Log in

Relevant bibliographies by topics / Gtl2 / Journal articles

To see the other types of publications on this topic, follow the link: Gtl2.

Journal articles on the topic 'Gtl2'

Author: Grafiati

Published: 4 June 2021

Last updated: 15 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Gtl2.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Kawano, J., S. Ide, T. Oinuma, and T. Suganuma. "A protein-specific monoclonal antibody to rat liver beta 1-->4 galactosyltransferase and its application to immunohistochemistry." Journal of Histochemistry & Cytochemistry 42, no. 3 (March 1994): 363–69. http://dx.doi.org/10.1177/42.3.8308253.

Full text

Abstract:

We have produced a new protein-specific monoclonal antibody (MAb) to rat liver beta 1-->4 galactosyltransferase. This MAb, GTL2, was selected as the most reactive IgG to a periodate-treated antigen. Antigen and protein specificities of GTL2 were verified by immunoblotting of a non-glycosylated recombinant protein of human galactosyltransferase and enzymatically deglycosylated rat galactosyltransferase. Using GTL2, an immunohistochemical study was done in rat liver, epididymis, and salivary glands. Intense staining was observed in Golgi areas of epididymal duct epithelial cells, and submandibular and sublingual acinar cells. Hepatocytes showed weaker staining. Immunoelectron microscopic observation revealed that the staining was exclusively localized in trans-Golgi membranes of these cells.

APA, Harvard, Vancouver, ISO, and other styles

2

Qian, Pengxu, Xi He, Ariel Paulson, Jeffrey S. Haug, and Linheng Li. "The Imprinted Dlk1-Gtl2 Locus Epigenetically Regulates Primitive Hematopoietic Stem Cell Mitochondrial Function and Energy Metabolism Via Repression of PI3K/Akt/mTOR Pathway." Blood 124, no. 21 (December 6, 2014): 243. http://dx.doi.org/10.1182/blood.v124.21.243.243.

Full text

Abstract:

Abstract Balanced regulation is essential for the long-term preservation of stem cells while providing for ongoing tissue maintenance. We and others have previously shown that these dichotomous functions are accomplished through the co-existence of at least two stem cell populations—reserve and primed stem cells. This balance has been shown previously to be regulated by protein-coding genes; however, the potential roles of noncoding RNAs (ncRNAs) and their relationships with protein-coding genes in regulating hematopoietic stem cells (HSCs) remain largely unknown. To systematically identify ncRNAs involved in the murine hematopoiesis, we used RNA sequencing and identified unique, differentially expressed (fingerprint) ncRNAs representing reserve HSCs, primed HSCs, and more active stem/progenitor cells. These were also compared with committed progenitors and all major mature hematopoietic lineages. Intriguingly, all of the fingerprint ncRNAs uniquely expressed in reserve HSCs were derived from the imprinted Dlk1-Gtl2 locus, which spans a 780kb region on the mouse chromosome 12qF1 and is precisely controlled by the Intergenic Germ line-derived Differentially Methylated Region (IG-DMR). The Gtl2 locus contains a large cluster of snoRNAs (23 snoRNAs) and the largest cluster of mammalian miRNAs (57 miRNAs) as part of a single transcript of long length ncRNA downstream of Gtl2. To determine the role of Dlk1-Gtl2 locus in hematopoiesis, we utilized the IG-DMR knockout mouse model and carried out phenotypic and functional assays in E15.0 fetal liver HSCs since the embryos loss of maternal IG-DMR are lethal after E16. We observed that deletion of the maternal IG-DMR (ΔmIG-DMR), but not the paternal one, leads to 2-fold reduction in CD93+ fetal liver HSC number and 4-fold decrease of reconstitution ability after tertiary transplantation. Further, we employed RNA-seq using fetal liver HSCs from wt and ΔmIG-DMR and found that several pathways involved in growth control, mitochondrial function and energy metabolism, such as mTOR, PI3K/Akt and Wnt, are significantly enhanced in ΔmIG-DMR HSCs. We also carried out small RNA-seq in both adult HSCs and fetal liver HSCs and identified 13 HSC-specific miRNAs, which are predominantly expressed in reserve HSCs and predicted to target multiple proteins in PI3K/Akt/mTOR pathway. Mechanistically, maternal IG-DMR deletion leads to down-regulation of Gtl2-derived 13 miRNAs and hyperactivation of PI3K/Akt/mTOR pathway, which further enhances mitochondrial activity and biogenesis, increases oxidative phosphorylation (OXPHOS) mediated ATP production and ROS levels, and eventually causes HSC exhaustion. Moreover, either pharmacological inhibition of the mTOR activity by rapamycin or overexpression of Gtl2-derived miRNAs could partially, if not all, rescues the defective HSC phenotype and bioenergetic activities caused by mIG-DMR deletion. Collectively, our work provides a global landscape of murine hematopoietic lncRNAs and demonstrates that Dlk1-Gtl2 locus is critical in maintaining primitive HSCs with a fundamentally epigenetic regulation of mitochondrial function, energy metabolism via repression of PI3K/Akt/mTOR pathway. Disclosures No relevant conflicts of interest to declare.

