.yjmcc.2011.12.001.

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23

Fu, Jian, та Mark B. Taubman. "Prolyl Hydroxylase EGLN3 Regulates Skeletal Myoblast Differentiation through an NF-κB-dependent Pathway". Journal of Biological Chemistry 285, № 12 (2010): 8927–35. http://dx.doi.org/10.1074/jbc.m109.078600.

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24

Lee, Sungwoo, Eijiro Nakamura, Haifeng Yang, et al. "Neuronal apoptosis linked to EglN3 prolyl hydroxylase and familial pheochromocytoma genes: Developmental culling and cancer." Cancer Cell 8, no. 2 (2005): 155–67. http://dx.doi.org/10.1016/j.ccr.2005.06.015.

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25

Yue, Yongjun, Jinsheng Cui, Yu Zhao, Shangying Liu, and Weixing Niu. "Circ_101341 Deteriorates the Progression of Clear Cell Renal Cell Carcinoma Through the miR- 411/EGLN3 Axis." Cancer Management and Research Volume 12 (December 2020): 13513–25. http://dx.doi.org/10.2147/cmar.s272287.

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26

Zhang, Gang, Jianqiang Wang, Wei Tan, et al. "Circular RNA EGLN3 silencing represses renal cell carcinoma progression through the miR-1224-3p/HMGXB3 axis." Acta Histochemica 123, no. 6 (2021): 151752. http://dx.doi.org/10.1016/j.acthis.2021.151752.

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27

Schlisio, S., R. S. Kenchappa, L. C. W. Vredeveld, et al. "The kinesin KIF1B acts downstream from EglN3 to induce apoptosis and is a potential 1p36 tumor suppressor." Genes & Development 22, no. 7 (2008): 884–93. http://dx.doi.org/10.1101/gad.1648608.

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28

Fu, J., and M. B. Taubman. "EGLN3 Inhibition of NF- B Is Mediated by Prolyl Hydroxylase-Independent Inhibition of I B Kinase Ubiquitination." Molecular and Cellular Biology 33, no. 15 (2013): 3050–61. http://dx.doi.org/10.1128/mcb.00273-13.

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29

Lin, Ling, and Jianhua Cai. "Circular RNA circ‐EGLN3 promotes renal cell carcinoma proliferation and aggressiveness via miR‐1299‐mediated IRF7 activation." Journal of Cellular Biochemistry 121, no. 11 (2020): 4377–85. http://dx.doi.org/10.1002/jcb.29620.

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30

Padovano, Valeria, Ivana Y. Kuo, Lindsey K. Stavola, et al. "The polycystins are modulated by cellular oxygen-sensing pathways and regulate mitochondrial function." Molecular Biology of the Cell 28, no. 2 (2017): 261–69. http://dx.doi.org/10.1091/mbc.e16-08-0597.

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Autosomal dominant polycystic kidney disease is caused by mutations in the genes encoding polycystin-1 (PC1) and polycystin-2 (PC2), which form an ion channel complex that may mediate ciliary sensory processes and regulate endoplasmic reticulum (ER) Ca2+ release. Loss of PC1 expression profoundly alters cellular energy metabolism. The mechanisms that control the trafficking of PC1 and PC2, as well as their broader physiological roles, are poorly understood. We found that O2 levels regulate the subcellular localization and channel activity of the polycystin complex through its interaction with

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31

Kubicka, Stefan, Roger Von Moos, Richard Greil, et al. "Bevacizumab (BEV) continued beyond first progression in patients (pts) with metastatic colorectal cancer (mCRC) previously treated with BEV + chemotherapy (CT): Biomarker findings from ML18147." Journal of Clinical Oncology 31, no. 4_suppl (2013): 452. http://dx.doi.org/10.1200/jco.2013.31.4_suppl.452.

