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Journal articles on the topic 'H19/IGF2'

Author: Grafiati

Published: 4 June 2021

Last updated: 17 February 2022

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1

Lawson, Elizabeth A., Xun Zhang, Jonathan T. Crocker, Wei-Lien Wang, and Anne Klibanski. "Hypoglycemia from IGF2 Overexpression Associated with Activation of Fetal Promoters and Loss of Imprinting in a Metastatic Hemangiopericytoma." Endocrine Reviews 30, no. 4 (2009): 413. http://dx.doi.org/10.1210/edrv.30.4.9990.

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ABSTRACT Context The mechanism of IGF2 overexpression in non-islet-cell tumor hypoglycemia is not understood. Objective We investigated the imprinting control and promoter usage for IGF2 expression to identify a mechanism for increased IGF-II production in non-islet-cell tumor hypoglycemia. Patient and Methods A patient with metastatic hemangiopericytoma was studied. Tissue from the original hemangiopericytoma, metastatic tumor, and uninvolved liver was analyzed for IGF-II immunohistochemistry. IGF2, a paternally imprinted gene, shares a control region with maternally imprinted H19, a putative

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Lawson, Elizabeth A., Xun Zhang, Jonathan T. Crocker, Wei-Lien Wang, and Anne Klibanski. "Hypoglycemia from IGF2 Overexpression Associated with Activation of Fetal Promoters and Loss of Imprinting in a Metastatic Hemangiopericytoma." Journal of Clinical Endocrinology & Metabolism 94, no. 7 (2009): 2226–31. http://dx.doi.org/10.1210/jc.2009-0153.

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Context: The mechanism of IGF2 overexpression in non-islet-cell tumor hypoglycemia is not understood. Objective: We investigated the imprinting control and promoter usage for IGF2 expression to identify a mechanism for increased IGF-II production in non-islet-cell tumor hypoglycemia. Patient and Methods: A patient with metastatic hemangiopericytoma was studied. Tissue from the original hemangiopericytoma, metastatic tumor, and uninvolved liver was analyzed for IGF-II immunohistochemistry. IGF2, a paternally imprinted gene, shares a control region with maternally imprinted H19, a putative tumor

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Drewell, Robert A., Katharine L. Arney, Takahiro Arima, Sheila C. Barton, James D. Brenton, and M. Azim Surani. "Novel conserved elements upstream of theH19gene are transcribed and act as mesodermal enhancers." Development 129, no. 5 (2002): 1205–13. http://dx.doi.org/10.1242/dev.129.5.1205.

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The reciprocally imprinted H19 and Igf2 genes form a co-ordinately regulated 130 kb unit in the mouse controlled by widely dispersed enhancers, epigenetically modified silencers and an imprinting control region (ICR). Comparative human and mouse genomic sequencing between H19 and Igf2 revealed two novel regions of strong homology upstream of the ICR termed H19 upstream conserved regions (HUCs). Mouse HUC1 and HUC2 act as potent enhancers capable of driving expression of an H19 reporter gene in a range of mesodermal tissues. Intriguingly, the HUC sequences are also transcribed bi-allelically in

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Berteaux, Nathalie, Nathalie Aptel, Guy Cathala, et al. "A Novel H19 Antisense RNA Overexpressed in Breast Cancer Contributes to Paternal IGF2 Expression." Molecular and Cellular Biology 28, no. 22 (2008): 6731–45. http://dx.doi.org/10.1128/mcb.02103-07.

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ABSTRACT The H19/IGFf2 locus belongs to a large imprinted domain located on human chromosome 11p15.5 (homologue to mouse distal chromosome 7). The H19 gene is expressed from the maternal allele, while IGF2 is paternally expressed. Natural antisense transcripts and intergenic transcription have been involved in many aspects of eukaryotic gene expression, including genomic imprinting and RNA interference. However, apart from the identification of some IGF2 antisense transcripts, few data are available on that topic at the H19/IGF2 locus. We identify here a novel transcriptional activity at both

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Pathak, Shilpa, Madhurima Saxena, Ryan D'Souza, and N. H. Balasinor. "Disrupted imprinting status at the H19 differentially methylated region is associated with the resorbed embryo phenotype in rats." Reproduction, Fertility and Development 22, no. 6 (2010): 939. http://dx.doi.org/10.1071/rd09154.

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Igf2, an imprinted gene that is paternally expressed in embryos, encodes an embryonic growth factor. An important regulator of Igf2 expression is methylation of the H19 differentially methylated region (DMR). A significant association has been observed between sperm methylation status at the H19 DMR and post-implantation loss. In addition, tamoxifen treatment has been shown to increase post-implantation loss and reduce DNA methylation at the H19 DMR in rat spermatozoa. Because this DMR is a primary DMR transmitting epigenetic imprint information from the gametes to the embryo, the aim of the p

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Thorvaldsen, Joanne L., Andrew M. Fedoriw, Son Nguyen, and Marisa S. Bartolomei. "Developmental Profile of H19 Differentially Methylated Domain (DMD) Deletion Alleles Reveals Multiple Roles of the DMD in Regulating Allelic Expression and DNA Methylation at the Imprinted H19/Igf2 Locus." Molecular and Cellular Biology 26, no. 4 (2006): 1245–58. http://dx.doi.org/10.1128/mcb.26.4.1245-1258.2006.