APA, Harvard, Vancouver, ISO, and other styles

3

Smit, Maria, Karin Segers, Laura Garcia Carrascosa, Tracy Shay, Francesca Baraldi, Gabor Gyapay, Gary Snowder, Michel Georges, Noelle Cockett, and Carole Charlier. "Mosaicism of Solid Gold Supports the Causality of a Noncoding A-to-G Transition in the Determinism of the Callipyge Phenotype." Genetics 163, no. 1 (January 1, 2003): 453–56. http://dx.doi.org/10.1093/genetics/163.1.453.

Full text

Abstract:

Abstract To identify the callipyge mutation, we have resequenced 184 kb spanning the DLK1-, GTL2-, PEG11-, and MEG8-imprinted domain and have identified an A-to-G transition in a highly conserved dodecamer motif between DLK1 and GTL2. This was the only difference found between the callipyge (CLPG) allele and a phylogenetically closely related wild-type allele. We report that this SNP is in perfect association with the callipyge genotype. The demonstration that Solid Gold—the alleged founder ram of the callipyge flock—is mosaic for this SNP virtually proves the causality of this SNP in the determinism of the callipyge phenotype.

APA, Harvard, Vancouver, ISO, and other styles

4

Su, Hong, Dongjie Li, Xiaohui Hou, Beibei Tan, Jiaqi Hu, Cui Zhang, Yunping Dai, Ning Li, and Shijie Li. "Molecular structure of bovine Gtl2 gene and DNA methylation status of Dlk1-Gtl2 imprinted domain in cloned bovines." Animal Reproduction Science 127, no. 1-2 (August 2011): 23–30. http://dx.doi.org/10.1016/j.anireprosci.2011.07.002.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Wu, Qiong, Takuya Kumagai, Manabu Kawahara, Hidehiko Ogawa, Hitoshi Hiura, Yayoi Obata, Riya Takano, and Tomohiro Kono. "Regulated expression of two sets of paternally imprinted genes is necessary for mouse parthenogenetic development to term." Reproduction 131, no. 3 (March 2006): 481–88. http://dx.doi.org/10.1530/rep.1.00933.

Full text

Abstract:

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 investigated the expression levels of paternally imprinted genes in ngH19Δ13/fgwt PE throughout their development. In ngH19Δ13/fgwt Pes that died soon after recovery, the expression of Igf2 and H19 was restored to the appropriate levels except for low Igf2 expression in the liver after E15.5. Further, the paternally expressed Dlk1 and Dio3 were repressed, while the expression levels of the maternal Gtl2 and Mirg were twice those of the controls. However, the above-mentioned four genes showed almost normal expression in the surviving ngH19Δ13/fgwt PEs. The methylation analysis revealed that the intragenic DMR of the Dlk1-Gtl2 domain was hypermethylated in the ngH19Δ13/fgwt PEs that survived, but not in the PEs that died soon after recovery. The present study suggests that two sets of co-ordinately regulated but oppositely expressed genes, Igf2-H19 and Dlk1-Gtl2, act as a critical barrier to parthenogenetic development in order to render a paternal contribution obligatory for descendants in mammals.

APA, Harvard, Vancouver, ISO, and other styles

6

Dindot, S. V., P. Farin, C. Farin, J. Alexander, E. Crosier, S. Walker, C. Long, and J. A. Piedrahita. "35ANALYSIS OF EPIGENETIC MODIFICATIONS AND GENOMIC IMPRINTING IN NUCLEAR TRANSFER DERIVED BOS GAURUS×B. TAURUS CONCEPTI." Reproduction, Fertility and Development 16, no. 2 (2004): 140. http://dx.doi.org/10.1071/rdv16n1ab35.