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452 Background: In ML18147, BEV + standard CT was continued as 2nd-line treatment for pts with mCRC progressing after 1st-line BEV + CT. ML18147 met its primary and secondary endpoints and had a comprehensive biomarker programme, including exploratory analyses of immunohistochemistry (IHC) and single nucleotide polymorphisms (SNPs). Methods: Tumour samples were analysed by IHC for VEGFA, VEGFR1, VEGFR2 and neuropilin-1; H-scores were generated. Tumor angiogenesis was determined by stereological analysis of CD31-stained microvessels; 183 SNPs of 30 mainly angiogenesis-related genes were genotyp

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Wang, Yicun, Xin Li, Wei Liu, et al. "MicroRNA-1205, encoded on chromosome 8q24, targets EGLN3 to induce cell growth and contributes to risk of castration-resistant prostate cancer." Oncogene 38, no. 24 (2019): 4820–34. http://dx.doi.org/10.1038/s41388-019-0760-3.

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Auburger, Georg, Suzana Gispert, and Nadine Brehm. "Methyl-Arginine Profile of Brain from Aged PINK1-KO+A53T-SNCA Mice Suggests Altered Mitochondrial Biogenesis." Parkinson's Disease 2016 (2016): 1–13. http://dx.doi.org/10.1155/2016/4686185.

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Hereditary Parkinson’s disease can be triggered by an autosomal dominant overdose of alpha-Synuclein (SNCA) or the autosomal recessive deficiency of PINK1. We recently showed that the combination of PINK1-knockout with overexpression of A53T-SNCA in double mutant (DM) mice potentiates phenotypes and reduces survival. Now we studied brain hemispheres of DM mice at age of 18 months in a hypothesis-free approach, employing a quantitative label-free global proteomic mass spectrometry scan of posttranslational modifications focusing on methyl-arginine. The strongest effects were documented for the

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Ang, Sonny, Maria Lima Da Silva, Margaret Dawson, et al. "NK Cell Proliferation and Cytolytic Function Are Compromised In the Hypoxic Tumor Microenvironment." Blood 116, no. 21 (2010): 4291. http://dx.doi.org/10.1182/blood.v116.21.4291.4291.

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Abstract Abstract 4291 Natural Killer (NK) cells have important and potent innate immunoregulatory and immune surveillance functions against tumor. The paradoxical coexistence of tumors and anti-tumor immune cells (“Hellstrom Paradox”) may in part be explained by the pathophysiology of the “hostile” tumor microenvironment which suppress immune-cell function, such as hypoxia, low pH, low tissue glucose, and the presence of immunosuppressive cytokines and metabolites. However, the effect of the malignant environment on the ability of NK cells to infiltrate tumor and exhibit effector function is

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Straub, Isabella R., Woranontee Weraarpachai, and Eric A. Shoubridge. "Multi-OMICS study of a CHCHD10 variant causing ALS demonstrates metabolic rewiring and activation of endoplasmic reticulum and mitochondrial unfolded protein responses." Human Molecular Genetics 30, no. 8 (2021): 687–705. http://dx.doi.org/10.1093/hmg/ddab078.

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Abstract Mutations in CHCHD10, coding for a mitochondrial intermembrane space protein, are a rare cause of autosomal dominant amyotrophic lateral sclerosis. Mutation-specific toxic gain of function or haploinsufficiency models have been proposed to explain pathogenicity. To decipher the metabolic dysfunction associated with the haploinsufficient p.R15L variant, we integrated transcriptomic, metabolomic and proteomic data sets in patient cells subjected to an energetic stress that forces the cells to rely on oxidative phosphorylation for ATP production. Patient cells had a complex I deficiency

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Zhong, ChengLin, SiChen Li, JingJing Li та ін. "Polymorphisms in the Egl nine homolog 3 (EGLN3) and Peroxisome proliferator activated receptor-alpha (PPARα) genes and their correlation with hypoxia adaptation in Tibetan chickens". PLOS ONE 13, № 3 (2018): e0194156. http://dx.doi.org/10.1371/journal.pone.0194156.

