@article{fallah_ifng/ifng-as1_2019,
	title = {{IFNG}/{IFNG}-{AS1} expression level balance: implications for autism spectrum disorder},
	issn = {1573-7365},
	shorttitle = {{IFNG}/{IFNG}-{AS1} expression level balance},
	doi = {10.1007/s11011-019-00510-4},
	abstract = {Autism spectrum disorder (ASD) is a neurodevelopmental disorder associated with different epidemiological, genetic, epigenetic, and environmental factors. Although its etiology is not fully understood, immune dysfunction is implicated in this disease. Recently, a large number of genes encoding long noncoding RNAs (lncRNAs) were discovered which act as positive or negative regulators of neighboring target genes. The lncRNA, Interferon gamma-antisense RNA (IFNG-AS1), regulates expression levels of the Interferon gamma (IFNG) gene. In the present study, we investigated expression of IFNG and IFNG-AS1 in 50 children with ASD (15 females and 35 males, mean age: 6 ± 1.4 years) and 50 healthy controls (14 females and 36 males, mean age: 6 ± 1.74 years) by real time PCR technique. The results showed significant up-regulation of IFNG and down-regulation of IFNG-AS1 expression in children with ASD compared to controls (Fold change = 1.5, P {\textless} 0.0001; Fold change = -0.143, P = 0.013, respectively). The IFNG expression level increase was more pronounced in male ASD children (Fold change = 1.621; p {\textless} 0.0001). Our data reveal a functional disruption in the interactive network of IFNG/IFNG-AS1 regulation, which could be a contributing factor in the chronic inflammatory aspect of ASD. Our findings can help understanding the underlying contributors to ASD pathogenesis and find novel treatment options for children with ASD.},
	language = {eng},
	journal = {Metabolic Brain Disease},
	author = {Fallah, Hamid and Sayad, Arezou and Ranjbaran, Fatemeh and Talebian, Fatemeh and Ghafouri-Fard, Soudeh and Taheri, Mohammad},
	month = nov,
	year = {2019},
	pmid = {31728886},
	keywords = {Autism spectrum disorder (ASD), INFG, INFG-AS1},
}

{"_id":"BoQaEJBMjQjHatLDz","bibbaseid":"fallah-sayad-ranjbaran-talebian-ghafourifard-taheri-ifngifngas1expressionlevelbalanceimplicationsforautismspectrumdisorder-2019","author_short":["Fallah, H.","Sayad, A.","Ranjbaran, F.","Talebian, F.","Ghafouri-Fard, S.","Taheri, M."],"bibdata":{"bibtype":"article","type":"article","title":"IFNG/IFNG-AS1 expression level balance: implications for autism spectrum disorder","issn":"1573-7365","shorttitle":"IFNG/IFNG-AS1 expression level balance","doi":"10.1007/s11011-019-00510-4","abstract":"Autism spectrum disorder (ASD) is a neurodevelopmental disorder associated with different epidemiological, genetic, epigenetic, and environmental factors. Although its etiology is not fully understood, immune dysfunction is implicated in this disease. Recently, a large number of genes encoding long noncoding RNAs (lncRNAs) were discovered which act as positive or negative regulators of neighboring target genes. The lncRNA, Interferon gamma-antisense RNA (IFNG-AS1), regulates expression levels of the Interferon gamma (IFNG) gene. In the present study, we investigated expression of IFNG and IFNG-AS1 in 50 children with ASD (15 females and 35 males, mean age: 6 ± 1.4 years) and 50 healthy controls (14 females and 36 males, mean age: 6 ± 1.74 years) by real time PCR technique. The results showed significant up-regulation of IFNG and down-regulation of IFNG-AS1 expression in children with ASD compared to controls (Fold change = 1.5, P \\textless 0.0001; Fold change = -0.143, P = 0.013, respectively). The IFNG expression level increase was more pronounced in male ASD children (Fold change = 1.621; p \\textless 0.0001). Our data reveal a functional disruption in the interactive network of IFNG/IFNG-AS1 regulation, which could be a contributing factor in