Full text

Abstract:

Somatic cell nuclear transfer in cattle is an inefficient process hindered by low pregnancy rates and fetal placental abnormalities. Improper or incomplete epigenetic reprogramming of the donor genome has been implicated as a cause for these aberrations and has been investigated extensively in mice. Here we report the use of a bovine interspecies model (Bos gaurus×B. taurus) for the assessment and characterization of epigenetic modifications and genomic imprinting in 40-day-old female nuclear transfer (NT)-derived fetuses and placentas. Previously, we identified genomic imprinting at the IGF2, GTL2 and XIST loci in the Bos gaurus×B. taurus fetuses. These results indicated maternal and paternal imprinting of the IGF2 and GTL2 loci, respectively, in the chorion, allantois, liver, lung and brain, whereas the XIST locus was maternally imprinted solely in the chorion of females. We extended this analysis to 40-day-old NT fetuses derived from a hybrid lung fibroblast cell line (female). Analysis of the donor cell line indicated conservation of imprinting of the IGF2 and GTL2 loci and bialleic expression of the XIST locus, presumably from the random patterns of X-chromosome inactivation. Analysis of three NT and three control pregnancies indicated disruption of genomic imprinting at the XIST locus in the chorions of all three clones compared to controls. In contrast, proper allelic expression of the IGF2 and GTL2 loci was observed in all fetuses and placentas. Quantification of maternal and paternal XIST transcripts in the chorion of clones and controls demonstrated a significant skewing from preferential paternal expression in controls (95.0±0.882, mean±S.E.) to mixed paternal and maternal expression in clones (73.6±5.2), (t-test; P<0.05). In an attempt to determine the cause for the abnormal allelic expression of the XIST locus in the chorion of the clones, methylation analysis of the XIST Differentially Methylated Region (DMR) was performed. Methylation-sensitive restriction digests and subsequent PCR of the XIST DMR indicated patterns were not different between controls and clones. However, when genome-wide and promoter-specific methylation analysis (bisulfite sequencing) was extended to the satellite I repeat element and epidermal cytokeratin promoter, hypermethylation was observed in the chorion of clones. These results demonstrate disruption of genomic imprinting in XIST locus in the placenta of 40-day-old clones independent of DMR methylation. They also indicate that cloning is associated with increased levels of methylation in selected genomic regions in the chorion.

APA, Harvard, Vancouver, ISO, and other styles

7

JIANG, Cao-de, and Zong-lin YANG. "Characterization, Imprinting Status and Tissue Distribution of Porcine GTL2 Gene." Agricultural Sciences in China 8, no. 2 (February 2009): 216–22. http://dx.doi.org/10.1016/s1671-2927(09)60029-8.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Royo, Hélène, Eugenia Basyuk, Virginie Marty, Maud Marques, Edouard Bertrand, and Jérôme Cavaillé. "Bsr, a Nuclear-retained RNA with Monoallelic Expression." Molecular Biology of the Cell 18, no. 8 (August 2007): 2817–27. http://dx.doi.org/10.1091/mbc.e06-10-0920.

Full text

Abstract:

The imprinted Dlk1-Gtl2 and Prader-Willi syndrome (PWS) regions are characterized by a complex noncoding transcription unit spanning arrays of tandemly repeated C/D RNA genes. These noncoding RNAs (ncRNAs) are thought to play an essential but still poorly understood role. To better understand the intracellular fate of these large ncRNAs, fluorescence in situ hybridization was carried out at the rat Dlk1-Gtl2 domain. This locus contains a ∼100-kb-long gene cluster comprising 86 homologous RBII-36 C/D RNA gene copies, all of them intron-encoded within the ncRNA gene Bsr. Here, we demonstrate that the Bsr gene is monoallelically expressed in primary rat embryonic fibroblasts as well as in hypothalamic neurons and yields a large amount of unspliced and spliced RNAs at the transcription site, mostly as elongated RNA signals. Surprisingly, spliced Bsr RNAs released from the transcription site mainly concentrate as numerous, stable nuclear foci that do not colocalize with any known subnuclear structures. On drug treatments, a fraction of Bsr RNA relocalizes to the cytoplasm and associates with stress granules (SGs), but not with P-bodies, pointing to a potential link between SGs and the metabolism of ncRNA. Thus, Bsr might represent a novel type of nuclear-retained transcript.

APA, Harvard, Vancouver, ISO, and other styles

9

Hitachi, Keisuke, Masashi Nakatani, Shiori Funasaki, Ikumi Hijikata, Mizuki Maekawa, Masahiko Honda, and Kunihiro Tsuchida. "Expression Levels of Long Non-Coding RNAs Change in Models of Altered Muscle Activity and Muscle Mass." International Journal of Molecular Sciences 21, no. 5 (February 27, 2020): 1628. http://dx.doi.org/10.3390/ijms21051628.

