Differential roles of hypoxia-inducible factor 1alpha (HIF-1alpha) and HIF-2alpha in hypoxic gene regulation.

By Cheng-Jun Hu, Liyi Wang, L. Chodosh, B. Keith, M. C. Simon. Molecular and Cellular Biology, 2003

710 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/5786408c352c362503a253eb444ed7c9ffb7938d

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Citations in the corpus

Oxygen sensing by mitochondria at complex III: the paradox of increased reactive oxygen species during hypoxia (2006, background): “…of genes involved in glucose uptake, glucose metabolism, cell survival, vascular tone, cytoskeletal organization, apoptosis, extracellular matrix metabolism, cell adhesion and iron metabolism (Wykoff et al. 2000; Hu et al. 2003; Wykoff et al. 2004; Gunton et al. 2005; Greijer et al. 2005).”
Hypoxia-inducible factors in stem cells and cancer (2009, unknown): “Given that some hypoxic effects on stem cells parallel stem cell regulation by signalling pathways, and because a correlation between hypoxia and signalling pathways has been observed [47, 54], it is possible that altered stem cell behaviour under low O2 involves hypoxic regulation of stem cell path”
SIRT3 opposes reprogramming of cancer cell metabolism through HIF1α destabilization (2011, background): “SIRT3 Opposes the Warburg Effect by Destabilizing HIF1a HIF1, the heterodimer of HIF1a andHIF1b, is the primary driver of increased glycolysis and lactate production during hypoxia (Gordan and Simon, 2007; Hu et al., 2003; Seagroves et al., 2001).”
HIF-2alpha promotes hypoxic cell proliferation by enhancing c-myc transcriptional activity. (2007, methodology): “HIF-1a uniquely activates glycolytic enzyme genes, while HIF-2a preferentially activates VEGF, transforming growth factor-a (TGFa), lysyl oxidase, Oct4, and Cyclin D1 (Baba et al., 2003; Covello et al., 2006; Erler et al., 2006; Gunaratnam et al., 2003; Hu et al., 2003; Wang et al., 2005).”
Therapeutic targeting of hypoxia and hypoxia-inducible factors in cancer. (2016, background): “Early studies showed that HIF-1 (but not HIF-2) induced expression of several glycolytic genes in various cell types,while unique HIF-2 target genes seemed to be cell type specific (Hu et al., 2003; Raval et al., 2005).”
Regulation of glycolysis by the hypoxia‐inducible factor (HIF): implications for cellular physiology (2020, background): “While HIF-1α and HIF-2α regulated genes can overlap, multiple studies have reported that glycolytic genes are exclusively regulated by HIF-1α (Hu et al. 2003, 2007; Wang et al. 2005).”
Oxygen in stem cell biology: a critical component of the stem cell niche. (2010, background): “Confirmation of this hypothesis was underscored by the observation that HIF-1a and HIF-2a harbor different transactivation domains, despite the structural similarity of their DNA binding and dimerization domains (Hu et al., 2003).”
The role of hypoxia-inducible factors in tumorigenesis (2008, background): “Like HIF-1a, HIF-2a heterodimerizes with ARNT and can induce gene expression.(10) In contrast to HIF-1a, HIF-2a expression is restricted to specific cell types that include endothelial cells, glial cells, type II pneumocytes, cardiomyocytes, fibroblasts of the kidney, interstitial cells of the pancr”
Activation of a metabolic gene regulatory network downstream of mTOR complex 1. (2010, background): “The HIFα subunit appears to dictate the target specificity of the HIF1 heterodimer (Hu et al., 2003), and TSC-deficient cells display mTORC1-dependent transcriptional upregulation of targets specific to HIF1α(e.”
The N-Terminal Transactivation Domain Confers Target Gene Specificity of Hypoxia-inducible Factors HIF-1α and HIF-2α (2007, methodology): “For example, HIF-1 specifically regulates glycolytic genes (including phosphoglycerate kinase [PGK] and lactate dehydrogenase A [LDHA]) (Hu et al., 2003; Rankin et al., 2005; Wang et al., 2005), as well as carbonic hydrase-9 (CA IX) (Grabmaier et al.”
HIF Transcription Factors, Inflammation, and Immunity (2014, background): “…mRNA and protein, especially in the proinflammatory T helper 17 (Th17) CD4 + T cell lineage, by a mechanism dependent on STAT3 (Dang et al., 2011; Ikejiri et al., 2012; Nakamura et al., 2005; Shi et al., 2011; Wang et al., 2014), where IL-6 and transforming growth factor-b (TGF-b) enhance HIF-1a…”