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ABSTRACT The differentially methylated domain (DMD) of the mouse H19 gene is a methylation-sensitive insulator that blocks access of the Igf2 gene to shared enhancers on the maternal allele and inactivates H19 expression on the methylated paternal allele. By analyzing H19 DMD deletion alleles H19ΔDMD and H19Δ3.8kb-5′H19 in pre- and postimplantation embryos, we show that the DMD exhibits positive transcriptional activity and is required for H19 expression in blastocysts and full activation of H19 during subsequent development. We also show that the DMD is required to establish Igf2 imprinting b

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Mitalipov, Shoukhrat M. "Genomic imprinting in primate embryos and embryonic stem cells." Reproduction, Fertility and Development 18, no. 8 (2006): 817. http://dx.doi.org/10.1071/rd06112.

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Embryonic stem (ES) cells hold promise for cell and tissue replacement approaches to treating human diseases. However, long-term in vitro culture and manipulations of ES cells may adversely affect their epigenetic integrity including imprinting. Disruption or inappropriate expression of imprinted genes is associated with several clinically significant syndromes and tumorigenesis in humans. We demonstrated aberrant biallelic expression of IGF2 and H19 in several rhesus monkey ES cell lines while SNRPN and NDN were normally imprinted and expressed from the paternal allele. In contrast, expanded

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Ainscough, J. F., T. Koide, M. Tada, S. Barton, and M. A. Surani. "Imprinting of Igf2 and H19 from a 130 kb YAC transgene." Development 124, no. 18 (1997): 3621–32. http://dx.doi.org/10.1242/dev.124.18.3621.

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A stringent test for imprint control elements is to examine their function at ectopic loci in transgenic experiments. Igf2 and H19 are part of a larger imprinting region and as a first step, we examined these reciprocally imprinted genes in transgenic experiments using a 130 kb YAC clone. After paternal inheritance, H19 was appropriately repressed and Igf2 was expressed, irrespective of copy number or genetic background. After maternal inheritance H19 was consistently expressed, albeit with some variability. The levels of H19 expression per copy of the transgene inversely correlated with Igf2

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9

Gatford, K. L., G. K. Heinemann, S. D. Thompson, et al. "Circulating IGF1 and IGF2 and SNP genotypes in men and pregnant and non-pregnant women." Endocrine Connections 3, no. 3 (2014): 138–49. http://dx.doi.org/10.1530/ec-14-0068.

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Circulating IGFs are important regulators of prenatal and postnatal growth, and of metabolism and pregnancy, and change with sex, age and pregnancy. Single-nucleotide polymorphisms (SNPs) in genes coding for these hormones associate with circulating abundance of IGF1 and IGF2 in non-pregnant adults and children, but whether this occurs in pregnancy is unknown. We therefore investigated associations of plasma IGF1 and IGF2 with age and genotype at candidate SNPs previously associated with circulating IGF1, IGF2 or methylation of the INS–IGF2–H19 locus in men (n=134), non-pregnant women (n=74) a

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Han, Li, Dong-Hoon Lee, and Piroska E. Szabó. "CTCF Is the Master Organizer of Domain-Wide Allele-Specific Chromatin at the H19/Igf2 Imprinted Region." Molecular and Cellular Biology 28, no. 3 (2007): 1124–35. http://dx.doi.org/10.1128/mcb.01361-07.

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ABSTRACT A paternally methylated imprinting control region (ICR) directs allele-specific expression of the imprinted H19 and Igf2 genes. CTCF protein binding in the ICR is required in the maternal chromosome for insulating Igf2 from the shared enhancers, initiation of the H19 promoter transcription, maintaining DNA hypomethylation, and chromosome loop formation. Using novel quantitative allele-specific chromatin immunoprecipitation-single-nucleotide primer extension assays, we measured the chromatin composition along the H19/Igf2 imprinted domain in cells with engineered mutations at the four

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Davies, Karen, Lucy Bowden, Paul Smith, et al. "Disruption of mesodermal enhancers forIgf2in the minute mutant." Development 129, no. 7 (2002): 1657–68. http://dx.doi.org/10.1242/dev.129.7.1657.

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The radiation-induced mutation minute (Mnt) in the mouse leads to intrauterine growth retardation with paternal transmission and has been linked to the distal chromosome 7 cluster of imprinted genes. We show that the mutation is an inversion, whose breakpoint distal to H19 disrupts and thus identifies an enhancer for Igf2 expression in skeletal muscle and tongue, and separates the gene from other mesodermal and extra-embryonic enhancers. Paternal transmission of Mnt leads to drastic downregulation of Igf2 transcripts in all mesodermal tissues and the placenta. Maternal transmission leads to me

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Ohlsson, R., F. Hedborg, L. Holmgren, C. Walsh, and T. J. Ekstrom. "Overlapping patterns of IGF2 and H19 expression during human development: biallelic IGF2 expression correlates with a lack of H19 expression." Development 120, no. 2 (1994): 361–68. http://dx.doi.org/10.1242/dev.120.2.361.