Full text

Abstract:

Skeletal muscle is a highly plastic organ that is necessary for homeostasis and health of the human body. The size of skeletal muscle changes in response to intrinsic and extrinsic stimuli. Although protein-coding RNAs including myostatin, NF-κβ, and insulin-like growth factor-1 (IGF-1), have pivotal roles in determining the skeletal muscle mass, the role of long non-coding RNAs (lncRNAs) in the regulation of skeletal muscle mass remains to be elucidated. Here, we performed expression profiling of nine skeletal muscle differentiation-related lncRNAs (DRR, DUM1, linc-MD1, linc-YY1, LncMyod, Neat1, Myoparr, Malat1, and SRA) and three genomic imprinting-related lncRNAs (Gtl2, H19, and IG-DMR) in mouse skeletal muscle. The expression levels of these lncRNAs were examined by quantitative RT-PCR in six skeletal muscle atrophy models (denervation, casting, tail suspension, dexamethasone-administration, cancer cachexia, and fasting) and two skeletal muscle hypertrophy models (mechanical overload and deficiency of the myostatin gene). Cluster analyses of these lncRNA expression levels were successfully used to categorize the muscle atrophy models into two sub-groups. In addition, the expression of Gtl2, IG-DMR, and DUM1 was altered along with changes in the skeletal muscle size. The overview of the expression levels of lncRNAs in multiple muscle atrophy and hypertrophy models provides a novel insight into the role of lncRNAs in determining the skeletal muscle mass.

APA, Harvard, Vancouver, ISO, and other styles

10

Jiang, Ying, Yi-Chen Yu, Guo-Lian Ding, Qian Gao, Feng Chen, and Qiong Luo. "Intrauterine hyperglycemia induces intergenerational Dlk1-Gtl2 methylation changes in mouse placenta." Oncotarget 9, no. 32 (January 5, 2018): 22398–405. http://dx.doi.org/10.18632/oncotarget.23976.

Full text

APA, Harvard, Vancouver, ISO, and other styles

11

Begemann, Matthias, Sabrina Spengler, Ulrike Kordaß, Carmen Schröder, and Thomas Eggermann. "Segmental maternal uniparental disomy 7q associated with DLK1/GTL2 (14q32) hypomethylation." American Journal of Medical Genetics Part A 158A, no. 2 (January 13, 2012): 423–28. http://dx.doi.org/10.1002/ajmg.a.34412.

Full text

APA, Harvard, Vancouver, ISO, and other styles

12

Stouder, Christelle, and Ariane Paoloni-Giacobino. "Transgenerational effects of the endocrine disruptor vinclozolin on the methylation pattern of imprinted genes in the mouse sperm." REPRODUCTION 139, no. 2 (February 2010): 373–79. http://dx.doi.org/10.1530/rep-09-0340.

Full text

Abstract:

Endocrine-disrupting chemicals (EDCs), among which is the antiandrogen vinclozolin (VCZ), have been reported to affect the male reproductive system. In this study, VCZ was administered to pregnant mice at the time of embryo sex determination, and its possible effects on the differentially methylated domains (DMDs) of two paternally (H19 and Gtl2) and three maternally (Peg1, Snrpn, and Peg3) imprinted genes were tested in the male offspring. The CpGs methylation status within the five gene DMDs was analyzed in the sperm, tail, liver, and skeletal muscle DNAs by pyrosequencing. In the sperm of controls, the percentages of methylated CpGs were close to the theoretical values of 100 and 0% in paternally or maternally imprinted genes respectively. VCZ decreased the percentages of methylated CpGs of H19 and Gtl2 (respective values 83.1 and 91.5%) and increased those of Peg1, Snrpn, and Peg3 (respective values 11.3, 18.3, and 11.2%). The effects of VCZ were transgenerational, but they disappeared gradually from F1 to F3. The mean sperm concentration of the VCZ-administered female offspring was only 56% of that of the controls in the F1 offspring, and it was back to normal values in the F2 and F3 offspring. In the somatic cells of controls, the percentages of methylated CpGs were close to the theoretical value of 50% and, surprisingly, VCZ altered the methylation of Peg3. We propose that the deleterious effects of VCZ on the male reproductive system are mediated by imprinting defects in the sperm. The reported effects of EDCs on human male spermatogenesis might be mediated by analogous imprinting alterations.

APA, Harvard, Vancouver, ISO, and other styles

13

Miyoshi, Norikatsu, Jente M. Stel, Keiko Shioda, Na Qu, Junko Odajima, Shino Mitsunaga, Xiangfan Zhang, et al. "Erasure of DNA methylation, genomic imprints, and epimutations in a primordial germ-cell model derived from mouse pluripotent stem cells." Proceedings of the National Academy of Sciences 113, no. 34 (August 2, 2016): 9545–50. http://dx.doi.org/10.1073/pnas.1610259113.

