PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 34281283-1 2021 beta-thalassaemia is a rare genetic condition caused by mutations in the beta-globin gene that result in severe iron-loading anaemia, maintained by a detrimental state of ineffective erythropoiesis (IE). Iron 112-116 hemoglobin subunit beta Homo sapiens 73-84 11861299-4 2002 We generated beta-globin gene constructs with this mutation and an iron-responsive element in the 5" untranslated region, which allowed specific experimental activation and inactivation of translation and, hence, NMD of this transcript. Iron 67-71 hemoglobin subunit beta Homo sapiens 13-24 25541274-12 2015 Thus, monitoring of the dose of iron chelators, according to the type of mutation in the beta globin gene, may help improve the compliance of beta thalassemics to chelation therapy and prevent side-effects in patients with beta plus mutations. Iron 32-36 hemoglobin subunit beta Homo sapiens 89-100 6096143-2 1984 The results show that the replacement of the distal histidine of the hemoglobin beta chains by an arginine greatly enhances the susceptibility of the heme-iron to oxidative challenge. Iron 155-159 hemoglobin subunit beta Homo sapiens 69-84 33868836-2 2021 The salient features of beta thalassemia major, in which both alleles of the HBB gene are affected, are transfusion dependency and iron overload. Iron 131-135 hemoglobin subunit beta Homo sapiens 77-80 32517787-4 2020 RESULTS: Of the plasma proteins implicated in iron and heme metabolism, hemoglobin subunit beta (p = 0.001) was significantly increased in AD compared to CN individuals. Iron 46-50 hemoglobin subunit beta Homo sapiens 72-95 30988565-0 2019 Impact of Genotype of Beta Globin Gene on Hepatic and Myocardial Iron Content in Egyptian Patients with Beta Thalassemia. Iron 65-69 hemoglobin subunit beta Homo sapiens 22-33 29127682-2 2017 Because HBB protein is a critical component (along with alpha-globin, heme, and iron) of hemoglobin, the molecule essential for oxygen delivery to tissues, mutations in HBB can result in lethal diseases or diseases with multi-organ dysfunction. Iron 80-84 hemoglobin subunit beta Homo sapiens 8-11 29127682-2 2017 Because HBB protein is a critical component (along with alpha-globin, heme, and iron) of hemoglobin, the molecule essential for oxygen delivery to tissues, mutations in HBB can result in lethal diseases or diseases with multi-organ dysfunction. Iron 80-84 hemoglobin subunit beta Homo sapiens 169-172 32027058-2 2020 Herein, it is discovered that organic small molecule (hexabromobenzene, HBB) can activate commercial transition metal (Ni, Fe, and NiFe) foam by directly evolving metal nanomeshes embedded in graphene-like films (M-NM@G) through a facile Br-induced solid-phase migration process. Iron 123-125 hemoglobin subunit beta Homo sapiens 72-75 28806678-3 2017 Total iron (Fe) contents were 16.50, 24.40, and 13.08% for nZVI/BB, nZVI/PBB and nZVI/HBB, respectively. Iron 6-10 hemoglobin subunit beta Homo sapiens 86-89 28806678-3 2017 Total iron (Fe) contents were 16.50, 24.40, and 13.08% for nZVI/BB, nZVI/PBB and nZVI/HBB, respectively. Iron 12-14 hemoglobin subunit beta Homo sapiens 86-89 17135308-0 2007 Heterozygous beta-globin gene mutations as a risk factor for iron accumulation and liver fibrosis in chronic hepatitis C. BACKGROUND: Iron accumulation is a well-known risk factor for the progression of chronic hepatitis C (CHC) to fibrosis. Iron 61-65 hemoglobin subunit beta Homo sapiens 13-24 17135308-0 2007 Heterozygous beta-globin gene mutations as a risk factor for iron accumulation and liver fibrosis in chronic hepatitis C. BACKGROUND: Iron accumulation is a well-known risk factor for the progression of chronic hepatitis C (CHC) to fibrosis. Iron 134-138 hemoglobin subunit beta Homo sapiens 13-24 17135308-2 2007 AIM: To evaluate the relative role of haemachromatosis (HFE), ferroportin and beta-globin gene mutations in promoting iron accumulation and fibrosis in patients with CHC. Iron 118-122 hemoglobin subunit beta Homo sapiens 78-89 17135308-6 2007 Hepatic iron concentration (HIC) and hepatic stainable iron were significantly higher (p<0.05) in patients with CHC carrying beta-globin mutations than in those with HFE mutations or the wild-type alleles. Iron 8-12 hemoglobin subunit beta Homo sapiens 128-139 17135308-6 2007 Hepatic iron concentration (HIC) and hepatic stainable iron were significantly higher (p<0.05) in patients with CHC carrying beta-globin mutations than in those with HFE mutations or the wild-type alleles. Iron 55-59 hemoglobin subunit beta Homo sapiens 128-139 17135308-7 2007 Multivariate analysis confirmed that the presence of beta-globin mutations was independently associated with both HIC (p = 0.008) and hepatic-stainable iron (odds ratio (OR) 6.11; 95% CI 1.56 to 23.92; p = 0.009). Iron 152-156 hemoglobin subunit beta Homo sapiens 53-64 17135308-10 2007 CONCLUSIONS: Heterozygosis for beta-globin mutations is a novel risk factor for both hepatic iron accumulation and the progression to fibrosis in patients with CHC. Iron 93-97 hemoglobin subunit beta Homo sapiens 31-42 20739079-9 2010 CONCLUSIONS: In patients with NAFLD, predominant hepatocellular iron deposition is often related to genetic factors, among which beta-globin mutations play a major role, predisposing to parenchymal iron accumulation and to progressive liver fibrosis. Iron 64-68 hemoglobin subunit beta Homo sapiens 129-140 20739079-9 2010 CONCLUSIONS: In patients with NAFLD, predominant hepatocellular iron deposition is often related to genetic factors, among which beta-globin mutations play a major role, predisposing to parenchymal iron accumulation and to progressive liver fibrosis. Iron 198-202 hemoglobin subunit beta Homo sapiens 129-140