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The spatial patterns of IGF2 and H19 gene expression are strikingly similar during parts of human embryonic/fetal and early postnatal development. Notable exceptions were found with the ciliary anlage of the embryonic retina and the choroid plexus/leptomeninges, where transcripts from the IGF2 but not the H19 locus could be detected. Moreover, in contrast to the other tissue samples examined, the choroid plexus/leptomeninges expressed both parental IGF2 alleles. Whilst RNase protection analysis revealed a weak activity of the P1 promoter in the choroid plexus/leptomeninges, the P2, P3 and P4 p

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Rotwein, Peter. "Similarity and variation in the insulin-like growth factor 2 - H19 locus in primates." Physiological Genomics 50, no. 6 (2018): 425–39. http://dx.doi.org/10.1152/physiolgenomics.00030.2018.

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Insulin-like growth factor 2 (IGF2), a small, secreted protein, is critical for fetal and prenatal growth in humans and other mammals. The IGF2 gene and its mouse homolog comprise part of a conserved linkage group that is regulated by parental imprinting, with IGF2/ Igf2 being expressed from the paternal chromosome, and the adjacent H19 gene from the maternal chromosome. By using information extracted from public genomic and gene expression databases, I have now analyzed this locus in nine nonhuman primate species representing over 60 million years of evolutionary divergence from a common prog

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Singh, Vikrant, and Madhulika Srivastava. "Enhancer Blocking Activity of the Insulator at H19-ICR Is Independent of Chromatin Barrier Establishment." Molecular and Cellular Biology 28, no. 11 (2008): 3767–75. http://dx.doi.org/10.1128/mcb.00091-08.

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ABSTRACT Transcriptional insulators are cis regulatory elements that organize chromatin into independently regulated domains. At the imprinted murine Igf2/H19 locus, the H19-ICR insulator prevents the activation of the Igf2 promoter on the maternal allele by enhancers that activate H19 on the same chromosome. Given the well-demonstrated role of H19-ICR as an enhancer blocker, we investigated its ability to define a chromatin barrier, as the two activities are coincident on several insulators and may act in concert to define a functional chromatin boundary between adjacent genes with distinct t

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Wei, Y. C., Y. J. Huan, Z. F. Liu, J. Zhu, X. M. Zhang, and Z. H. Liu. "82 ABERRANT EXPRESSION AND METHYLATION STATUS OF PUTATIVELY IMPRINTED GENES IN CLONED PIG PLACENTA." Reproduction, Fertility and Development 22, no. 1 (2010): 199. http://dx.doi.org/10.1071/rdv22n1ab82.

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Unlike embryos derived from fertilization, most cloned embryos die during post-implantation development, and those that survive to term are frequently defective. Many of the observed defects involve the placenta. Abnormal placentation has been described in several cloned species, but rarely in pigs. Because imprinted genes are important regulators of placenta growth and may be subjected to faulty reprogramming during somatic cell nuclear transfer, we aimed to determine the expression levels and methylation patterns of imprinted genes in live cloned piglets and their placentas compared with dea

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Ohlsson, R., T. J. Ekström, G. Adam, et al. "Genetic imprinting of IGF2/H19 in Normal, Hyperplastic and Neoplastic Cells." Acta geneticae medicae et gemellologiae: twin research 45, no. 1-2 (1996): 91–92. http://dx.doi.org/10.1017/s0001566000001161.

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Genetic imprinting implies the preferential or exclusive expression of one of the parental alleles of a subset of autosomal loci. The insulin-like growth factor II (IGF2) and H19 loci are particularly interesting examples of this phenomenon since their products appear to display growth agonistic and antagonistic properties, respectively. In addition, IGF2 and H19 are only 90 kb apart, are expressed from opposite parental alleles [1,2] and show a striking similarity in their spatial expression patterns during human prenatal development [3]. One exception is the choroid plexus and leptomeninges

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Kaffer, Christopher R., Alex Grinberg, and Karl Pfeifer. "Regulatory Mechanisms at the MouseIgf2/H19 Locus." Molecular and Cellular Biology 21, no. 23 (2001): 8189–96. http://dx.doi.org/10.1128/mcb.21.23.8189-8196.2001.

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ABSTRACT The closely linked H19 and Igf2 genes show highly similar patterns of gene expression but are reciprocally imprinted. H19 is expressed almost exclusively from the maternally inherited chromosome, while Igf2 expression is mostly from the paternal chromosome. In humans, loss of imprinting at this locus is associated with tumors and with developmental disorders. Monoallelic expression at the imprinted Igf2/H19 locus occurs by at least two distinct mechanisms: a developmentally regulated silencing of the paternal H19 promoter, and transcriptional insulation of the maternal Igf2 promoters.

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Webber, Andrea L., and Shirley M. Tilghman. "The Absence of Enhancer Competition betweenIgf2 and H19 following Transfer into Differentiated Cells." Molecular and Cellular Biology 18, no. 4 (1998): 1903–10. http://dx.doi.org/10.1128/mcb.18.4.1903.

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ABSTRACT H19 and Igf2 are reciprocally imprinted genes that lie 90 kb apart on mouse chromosome 7. The two genes are coexpressed during development, with the H19 gene expressed exclusively from the maternal chromosome and Igf2 from the paternal chromosome. It has been proposed that their reciprocal imprinting is governed by a competition between the genes for a common set of enhancers. The competition on the paternal chromosome is influenced by extensive allele-specific methylation of theH19 gene and its 5′ flank, which acts to inhibitH19 transcription and thus indirectly leads to the activati

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Feil, R., J. Walter, N. D. Allen, and W. Reik. "Developmental control of allelic methylation in the imprinted mouse Igf2 and H19 genes." Development 120, no. 10 (1994): 2933–43. http://dx.doi.org/10.1242/dev.120.10.2933.