Full text

Abstract:

The genome-wide depletion of 5-methylcytosines (5meCs) caused by passive dilution through DNA synthesis without daughter strand methylation and active enzymatic processes resulting in replacement of 5meCs with unmethylated cytosines is a hallmark of primordial germ cells (PGCs). Although recent studies have shown that in vitro differentiation of pluripotent stem cells (PSCs) to PGC-like cells (PGCLCs) mimics the in vivo differentiation of epiblast cells to PGCs, how DNA methylation status of PGCLCs resembles the dynamics of 5meC erasure in embryonic PGCs remains controversial. Here, by differential detection of genome-wide 5meC and 5-hydroxymethylcytosine (5hmeC) distributions by deep sequencing, we show that PGCLCs derived from mouse PSCs recapitulated the process of genome-wide DNA demethylation in embryonic PGCs, including significant demethylation of imprint control regions (ICRs) associated with increased mRNA expression of the corresponding imprinted genes. Although 5hmeCs were also significantly diminished in PGCLCs, they retained greater amounts of 5hmeCs than intragonadal PGCs. The genomes of both PGCLCs and PGCs selectively retained both 5meCs and 5hmeCs at a small number of repeat sequences such as GSAT_MM, of which the significant retention of bisulfite-resistant cytosines was corroborated by reanalysis of previously published whole-genome bisulfite sequencing data for intragonadal PGCs. PSCs harboring abnormal hypermethylation at ICRs of the Dlk1-Gtl2-Dio3 imprinting cluster diminished these 5meCs upon differentiation to PGCLCs, resulting in transcriptional reactivation of the Gtl2 gene. These observations support the usefulness of PGCLCs in studying the germline epigenetic erasure including imprinted genes, epimutations, and erasure-resistant loci, which may be involved in transgenerational epigenetic inheritance.

APA, Harvard, Vancouver, ISO, and other styles

14

Schneider, Gabriela, Zachariah Payne Sellers, and Mariusz Z. Ratajczak. "Parentally imprinted genes regulate hematopoiesis—new evidence from the Dlk1–Gtl2 locus." Stem Cell Investigation 3 (July 22, 2016): 29. http://dx.doi.org/10.21037/sci.2016.06.09.

Full text

APA, Harvard, Vancouver, ISO, and other styles

15

Carr, Michael S., Aleksey Yevtodiyenko, Claudia L. Schmidt, and Jennifer V. Schmidt. "Allele-specific histone modifications regulate expression of the Dlk1–Gtl2 imprinted domain." Genomics 89, no. 2 (February 2007): 280–90. http://dx.doi.org/10.1016/j.ygeno.2006.10.005.

Full text

APA, Harvard, Vancouver, ISO, and other styles

16

Seitz, H. "A Large Imprinted microRNA Gene Cluster at the Mouse Dlk1-Gtl2 Domain." Genome Research 14, no. 9 (September 1, 2004): 1741–48. http://dx.doi.org/10.1101/gr.2743304.

Full text

APA, Harvard, Vancouver, ISO, and other styles

17

Nowak, Kamila, Geneva Stein, Lu Mei He, Elizabeth Powell, and Tamara Davis. "ANALYSIS OF PATERNAL ALLELE-SPECIFIC METHYLATION AT MOUSE Gtl2 DURING EARLY EMBRYOGENESIS." Biology of Reproduction 77, Suppl_1 (July 1, 2007): 165. http://dx.doi.org/10.1093/biolreprod/77.s1.165.

Full text

APA, Harvard, Vancouver, ISO, and other styles

18

Geuns, Elke, Nele De Temmerman, Pierre Hilven, André Van Steirteghem, Inge Liebaers, and Martine De Rycke. "Methylation analysis of the intergenic differentially methylated region of DLK1-GTL2 in human." European Journal of Human Genetics 15, no. 3 (January 10, 2007): 352–61. http://dx.doi.org/10.1038/sj.ejhg.5201759.

Full text

APA, Harvard, Vancouver, ISO, and other styles

19

Takeda, H., F. Caiment, M. Smit, S. Hiard, X. Tordoir, N. Cockett, M. Georges, and C. Charlier. "The callipyge mutation enhances bidirectional long-range DLK1-GTL2 intergenic transcription in cis." Proceedings of the National Academy of Sciences 103, no. 21 (May 11, 2006): 8119–24. http://dx.doi.org/10.1073/pnas.0602844103.