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Gavrilovskaya, Irina N., Elena E. Gorbunova, and Erich R. Mackow. "Hypoxia Induces Permeability and Giant Cell Responses of Andes Virus-Infected Pulmonary Endothelial Cells by Activating the mTOR-S6K Signaling Pathway." Journal of Virology 87, no. 23 (2013): 12999–3008. http://dx.doi.org/10.1128/jvi.02103-13.

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Andes virus (ANDV) is a South American hantavirus that causes a highly lethal hantavirus pulmonary syndrome (HPS) characterized by hypoxia, thrombocytopenia, and vascular leakage leading to acute pulmonary edema. ANDV infects human pulmonary microvascular and lymphatic endothelial cells (MECs and LECs, respectively) and nonlytically enhances the permeability of interendothelial cell adherence junctions in response to vascular endothelial growth factor (VEGF). Recent findings also indicate that ANDV causes the formation of giant endothelial cells. Here, we demonstrate that hypoxic conditions al

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Ortega, Miguel A., Beatriz Romero, Ángel Asúnsolo, et al. "Behavior of Smooth Muscle Cells under Hypoxic Conditions: Possible Implications on the Varicose Vein Endothelium." BioMed Research International 2018 (October 18, 2018): 1–9. http://dx.doi.org/10.1155/2018/7156150.

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Varicose veins are a disease with high incidence and prevalence. In the venous wall, the smooth muscle cells (SMCs) act in the vascular homeostasis that secretes multiple substances in response to stimuli. Any alteration of these cells can modify the function and structure of the other venous layers such as the endothelium, resulting in increases in endothelial permeability and release of substances. Therefore, knowing the cellular and molecular mechanisms of varicose veins is imperative. The aims of this study are to understand how SMCs of patients with varicose veins subjected to saphenectom

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Bjarnason, Georg A., Zsuzsanna Lichner, Salvador Mejia-Guerrero, et al. "Pleotrophic action of renal cell carcinoma: Dysregulated microRNAs on hypoxia-related signaling pathways." Journal of Clinical Oncology 30, no. 5_suppl (2012): 428. http://dx.doi.org/10.1200/jco.2012.30.5_suppl.428.

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428 Background: The von Hippel-Lindau (VHL) gene is lost in 70% of clear cell Renal Cell Carcinomas (ccRCC); however, additional mechanisms are proposed to regulate VHL expression, including suppression by microRNAs (miRNAs). miRNAs are a class of naturally occurring, small non-coding RNA molecules that downregulate gene expression of target mRNAs. We demonstrate that ccRCC-dysregulated miRNAs can target multiple members of the ccRCC-related signaling pathways. Methods: miR-17 and miR-224 mimics and inhibitors were transfected into ccRCC cell lines using siPORT (Ambion). PicTar and TargetScan

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Samidurai, Arun, Sean K. Roh, Meeta Prakash, et al. "STAT3-miR-17/20 signalling axis plays a critical role in attenuating myocardial infarction following rapamycin treatment in diabetic mice." Cardiovascular Research 116, no. 13 (2019): 2103–15. http://dx.doi.org/10.1093/cvr/cvz315.

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Abstract Aims Deregulation of mTOR (mammalian target of rapamycin) signalling occurs in diabetes, which exacerbates injury following myocardial infarction (MI). We therefore investigated the infarct-limiting effect of chronic treatment with rapamycin (RAPA, mTOR inhibitor) in diabetic mice following myocardial ischaemia/reperfusion (I/R) injury and delineated the potential protective mechanism. Methods and results Adult male diabetic (db/db) or wild-type (WT) (C57) mice were treated with RAPA (0.25 mg/kg/day, intraperitoneal) or vehicle (5% DMSO) for 28 days. The hearts from treated mice were

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Yasukochi, Yoshiki, Takayuki Nishimura, Juan Ugarte, et al. "Effect of EGLN1 Genetic Polymorphisms on Hemoglobin Concentration in Andean Highlanders." BioMed Research International 2020 (November 15, 2020): 1–16. http://dx.doi.org/10.1155/2020/3436581.