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The Insulin-like growth factor 2 (Igf2) and H19 genes are reciprocally imprinted and closely linked. Igf2 encodes a fetal growth-factor and is predominantly expressed from the paternal allele, while H19 is expressed from the maternal allele and encodes a transcript which may downregulate cellular proliferation. One of the epigenetic modifications thought to be involved in parental imprinting is DNA methylation. Here we analyse methylation in two regions of the Igf2 gene, one approx. 3 kb upstream of the gene and one in the 3′ part of the gene. Both regions are more methylated on the expressed

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Nielsen, Helene Myrtue, Alexandre How-Kit, Carole Guerin, et al. "Copy number variations alter methylation and parallel IGF2 overexpression in adrenal tumors." Endocrine-Related Cancer 22, no. 6 (2015): 953–67. http://dx.doi.org/10.1530/erc-15-0086.

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Overexpression of insulin growth factor 2 (IGF2) is a hallmark of adrenocortical carcinomas and pheochromocytomas. Previous studies investigating the IGF2/H19 locus have mainly focused on a single molecular level such as genomic alterations or altered DNA methylation levels and the causal changes underlying IGF2 overexpression are still not fully established. In the current study, we analyzed 62 tumors of the adrenal gland from patients with Conn's adenoma (CA, n=12), pheochromocytomas (PCC, n=10), adrenocortical benign tumors (ACBT, n=20), and adrenocortical carcinomas (ACC, n=20). Gene expre

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Szabó, Piroska E., Shih-Huey E. Tang, Michael R. Reed, Francisco J. Silva, Walter M. K. Tsark та Jeffrey R. Mann. "The chicken β-globin insulator element conveys chromatin boundary activity but not imprinting at the mouse Igf2/H19 domain". Development 129, № 4 (2002): 897–904. http://dx.doi.org/10.1242/dev.129.4.897.

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Imprinting of the mouse insulin-like growth factor 2 (Igf2) and H19 genes is regulated by an imprinting control region (ICR). The hypomethylated maternal copy functions as a chromatin insulator through the binding of CTCF and prevents Igf2 activation in cis, while hypermethylation of the paternal copy inactivates insulator function and leads to inactivation of H19 in cis. The specificity of the ICR sequence for mediating imprinting and chromatin insulation was investigated by substituting it for two copies of the chicken β-globin insulator element, (ChβGI)2, in mice. This introduced sequence r

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Thorvaldsen, Joanne L., Mellissa R. W. Mann, Okechukwu Nwoko, Kristen L. Duran, and Marisa S. Bartolomei. "Analysis of Sequence Upstream of the Endogenous H19 Gene Reveals Elements Both Essential and Dispensable for Imprinting." Molecular and Cellular Biology 22, no. 8 (2002): 2450–62. http://dx.doi.org/10.1128/mcb.22.8.2450-2462.2002.

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ABSTRACT Imprinting of the linked and oppositely expressed mouse H19 and Igf2 genes requires a 2-kb differentially methylated domain (DMD) that is located 2 kb upstream of H19. This element is postulated to function as a methylation-sensitive insulator. Here we test whether an additional sequence 5′ of H19 is required for H19 and Igf2 imprinting. Because repetitive elements have been suggested to be important for genomic imprinting, the requirement of a G-rich repetitive element that is located immediately 3′ to the DMD was first tested in two targeted deletions: a 2.9-kb deletion (ΔDMDΔG) tha

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Masunaga, Yohei, Takanobu Inoue, Kaori Yamoto, et al. "IGF2 Mutations." Journal of Clinical Endocrinology & Metabolism 105, no. 1 (2019): 116–25. http://dx.doi.org/10.1210/clinem/dgz034.

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Abstract Objective IGF2 is a paternally expressed growth-promoting gene. Here, we report five cases with IGF2 mutations and review IGF2 mutation-positive patients described in the literature. We also compare clinical features between patients with IGF2 mutations and those with H19/IGF2:IG-DMR epimutations. Results We recruited five cases with IGF2 mutations: case 1 with a splice site mutation (c.–6–1G&gt;C) leading to skipping of exon 2 and cases 2–5 with different missense mutations (p.(Cys70Tyr), p.(Cys71Arg), p.(Cys33Ser), and p.(Cys45Ser)) affecting cysteine residues involved in the S-

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Tiwari, M., N. Rawat, P. Vats, et al. "89 METHYLATION STATUS OF IGF2/H19 DMR3 REGION AFFECTS IN VITRO BLASTOCYST PRODUCTION IN GOAT (CAPRA HIRCUS)." Reproduction, Fertility and Development 29, no. 1 (2017): 152. http://dx.doi.org/10.1071/rdv29n1ab89.

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Parthenogenesis has been observed in lower animals but no known instance has been reported in mammals because both maternal and paternal genomes are a fundamental prerequisite for embryogenesis. A major reason for developmental failure of uniparental zygotes is expression of certain genes in a parent-of-origin-specific manner, i.e. genomic imprinting of genes. Out of many imprinted genes identified so far, IGF2/H19 have been extensively studied and known to play an important role in fetal and placental development. Gene IGF2 is expressed by the paternal allele, H19 is transcribed from the mate

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Biniszkiewicz, Detlev, Joost Gribnau, Bernard Ramsahoye, et al. "Dnmt1 Overexpression Causes Genomic Hypermethylation, Loss of Imprinting, and Embryonic Lethality." Molecular and Cellular Biology 22, no. 7 (2002): 2124–35. http://dx.doi.org/10.1128/mcb.22.7.2124-2135.2002.