Full text

APA, Harvard, Vancouver, ISO, and other styles

20

SCHNEIDER, GABRIELA, MARK J. BOWSER, DONG-MYUNG SHIN, FREDERIC G. BARR, and MARIUSZ Z. RATAJCZAK. "The paternally imprinted DLK1-GTL2 locus is differentially methylated in embryonal and alveolar rhabdomyosarcomas." International Journal of Oncology 44, no. 1 (October 29, 2013): 295–300. http://dx.doi.org/10.3892/ijo.2013.2153.

Full text

APA, Harvard, Vancouver, ISO, and other styles

21

Sato, Shun, Wataru Yoshida, Hidenobu Soejima, Kazuhiko Nakabayashi, and Kenichiro Hata. "Methylation dynamics of IG-DMR and Gtl2-DMR during murine embryonic and placental development." Genomics 98, no. 2 (August 2011): 120–27. http://dx.doi.org/10.1016/j.ygeno.2011.05.003.

Full text

APA, Harvard, Vancouver, ISO, and other styles

22

Bidwell, C. A., T. L. Shay, M. Georges, J. E. Beever, S. Berghmans, and N. E. Cockett. "Differential expression of the GTL2 gene within the callipyge region of ovine chromosome 18." Animal Genetics 32, no. 5 (October 2001): 248–56. http://dx.doi.org/10.1046/j.1365-2052.2001.00776.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

23

Dindot, Scott V., Kathleen C. Kent, Bret Evers, Naida Loskutoff, James Womack, and Jorge A. Piedrahita. "Conservation of genomic imprinting at the XIST, IGF2, and GTL2 loci in the bovine." Mammalian Genome 15, no. 12 (December 2004): 966–74. http://dx.doi.org/10.1007/s00335-004-2407-z.

Full text

APA, Harvard, Vancouver, ISO, and other styles

24

Yevtodiyenko, Aleksey, Michael S. Carr, Nafisa Patel, and Jennifer V. Schmidt. "Analysis of candidate imprinted genes linked to Dlk1-Gtl2 using a congenic mouse line." Mammalian Genome 13, no. 11 (November 1, 2002): 633–38. http://dx.doi.org/10.1007/s00335-002-2208-1.

Full text

APA, Harvard, Vancouver, ISO, and other styles

25

Croteau, Sylvie, Marie-Claude Charron, Keith E. Latham, and Anna K. Naumova. "Alternative splicing and imprinting control of the Meg3/Gtl2-Dlk1 locus in mouse embryos." Mammalian Genome 14, no. 4 (April 1, 2003): 231–41. http://dx.doi.org/10.1007/s00335-002-2244-x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

26

Kumamoto, Soichiro, Nozomi Takahashi, Kayo Nomura, Makoto Fujiwara, Megumi Kijioka, Yoshinobu Uno, Yoichi Matsuda, Yusuke Sotomaru, and Tomohiro Kono. "Overexpression of microRNAs from the Gtl2-Rian locus contributes to postnatal death in mice." Human Molecular Genetics 26, no. 19 (June 15, 2017): 3653–62. http://dx.doi.org/10.1093/hmg/ddx223.

Full text

APA, Harvard, Vancouver, ISO, and other styles

27

Sekita, Y., H. Wagatsuma, M. Irie, S. Kobayashi, T. Kohda, J. Matsuda, M. Yokoyama, et al. "Aberrant regulation of imprinted gene expression in Gtl2^lacZ mice." Cytogenetic and Genome Research 113, no. 1-4 (2006): 223–29. http://dx.doi.org/10.1159/000090836.

Full text

APA, Harvard, Vancouver, ISO, and other styles

28

Schuster-Gossler, K., D. Simon-Chazottes, J. L. Guénet, J. Zachgo, and A. Gossler. "Gtl2 lacZ , an insertional mutation on mouse Chromosome 12 with parental origin-dependent phenotype." Mammalian Genome 7, no. 1 (January 1996): 20–24. http://dx.doi.org/10.1007/s003359900006.

Full text

APA, Harvard, Vancouver, ISO, and other styles

29

Jiang, Y., Q. Luo, Q. Gao, G. Ding, J. Sheng, and H. Huang. "Intrauterine high-glucose environment influences placental development through imprinting regulation of Dlk1/Gtl2 region." Fertility and Sterility 100, no. 3 (September 2013): S48. http://dx.doi.org/10.1016/j.fertnstert.2013.07.1826.

Full text

APA, Harvard, Vancouver, ISO, and other styles

30

Tierling, Sascha, Simone Dalbert, Sandra Schoppenhorst, Chen-En Tsai, Sven Oliger, Anne C. Ferguson-Smith, Martina Paulsen, and Jörn Walter. "High-resolution map and imprinting analysis of the Gtl2–Dnchc1 domain on mouse chromosome 12." Genomics 87, no. 2 (February 2006): 225–35. http://dx.doi.org/10.1016/j.ygeno.2005.09.018.