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The physiological characteristics of Andean natives living at high altitudes have been investigated extensively, with many studies reporting that Andean highlanders have a higher hemoglobin (Hb) concentration than other highlander populations. It has previously been reported that positive natural selection has acted independently on the egl-9 family hypoxia inducible factor 1 (EGLN1) gene in Tibetan and Andean highlanders and is related to Hb concentration in Tibetans. However, no study has yet revealed the genetic determinants of Hb concentration in Andeans even though several single-nucleoti

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Mishra, Aastha, Ghulam Mohammad, Tashi Thinlas, and M. A. Qadar Pasha. "EGLN1 variants influence expression and SaO2 levels to associate with high-altitude pulmonary oedema and adaptation." Clinical Science 124, no. 7 (2012): 479–89. http://dx.doi.org/10.1042/cs20120371.

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EGLN1 [encoding HIF (hypoxia-inducible factor)-prolyl hydroxylase 2] plays a pivotal role in the HIF pathway and has emerged as one of the most intriguing genes with respect to physiology at HA (high altitude). EGLN1, being an actual oxygen sensor, appears to have a potential role in the functional adaptation to the hypobaric hypoxic environment. In the present study, we screened 30 polymorphisms of EGLN1, evaluated its gene expression and performed association analyses. In addition, the role of allelic variants in altering TF (transcription factor)-binding sites and consequently the replaceme

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Brutsaert, Tom D., Melisa Kiyamu, Gianpietro Elias Revollendo, et al. "Association of EGLN1 gene with high aerobic capacity of Peruvian Quechua at high altitude." Proceedings of the National Academy of Sciences 116, no. 48 (2019): 24006–11. http://dx.doi.org/10.1073/pnas.1906171116.

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Highland native Andeans have resided at altitude for millennia. They display high aerobic capacity (VO2max) at altitude, which may be a reflection of genetic adaptation to hypoxia. Previous genomewide (GW) scans for natural selection have nominated Egl-9 homolog 1 gene (EGLN1) as a candidate gene. The encoded protein, EGLN1/PHD2, is an O2 sensor that controls levels of the Hypoxia Inducible Factor-α (HIF-α), which regulates the cellular response to hypoxia. From GW association and analysis of covariance performed on a total sample of 429 Peruvian Quechua and 94 US lowland referents, we identif

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Chiang, Han-Lin, Chiung Mei Chen, Yi-Chun Chen, Chih-Ying Chao, Yih-Ru Wu, and Guey-Jen Lee-Chen. "Genetic Analysis of EGLN1 C127S Variant in Taiwanese Parkinson’s Disease." Parkinson's Disease 2020 (April 25, 2020): 1–4. http://dx.doi.org/10.1155/2020/9582317.

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Parkinson’s disease (PD) is a neurodegenerative disorder related to nigrostriatal dopaminergic neuron degeneration and iron accumulation. As a cellular oxygen sensor, prolyl hydroxylase domain containing protein 2 (PHD2, encoded by egl-9 family hypoxia inducible factor 1, EGLN1) modifies hypoxia-inducible factor alpha (HIF-α) protein for proteasomal destruction under normoxic condition. In addition, 2-oxoglutarate- (OG-) dependent dioxygenase activity of PHD2 is involved in the oxygen and iron regulation of iron-responsive element binding protein 2 (IRP2) stability. Previously increased expres

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Oliveira, Jennifer L., Lori A. Frederick, Lea M. Coon, et al. "Spectrum of Mutations Associated with Hereditary Erythrocytosis." Blood 126, no. 23 (2015): 2140. http://dx.doi.org/10.1182/blood.v126.23.2140.2140.