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ABSTRACT Biallelic expression of Igf2 is frequently seen in cancers because Igf2 functions as a survival factor. In many tumors the activation of Igf2 expression has been correlated with de novo methylation of the imprinted region. We have compared the intrinsic susceptibilities of the imprinted region of Igf2 and H19, other imprinted genes, bulk genomic DNA, and repetitive retroviral sequences to Dnmt1 overexpression. At low Dnmt1 methyltransferase levels repetitive retroviral elements were methylated and silenced. The nonmethylated imprinted region of Igf2 and H19 was resistant to methylatio

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Banerjee, Subhasis, Alan Smallwood, Scott Lamond, Stuart Campbell, and Geeta Nargund. "Igf2/H19 Imprinting Control Region (ICR): An Insulator or a Position-Dependent Silencer?" Scientific World JOURNAL 1 (2001): 218–24. http://dx.doi.org/10.1100/tsw.2001.50.

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The imprinting control region (ICR) located far upstream of the H19 gene, in conjunction with enhancers, modulates the transcription of Igf2 and H19 genes in an allele-specific manner. On paternal inheritance, the methylated ICR silences the H19 gene and indirectly facilitates transcription from the distant Igf2 promoter, whereas on the maternal chromosome the unmethylated ICR, together with enhancers, activates transcription of the H19 gene and thereby contributes to the repression of Igf2. This repression of maternal Igf2 has recently been postulated to be due to a chromatin boundary or insu

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Agba, Ogechukwu Brenda, Ludwig Lausser, Klaus Huse, et al. "Tissue-, sex-, and age-specific DNA methylation of rat glucocorticoid receptor gene promoter and insulin-like growth factor 2 imprinting control region." Physiological Genomics 49, no. 11 (2017): 690–702. http://dx.doi.org/10.1152/physiolgenomics.00009.2017.

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Tissue-, sex-, and age-specific epigenetic modifications such as DNA methylation are largely unknown. Changes in DNA methylation of the glucocorticoid receptor gene ( NR3C1) and imprinting control region (ICR) of IGF2 and H19 genes during the lifespan are particularly interesting since these genes are susceptible to epigenetic modifications by prenatal stress or malnutrition. They are important regulators of development and aging. Methylation changes of NR3C1 affect glucocorticoid receptor expression, which is associated with stress sensitivity and stress-related diseases predominantly occurri

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Casola, S., M. Vernucci, P. Ungaro, C. B. Bruni, and A. Riccio. "Preferential Loss of Heterozygosity of Chromosome 7 Loci in Simian Virus 40 t/T Antigen-Induced Mouse Hepatocellular Carcinomas Does Not Involve H-ras Muatations." Acta geneticae medicae et gemellologiae: twin research 45, no. 1-2 (1996): 221–25. http://dx.doi.org/10.1017/s0001566000001343.

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Genetic complementation experiments have indicated that both a maternal and a paternal copy of the distal region of mouse chromosome 7 are essential for normal development [1]. This suggested the presence of genes whose expression is dependent on the gamete of origin in this chromosomal region. Two such imprinted genes, namely insulin-like growth factor II (Igf2) and H19, have been identified so far [2, 3]. The first encodes a peptide with mitotic activity towards several cell types, that contributes significantly to prenatal growth of mammals, whereas the second has, as yet, no defined role a

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Ainscough, J. F., R. M. John, S. C. Barton, and M. A. Surani. "A skeletal muscle-specific mouse Igf2 repressor lies 40 kb downstream of the gene." Development 127, no. 18 (2000): 3923–30. http://dx.doi.org/10.1242/dev.127.18.3923.

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Igf2 and H19 are closely linked and reciprocally expressed genes on distal chromosome 7 in the mouse. We have previously shown that a 130 kb YAC transgene contains multiple tissue-specific enhancers for expression of both genes during embryogenesis. The YAC also contains all the crucial elements responsible for initiating and maintaining appropriate parent-of-origin-specific expression of these genes at ectopic sites, with expression of Igf2 after paternal inheritance and of H19 after maternal inheritance. Located centrally between Igf2 and H19 are two prominent DNaseI hypersensitive sites, an

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Freschi, Andrea, Rosita Del Prete, Laura Pignata, et al. "The number of the CTCF binding sites of the H19/IGF2:IG-DMR correlates with DNA methylation and expression imprinting in a humanized mouse model." Human Molecular Genetics 30, no. 16 (2021): 1509–20. http://dx.doi.org/10.1093/hmg/ddab132.

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Abstract The reciprocal parent of origin-specific expression of H19 and IGF2 is controlled by the H19/IGF2:IG-DMR (IC1), whose maternal allele is unmethylated and acts as a CTCF-dependent insulator. In humans, internal IC1 deletions are associated with Beckwith–Wiedemann syndrome (BWS) and Silver-Russell syndrome (SRS), depending on their parental origin. These genetic mutations result in aberrant DNA methylation, deregulation of IGF2/H19 and disease with incomplete penetrance. However, the mechanism linking the microdeletions to altered molecular and clinical phenotypes remains unclear. To ad

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Arney, Katharine L. "H19 and Igf2 – enhancing the confusion?" Trends in Genetics 19, no. 1 (2003): 17–23. http://dx.doi.org/10.1016/s0168-9525(02)00004-5.