Full text

APA, Harvard, Vancouver, ISO, and other styles

31

Kircher, Martin, Christoph Bock, and Martina Paulsen. "Structural conservation versus functional divergence of maternally expressed microRNAs in the Dlk1/Gtl2 imprinting region." BMC Genomics 9, no. 1 (2008): 346. http://dx.doi.org/10.1186/1471-2164-9-346.

Full text

APA, Harvard, Vancouver, ISO, and other styles

32

Takahashi, Nozomi, Akira Okamoto, Motomu Shirai, Ryota Kobayashi, and Tomohiro Kono. "Deletion of the Maternally Expressed Imprinted Gene, Gtl2, Resulted in Parental-specific Lethality in Mice." Biology of Reproduction 78, Suppl_1 (May 1, 2008): 305–6. http://dx.doi.org/10.1093/biolreprod/78.s1.305c.

Full text

APA, Harvard, Vancouver, ISO, and other styles

33

Zhou, Y., P. Cheunsuchon, Y. Nakayama, M. W. Lawlor, Y. Zhong, K. A. Rice, L. Zhang, et al. "Activation of paternally expressed genes and perinatal death caused by deletion of the Gtl2 gene." Development 137, no. 16 (July 7, 2010): 2643–52. http://dx.doi.org/10.1242/dev.045724.

Full text

APA, Harvard, Vancouver, ISO, and other styles

34

Luo, Jian, Yiyuan Zhang, Yanhua Guo, Hong Tang, Haixia Wei, Shouren Liu, Xinhua Wang, Limin Wang, and Ping Zhou. "TRIM28 regulates Igf2-H19 and Dlk1-Gtl2 imprinting by distinct mechanisms during sheep fibroblast proliferation." Gene 637 (December 2017): 152–60. http://dx.doi.org/10.1016/j.gene.2017.09.048.

Full text

APA, Harvard, Vancouver, ISO, and other styles

35

Takada, S., M. Tevendale, J. Baker, P. Georgiades, E. Campbell, T. Freeman, M. H. Johnson, M. Paulsen, and A. C. Ferguson-Smith. "Delta-like and Gtl2 are reciprocally expressed, differentially methylated linked imprinted genes on mouse chromosome 12." Current Biology 10, no. 18 (September 2000): 1135–38. http://dx.doi.org/10.1016/s0960-9822(00)00704-1.

Full text

APA, Harvard, Vancouver, ISO, and other styles

36

Yevtodiyenko, Aleksey, Ekaterina Y. Steshina, Scott C. Farner, John M. Levorse, and Jennifer V. Schmidt. "A 178-kb BAC transgene imprints the mouse Gtl2 gene and localizes tissue-specific regulatory elements." Genomics 84, no. 2 (August 2004): 277–87. http://dx.doi.org/10.1016/j.ygeno.2004.04.005.

Full text

APA, Harvard, Vancouver, ISO, and other styles

37

McLaughlin, D., M. Vidaki, E. Renieri, and D. Karagogeos. "Expression pattern of the maternally imprinted gene Gtl2 in the forebrain during embryonic development and adulthood." Gene Expression Patterns 6, no. 4 (April 2006): 394–99. http://dx.doi.org/10.1016/j.modgep.2005.09.007.

Full text

APA, Harvard, Vancouver, ISO, and other styles

38

Davis, Tamara L., Alyssa Gagne, Mahvish Qureshi, Kayla McDaniel, and Jeanette Bates. "Comparative Analysis of DNA Methylation Acquisition at the Imprinted Gtl2/Dlk1 Locus During Mouse Embryonic Development." Biology of Reproduction 87, Suppl_1 (August 1, 2012): 279. http://dx.doi.org/10.1093/biolreprod/87.s1.279.

Full text

APA, Harvard, Vancouver, ISO, and other styles

39

Seibt, Julie, Olivier Armant, Anne Le Digarcher, Diogo Castro, Vidya Ramesh, Laurent Journot, François Guillemot, Pierre Vanderhaeghen, and Tristan Bouschet. "Expression at the Imprinted Dlk1-Gtl2 Locus Is Regulated by Proneural Genes in the Developing Telencephalon." PLoS ONE 7, no. 11 (November 6, 2012): e48675. http://dx.doi.org/10.1371/journal.pone.0048675.

Full text

APA, Harvard, Vancouver, ISO, and other styles

40

Snyder, C. M., A. L. Rice, N. L. Estrella, A. Held, S. C. Kandarian, and F. J. Naya. "MEF2A regulates the Gtl2-Dio3 microRNA mega-cluster to modulate WNT signaling in skeletal muscle regeneration." Development 140, no. 1 (November 15, 2012): 31–42. http://dx.doi.org/10.1242/dev.081851.