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Abstract Background: Mechanisms of hereditary erythrocytosis have been elucidated recently. These include high oxygen affinity (HOA) hemoglobin (Hb) variants, bisphosphoglycerate mutase (BPGM) deficiency, abnormalities in the erythropoietin receptor (EPOR) and oxygen-sensing pathway (OSP) proteins prolyl hydroxylase domain-2 (PHD2), hypoxia-inducible factor-2 alpha subunit (HIF2A), and von Hippel-Lindau (VHL). We present our experience with these disorders. Methods: Evaluation of erythrocytosis patients' blood samples for HOA Hb variants by protein or DNA sequencing methods has been performed

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Yi, Dan, Bin Liu, Ting Wang, et al. "Endothelial Autocrine Signaling through CXCL12/CXCR4/FoxM1 Axis Contributes to Severe Pulmonary Arterial Hypertension." International Journal of Molecular Sciences 22, no. 6 (2021): 3182. http://dx.doi.org/10.3390/ijms22063182.

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Endothelial autocrine signaling is essential to maintain vascular homeostasis. There is limited information about the role of endothelial autocrine signaling in regulating severe pulmonary vascular remodeling during the onset of pulmonary arterial hypertension (PAH). In this study, we employed the first severe pulmonary hypertension (PH) mouse model, Egln1Tie2Cre (Tie2Cre-mediated disruption of Egln1) mice, to identify the novel autocrine signaling mediating the pulmonary vascular endothelial cell (PVEC) proliferation and the pathogenesis of PAH. PVECs isolated from Egln1Tie2Cre lung expressed

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Zhang, Jing, Xingnan Zheng, and Qing Zhang. "EglN2 positively regulates mitochondrial function in breast cancer." Molecular & Cellular Oncology 3, no. 2 (2015): e1120845. http://dx.doi.org/10.1080/23723556.2015.1120845.

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Kaelin, William G. "IDH Mutations, 2-Oxoglutarate-dependent Dioxygenases, and Leukemia." Blood 124, no. 21 (2014): SCI—6—SCI—6. http://dx.doi.org/10.1182/blood.v124.21.sci-6.sci-6.

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Abstract Somatic isocitrate dehydrogenase 1 (IDH1) and IDH2 mutations have been discovered in a variety of neoplasms, including glioblastomas and acute myelogenous leukemias. Cancer-associated IDH mutants produce large quantities (low mM) of the R enantiomer of 2-hydroxyglutarate (R-2HG). R-2HG resembles 2-oxoglutarate, which is a Krebs Cycle intermediate and an essential cofactor for a variety of enzymes including the ~70 2-oxoglutarate-dependent dioxygenases. Included among these enzymes are the EglN prolyl hydroxylases that earmark the hypoxia-inducible factor (HIF) for destruction under no

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Yang, Minghua, Pan Chen, Jiao Liu, et al. "Clockophagy is a novel selective autophagy process favoring ferroptosis." Science Advances 5, no. 7 (2019): eaaw2238. http://dx.doi.org/10.1126/sciadv.aaw2238.

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Ferroptosis is a form of nonapoptotic regulated cell death driven by iron-dependent lipid peroxidation. Autophagy involves a lysosomal degradation pathway that can either promote or impede cell death. A high level of autophagy has been associated with ferroptosis, but the mechanisms underpinning this relationship are largely elusive. We characterize the contribution of autophagy to ferroptosis in human cancer cell lines and mouse tumor models. We show that “clockophagy,” the selective degradation of the core circadian clock protein ARNTL by autophagy, is critical for ferroptosis. We identify S

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Petousi, Nayia, Quentin P. P. Croft, Gianpiero L. Cavalleri, et al. "Tibetans living at sea level have a hyporesponsive hypoxia-inducible factor system and blunted physiological responses to hypoxia." Journal of Applied Physiology 116, no. 7 (2014): 893–904. http://dx.doi.org/10.1152/japplphysiol.00535.2013.

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Tibetan natives have lived on the Tibetan plateau (altitude ∼4,000 m) for at least 25,000 years, and as such they are adapted to life and reproduction in a hypoxic environment. Recent studies have identified two genetic loci, EGLN1 and EPAS1, that have undergone natural selection in Tibetans, and further demonstrated an association of EGLN1/ EPAS1 genotype with hemoglobin concentration. Both genes encode major components of the hypoxia-inducible factor (HIF) transcriptional pathway, which coordinates an organism's response to hypoxia. Patients living at sea level with genetic disease of the HI

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