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Lou, Hangying, Fang Le, Minhao Hu, et al. "Aberrant DNA Methylation of IGF2-H19 Locus in Human Fetus and in Spermatozoa From Assisted Reproductive Technologies." Reproductive Sciences 26, no. 7 (2018): 997–1004. http://dx.doi.org/10.1177/1933719118802052.

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Given the higher risk of developing imprinting disorders in assisted reproductive technology (ART)-conceived children, we hypothesized that ART may affect DNA methylation of the insulin-like growth factor 2 (IGF2), H19, small nuclear ribonucleoprotein polypeptide N (SNRPN) differentially methylated regions (DMRs) at the fetal stage, which in turn may be associated with sperm abnormalities. A total of 4 patient groups were recruited, namely, multifetal reduction following in vitro fertilization (IVF)/ intracytoplasmic sperm injection (ICSI; n = 56), multifetal reduction following controlled ova

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Lee, Ho-Sun, Albino Barraza-Villarreal, Carine Biessy, et al. "Dietary supplementation with polyunsaturated fatty acid during pregnancy modulates DNA methylation at IGF2/H19 imprinted genes and growth of infants." Physiological Genomics 46, no. 23 (2014): 851–57. http://dx.doi.org/10.1152/physiolgenomics.00061.2014.

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Epigenetic regulation of imprinted genes is regarded as a highly plausible explanation for linking dietary exposures in early life with the onset of diseases during childhood and adulthood. We sought to test whether prenatal dietary supplementation with docosahexaenoic acid (DHA) during pregnancy may modulate epigenetic states at birth. This study was based on a randomized intervention trial conducted in Mexican pregnant women supplemented daily with 400 mg of DHA or a placebo from gestation week 18–22 to parturition. We applied quantitative profiling of DNA methylation states at IGF2 promoter

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Gao, L., Y. Liu, Y. Wen, and W. Wu. "LncRNA H19-mediated mouse cleft palate induced by all-trans retinoic acid." Human & Experimental Toxicology 36, no. 4 (2016): 395–401. http://dx.doi.org/10.1177/0960327116651121.

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Long noncoding RNAs (lncRNAs) are the new class of transcripts and pervasively transcribed in the genome, which have been found to play important functional roles in many tissues and organs. LncRNAs can interact with target gene to exert their functions. However, the function and mechanism of lncRNA in cleft palate (CP) development remain elusive. Here, we investigated the role of lncRNA H19 and its target gene insulin-like growth factor 2 (IGF2) in CP of mice. All-trans retinoic acid (atRA) is a well-known teratogenic effecter of CP. After establishment of the CP mouse model using atRA in viv

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Park, Kye-Yoon, Elizabeth A. Sellars, Alexander Grinberg, Sing-Ping Huang, and Karl Pfeifer. "The H19 Differentially Methylated Region Marks the Parental Origin of a Heterologous Locus without Gametic DNA Methylation." Molecular and Cellular Biology 24, no. 9 (2004): 3588–95. http://dx.doi.org/10.1128/mcb.24.9.3588-3595.2004.

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ABSTRACT Igf2 and H19 are coordinately regulated imprinted genes physically linked on the distal end of mouse chromosome 7. Genetic analyses demonstrate that the differentially methylated region (DMR) upstream of the H19 gene is necessary for three distinct functions: transcriptional insulation of the maternal Igf2 allele, transcriptional silencing of paternal H19 allele, and marking of the parental origin of the two chromosomes. To test the sufficiency of the DMR for the third function, we inserted DMR at two heterologous positions in the genome, downstream of H19 and at the alpha-fetoprotein

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Williams-Wyss, Olivia, Song Zhang, Severence M. MacLaughlin, et al. "Embryo number and periconceptional undernutrition in the sheep have differential effects on adrenal epigenotype, growth, and development." American Journal of Physiology-Endocrinology and Metabolism 307, no. 2 (2014): E141—E150. http://dx.doi.org/10.1152/ajpendo.00051.2012.

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Exposure to poor maternal nutrition around the time of conception results in an early prepartum activation of the fetal pituitary-adrenal axis and in increased adrenal growth and stress response after birth associated with epigenetic changes in a differentially methylated region (DMR) of adrenal IGF2/H19. We have determined the effects of maternal undernutrition during the periconceptional period (PCUN: 70% of control intake from 60 days before until 6 days after conception) and early preimplantation period (PIUN: 70% of control intake for 6 days after conception) on fetal plasma ACTH and cort

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Szabó, Piroska E., Shih-Huey E. Tang, Francisco J. Silva, Walter M. K. Tsark, and Jeffrey R. Mann. "Role of CTCF Binding Sites in the Igf2/H19 Imprinting Control Region." Molecular and Cellular Biology 24, no. 11 (2004): 4791–800. http://dx.doi.org/10.1128/mcb.24.11.4791-4800.2004.

