Disease relevance of HIGD1A

• In cultured cells, HIG1 and HIG2 expression is induced by hypoxia and by glucose deprivation, but their expression is not induced by serum deprivation, UV, or ionizing radiation [1].
• The purpose of this review is to present an update of selected issues regarding hypoxia-inducible gene expression and how this affects prognosis, angiogenesis and metastasis [2].

High impact information on HIGD1A

• Inhibitory PAS domain protein is a negative regulator of hypoxia-inducible gene expression [3].
• A Fenton reaction at the endoplasmic reticulum is involved in the redox control of hypoxia-inducible gene expression [4].
• Nickel (Ni2+) and cobalt (Co2+) mimic hypoxia and were used as a tool to study the role of oxygen sensing and signaling cascades in the regulation of hypoxia-inducible gene expression [5].
• Hypoxia modifies the transcriptome of primary human monocytes: modulation of novel immune-related genes and identification of CC-chemokine ligand 20 as a new hypoxia-inducible gene [6].
• Here we provide evidence that lactate and pyruvate regulate hypoxia-inducible gene expression independently of hypoxia by stimulating the accumulation of hypoxia-inducible Factor 1alpha (HIF-1alpha) [7].

Biological context of HIGD1A

• The putative HIG1 and HIG2 open reading frames are expressed in cells, as confirmed by epitope tagging [1].
• These experiments show the utility of mutagenesis and selection of mutant cells in the analysis of mammalian transcriptional responses to hypoxia and demonstrate the operation of HIF-1alpha-dependent and HIF-1alpha-independent pathways of hypoxia-inducible gene expression in Chinese hamster ovary cells [8].
• Taken together, our results demonstrate that visfatin is a new hypoxia-inducible gene of which expression is stimulated through the interaction of HIF-1 with HRE sites in its promoter region [9].
• Hypoxia-inducible gene expression system using the erythropoietin enhancer and 3'-untranslated region for the VEGF gene therapy [10].

Anatomical context of HIGD1A

• These data demonstrate that leptin is a new hypoxia-inducible gene, which is stimulated in a placental cell line through HIF-1 interaction with a consensus HRE site located at -116 in the proximal promoter [11].
• Remarkably, in response to hypoxia, Ad/5HRE-3NRSE showed strong hypoxia-inducible gene expression selectively in neurons (12-fold induction in CGNs and 22-fold in NT2/Ns), but not in glial cells [12].
• A hypoxia-inducible gene expression system using erythropoietin 3' untranslated region for the gene therapy of rat spinal cord injury [13].

Associations of HIGD1A with chemical compounds

• The expression of the glucose transporter isoform 1 (GLUT-1) mRNA, a well known hypoxia inducible gene, was also increased [14].
• Nitric oxide (NO) is believed to play an important, but as yet undefined, role in regulating hypoxia inducible gene expression [15].
• Apigenin also suppressed the expression of erythropoietin mRNA, which is a typical hypoxia-inducible gene, via the degradation of hypoxia-inducible factor 1 (HIF-1) alpha [16].

Other interactions of HIGD1A

• The finding suggest that STAT3-dependent pathway is involved in the activation and proliferation of PASMC stimulated by hypoxia, and SOCS3 is a rapidly hypoxia-inducible gene and acts to inhibit activation of cellular signaling pathway in a classical negative feedback loop [17].

Analytical, diagnostic and therapeutic context of HIGD1A

• In addition, tumor xenografts derived from human cervical cancer cells display increased expression of HIG1 and HIG2 when they are deprived of oxygen [1].

References