the chronic inflammatory aspect of ASD. Our findings can help understanding the underlying contributors to ASD pathogenesis and find novel treatment options for children with ASD.","language":"eng","journal":"Metabolic Brain Disease","author":[{"propositions":[],"lastnames":["Fallah"],"firstnames":["Hamid"],"suffixes":[]},{"propositions":[],"lastnames":["Sayad"],"firstnames":["Arezou"],"suffixes":[]},{"propositions":[],"lastnames":["Ranjbaran"],"firstnames":["Fatemeh"],"suffixes":[]},{"propositions":[],"lastnames":["Talebian"],"firstnames":["Fatemeh"],"suffixes":[]},{"propositions":[],"lastnames":["Ghafouri-Fard"],"firstnames":["Soudeh"],"suffixes":[]},{"propositions":[],"lastnames":["Taheri"],"firstnames":["Mohammad"],"suffixes":[]}],"month":"November","year":"2019","pmid":"31728886","keywords":"Autism spectrum disorder (ASD), INFG, INFG-AS1","bibtex":"@article{fallah_ifng/ifng-as1_2019,\n\ttitle = {{IFNG}/{IFNG}-{AS1} expression level balance: implications for autism spectrum disorder},\n\tissn = {1573-7365},\n\tshorttitle = {{IFNG}/{IFNG}-{AS1} expression level balance},\n\tdoi = {10.1007/s11011-019-00510-4},\n\tabstract = {Autism spectrum disorder (ASD) is a neurodevelopmental disorder associated with different epidemiological, genetic, epigenetic, and environmental factors. Although its etiology is not fully understood, immune dysfunction is implicated in this disease. Recently, a large number of genes encoding long noncoding RNAs (lncRNAs) were discovered which act as positive or negative regulators of neighboring target genes. The lncRNA, Interferon gamma-antisense RNA (IFNG-AS1), regulates expression levels of the Interferon gamma (IFNG) gene. In the present study, we investigated expression of IFNG and IFNG-AS1 in 50 children with ASD (15 females and 35 males, mean age: 6 ± 1.4 years) and 50 healthy controls (14 females and 36 males, mean age: 6 ± 1.74 years) by real time PCR technique. The results showed significant up-regulation of IFNG and down-regulation of IFNG-AS1 expression in children with ASD compared to controls (Fold change = 1.5, P {\\textless} 0.0001; Fold change = -0.143, P = 0.013, respectively). The IFNG expression level increase was more pronounced in male ASD children (Fold change = 1.621; p {\\textless} 0.0001). Our data reveal a functional disruption in the interactive network of IFNG/IFNG-AS1 regulation, which could be a contributing factor in the chronic inflammatory aspect of ASD. Our findings can help understanding the underlying contributors to ASD pathogenesis and find novel treatment options for children with ASD.},\n\tlanguage = {eng},\n\tjournal = {Metabolic Brain Disease},\n\tauthor = {Fallah, Hamid and Sayad, Arezou and Ranjbaran, Fatemeh and Talebian, Fatemeh and Ghafouri-Fard, Soudeh and Taheri, Mohammad},\n\tmonth = nov,\n\tyear = {2019},\n\tpmid = {31728886},\n\tkeywords = {Autism spectrum disorder (ASD), INFG, INFG-AS1},\n}\n\n","author_short":["Fallah, H.","Sayad, A.","Ranjbaran, F.","Talebian, F.","Ghafouri-Fard, S.","Taheri, M."],"key":"fallah_ifng/ifng-as1_2019","id":"fallah_ifng/ifng-as1_2019","bibbaseid":"fallah-sayad-ranjbaran-talebian-ghafourifard-taheri-ifngifngas1expressionlevelbalanceimplicationsforautismspectrumdisorder-2019","role":"author","urls":{},"keyword":["Autism spectrum disorder (ASD)","INFG","INFG-AS1"],"metadata":{"authorlinks":{}}},"bibtype":"article","biburl":"https://bibbase.org/zotero/sstraume97","dataSources":["TyZEFir7kPZynooYn","cheJSdW6Nnp4Tryus"],"keywords":["autism spectrum disorder (asd)","infg","infg-as1"],"search_terms":["ifng","ifng","as1","expression","level","balance","implications","autism","spectrum","disorder","fallah","sayad","ranjbaran","talebian","ghafouri-fard","taheri"],"title":"IFNG/IFNG-AS1 expression level balance: implications for autism spectrum disorder","year":2019}