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ABSTRACT A ∼2.4-kb imprinting control region (ICR) regulates somatic monoallelic expression of the Igf2 and H19 genes. This is achieved through DNA methylation-dependent chromatin insulator and promoter silencing activities on the maternal and paternal chromosomes, respectively. In somatic cells, the hypomethylated maternally inherited ICR binds the insulator protein CTCF at four sites and blocks activity of the proximal Igf2 promoter by insulating it from its distal enhancers. CTCF binding is thought to play a direct role in inhibiting methylation of the ICR in female germ cells and in somati

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Wu, Qiong, Takuya Kumagai, Manabu Kawahara, et al. "Regulated expression of two sets of paternally imprinted genes is necessary for mouse parthenogenetic development to term." Reproduction 131, no. 3 (2006): 481–88. http://dx.doi.org/10.1530/rep.1.00933.

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Mouse parthenogenetic embryos (PEs) are developmentally arrested until embryo day (E) 9.5 because of genomic imprinting. However, we have shown that embryos containing genomes from non-growing (ng) and fully grown (fg) oocytes, i.e. ngwt/fgwt PE (wt, wild type), developed to E13.5. Moreover, parthenogenetic development could be extended to term by further regulation of Igf2 and H19 expression using mice with deletion of the H19 transcription unit (H19Δ13) together with its differentially unit (DMR). To gain an insight into the extended development of the parthenotes to term, we have here inves

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Dean, W., L. Bowden, A. Aitchison, et al. "Altered imprinted gene methylation and expression in completely ES cell-derived mouse fetuses: association with aberrant phenotypes." Development 125, no. 12 (1998): 2273–82. http://dx.doi.org/10.1242/dev.125.12.2273.

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In vitro manipulation of preimplantation mammalian embryos can influence differentiation and growth at later stages of development. In the mouse, culture of embryonic stem (ES) cells affects their totipotency and may give rise to fetal abnormalities. To investigate whether this is associated with epigenetic alterations in imprinted genes, we analysed two maternally expressed genes (Igf2r, H19) and two paternally expressed genes (Igf2, U2af1-rs1) in ES cells and in completely ES cell-derived fetuses. Altered allelic methylation patterns were detected in all four genes, and these were consistent

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Dejeux, Emelyne, Robert Olaso, Bertrand Dousset, et al. "Hypermethylation of the IGF2 differentially methylated region 2 is a specific event in insulinomas leading to loss-of-imprinting and overexpression." Endocrine-Related Cancer 16, no. 3 (2009): 939–52. http://dx.doi.org/10.1677/erc-08-0331.

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Prediction of the evolution of endocrine pancreatic tumors remains difficult based on histological criteria alone. We have previously demonstrated that epigenetic changes are an early event in a mouse model developing insulinomas. Particularly, overexpression of the imprinted IGF2 was caused by the hypermethylation of CpGs in the differentially methylated region 2 (DMR2). Here, we investigated whether IGF2 hypermethylation is also observed in human insulinomas and whether this alteration is common to other human endocrine tumors of the pancreas and the digestive tract. We analyzed the methylat

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Heo, J., Dong Myung Shin, Kasia Mierzejewska, et al. "New Molecular Evidence That Oct-4 Is Truly Expressed In a Rare Population Of Developmental Early Stem Cells In Human Umbilical Cord Blood (UCB) and That Epigenetic Modification Of Imprinting At Igf2-H19 Locus Regulates Their Quiescent State – Potential Implications For Regenerative Medicine." Blood 122, no. 21 (2013): 2393. http://dx.doi.org/10.1182/blood.v122.21.2393.2393.

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Abstract Background One of the most intriguing questions in stem cell biology is whether human umbilical cord blood (UCB) contains early-development stem cells that express markers of pluripotency and thus could be employed in regenerative medicine. Several groups have reported mRNAs for genes regulating stem cell pluripotency, such as Oct-4A, Nanog, and SSEA-1, in UCB cells. However, detection of the Oct-4A transcript may be hampered by the presence of several pseudogenes and Oct-4B isoform, which is not related to stem cell pluripotency. Another important question is: why are these primitive

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Shin, Dong-Myung, Ewa K. Zuba-Surma, Mariusz Z. Ratajczak, and Magdalena Kucia. "The Unique Pattern of Somatic Imprint in Oct-4+ Very Small Embryonic Like (VSEL) Stem Cells Isolated from Adult Tissues Further Supports Both Their Epiblast/Germ Line Origin and Explains Quiescent Status: Potential Modification of Somatic Imprint as a Key to Longevity?" Blood 112, no. 11 (2008): 385. http://dx.doi.org/10.1182/blood.v112.11.385.385.

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Abstract Recently, we identified a population of very small embryonic like (VSEL) SCs in adult bone marrow (BM) (Leukemia2006:20;857). These VSELs are: very small in size (~3.6 um); Oct-4+CXCR4+SSEA-1+Sca-1+CD45−lin−; possessing large nuclei containing unorganized chromatin (euchromatin); and we learned that in co-cultures with C2C12 cells, VSELs form embryoid body-like spheres (VSEL-DSs) that contain primitive SCs capable to differentiate into all three germ layers (e.g., myocardium, neural tissue, and pancreas). To better characterize this intriguing population of SCs, we employed bisulfite

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Holmgren, Claes, Chandrasekhar Kanduri, Ghislaine Dell, et al. "CpG methylation regulates the Igf2/H19 insulator." Current Biology 11, no. 14 (2001): 1128–30. http://dx.doi.org/10.1016/s0960-9822(01)00314-1.

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Banerjee, Subhasis, and Alan Smallwood. "A chromatin model of IGF2/H19 imprinting." Nature Genetics 11, no. 3 (1995): 237–38. http://dx.doi.org/10.1038/ng1195-237.

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Creemers, S. G., P. M. van Koetsveld, F. J. van Kemenade, et al. "Methylation of IGF2 regulatory regions to diagnose adrenocortical carcinomas." Endocrine-Related Cancer 23, no. 9 (2016): 727–37. http://dx.doi.org/10.1530/erc-16-0266.

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Adrenocortical carcinoma (ACC) is a rare malignancy with a poor prognosis. Discrimination of ACCs from adrenocortical adenomas (ACAs) is challenging on both imaging and histopathological grounds. High IGF2 expression is associated with malignancy, but shows large variability. In this study, we investigate whether specific methylation patterns of IGF2 regulatory regions could serve as a valuable biomarker in distinguishing ACCs from ACAs. Pyrosequencing was used to analyse methylation percentages in DMR0, DMR2, imprinting control region (ICR) (consisting of CTCF3 and CTCF6) and the H19 promoter

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Loke, Y. J., J. C. Galati, R. Saffery, and J. M. Craig. "Association of in vitro fertilization with global and IGF2/H19 methylation variation in newborn twins." Journal of Developmental Origins of Health and Disease 6, no. 2 (2015): 115–24. http://dx.doi.org/10.1017/s2040174415000161.

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In vitro fertilization (IVF) and its subset intracytoplasmic sperm injection (ICSI), are widely used medical treatments for conception. There has been controversy over whether IVF is associated with adverse short- and long-term health outcomes of offspring. As with other prenatal factors, epigenetic change is thought to be a molecular mediator of any in utero programming effects. Most studies focused on DNA methylation at gene-specific and genomic level, with only a few on associations between DNA methylation and IVF. Using buccal epithelium from 208 twin pairs from the Peri/Postnatal Epigenet

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Grünert, Sarah C., Uta Matysiak, Franka Hodde, et al. "Isolated Hypomethylation of IGF2 Associated with Severe Hypoglycemia Responsive to Growth Hormone Treatment." Diagnostics 11, no. 5 (2021): 749. http://dx.doi.org/10.3390/diagnostics11050749.

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Hypomethylation of H19 and IGF2 can cause Silver–Russell syndrome (SRS), a clinically and genetically heterogeneous condition characterized by intrauterine growth restriction, poor postnatal growth, relative macrocephaly, craniofacial abnormalities, body asymmetry, hypoglycemia and feeding difficulties. Isolated hypomethylation of IGF2 has been reported in single cases of SRS as well. Here, we report on a 19-month-old patient who presented with two episodes of hypoglycemic seizures. No intrauterine growth restriction was observed, the patient did not present with SRS-typical facial features, a

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Ekstrom, T. J., H. Cui, X. Li, and R. Ohlsson. "Promoter-specific IGF2 imprinting status and its plasticity during human liver development." Development 121, no. 2 (1995): 309–16. http://dx.doi.org/10.1242/dev.121.2.309.

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IGF2 has been shown to be expressed preferentially from the paternally derived allele, although the maternal allele can be found active during both prenatal and postnatal development as well as in neoplastic tumours in humans. We addressed here whether or not the biallelic expression patterns that can be seen during postnatal human liver development reflected a coordinated change in the activities of the four promoters of human IGF2. We show here that the P2, P3 and P4 promoters, but not the P1 promoter, display monoallelic activity in embryonic, neonatal and younger infant liver specimens. Th

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Caspary, Tamara, Michele A. Cleary, Catherine C. Baker, Xiao-Juan Guan, and Shirley M. Tilghman. "Multiple Mechanisms Regulate Imprinting of the Mouse Distal Chromosome 7 Gene Cluster." Molecular and Cellular Biology 18, no. 6 (1998): 3466–74. http://dx.doi.org/10.1128/mcb.18.6.3466.

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ABSTRACT Genomic imprinting is an epigenetic process that results in the preferential silencing of one of the two parental copies of a gene. Although the precise mechanisms by which genomic imprinting occurs are unknown, the tendency of imprinted genes to exist in chromosomal clusters suggests long-range regulation through shared regulatory elements. We characterize a 800-kb region on the distal end of mouse chromosome 7 that contains a cluster of four maternally expressed genes, H19, Mash2, Kvlqt1, andp57Kip2 , as well as two paternally expressed genes, Igf2 and Ins2, and assess the expressio

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Wu, Hao, Xiaorong Pan, Rong Li, Wangcheng Song, and Song Hua. "Excessive rumen-protected choline in the daily diet compromises sperm quality of male dairy goats as a result of aberrant DNA methylation modification." Animal Production Science 61, no. 13 (2021): 1329. http://dx.doi.org/10.1071/an20626.

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Context Choline is added to the diet of ruminants to improve animal growth, development and reproduction; however, little information is available regarding effects of dietary choline supplementation, in the form of rumen-protected choline (RPC), on fertility of male ruminants. Excess RPC in the diet might damage ram fertility through abnormal alteration of methylation patterns at the imprinting control region (ICR) of imprinted genes H19/IGF2. Aims The present study evaluated the influence of different levels of RPC supplementation on the sperm quality of male Saanen dairy goats. Methods Diff

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