Full text

APA, Harvard, Vancouver, ISO, and other styles

41

Song, Yang, and Lei Yang. "Transgenerational impaired spermatogenesis with sperm H19 and Gtl2 hypomethylation induced by the endocrine disruptor p,p’-DDE." Toxicology Letters 297 (November 2018): 34–41. http://dx.doi.org/10.1016/j.toxlet.2018.08.015.

Full text

APA, Harvard, Vancouver, ISO, and other styles

42

Shioda, Toshi, Noel Rosenthal, Haley Ellis, and Keiko Shioda. "Selective Repair of Epigenetic Aberrations at the Gtl2/Meg3 Imprinted Locus in Mouse Induced Primordial Germ Cells." Biology of Reproduction 85, Suppl_1 (July 1, 2011): 120. http://dx.doi.org/10.1093/biolreprod/85.s1.120.

Full text

APA, Harvard, Vancouver, ISO, and other styles

43

Manji, Shehnaaz S. M., Brita S. Sørensen, Tuomas Klockars, Timothy Lam, Wendy Hutchison, and Hans-Henrik M. Dahl. "Molecular characterization and expression of maternally expressed gene 3 (Meg3/Gtl2) RNA in the mouse inner ear." Journal of Neuroscience Research 83, no. 2 (February 1, 2006): 181–90. http://dx.doi.org/10.1002/jnr.20721.

Full text

APA, Harvard, Vancouver, ISO, and other styles

44

Prasasya, Rexxi, Kristen V. Grotheer, Linda D. Siracusa, and Marisa S. Bartolomei. "Temple syndrome and Kagami-Ogata syndrome: clinical presentations, genotypes, models and mechanisms." Human Molecular Genetics 29, R1 (June 27, 2020): R107—R116. http://dx.doi.org/10.1093/hmg/ddaa133.

Full text

Abstract:

Abstract Temple syndrome (TS) and Kagami-Ogata syndrome (KOS) are imprinting disorders caused by absence or overexpression of genes within a single imprinted cluster on human chromosome 14q32. TS most frequently arises from maternal UPD14 or epimutations/deletions on the paternal chromosome, whereas KOS most frequently arises from paternal UPD14 or epimutations/deletions on the maternal chromosome. In this review, we describe the clinical symptoms and genetic/epigenetic features of this imprinted region. The locus encompasses paternally expressed protein-coding genes (DLK1, RTL1 and DIO3) and maternally expressed lncRNAs (MEG3/GTL2, RTL1as and MEG8), as well as numerous miRNAs and snoRNAs. Control of expression is complex, with three differentially methylated regions regulating germline, placental and tissue-specific transcription. The strong conserved synteny between mouse chromosome 12aF1 and human chromosome 14q32 has enabled the use of mouse models to elucidate imprinting mechanisms and decipher the contribution of genes to the symptoms of TS and KOS. In this review, we describe relevant mouse models and highlight their value to better inform treatment options for long-term management of TS and KOS patients.

APA, Harvard, Vancouver, ISO, and other styles

45

Qian, Pengxu, Xi C. He, Ariel Paulson, Zhenrui Li, Fang Tao, John M. Perry, Fengli Guo, et al. "The Dlk1-Gtl2 Locus Preserves LT-HSC Function by Inhibiting the PI3K-mTOR Pathway to Restrict Mitochondrial Metabolism." Cell Stem Cell 18, no. 2 (February 2016): 214–28. http://dx.doi.org/10.1016/j.stem.2015.11.001.

Full text

APA, Harvard, Vancouver, ISO, and other styles

46

da Rocha, Simão T., Maxine Tevendale, Edward Knowles, Shuji Takada, Marie Watkins, and Anne C. Ferguson-Smith. "Restricted co-expression of Dlk1 and the reciprocally imprinted non-coding RNA, Gtl2: Implications for cis-acting control." Developmental Biology 306, no. 2 (June 2007): 810–23. http://dx.doi.org/10.1016/j.ydbio.2007.02.043.

Full text

APA, Harvard, Vancouver, ISO, and other styles

47

Astuti, D., F. Latif, K. Wagner, D. Gentle, W. N. Cooper, D. Catchpoole, R. Grundy, A. C. Ferguson-Smith, and E. R. Maher. "Epigenetic alteration at the DLK1-GTL2 imprinted domain in human neoplasia: analysis of neuroblastoma, phaeochromocytoma and Wilms' tumour." British Journal of Cancer 92, no. 8 (March 29, 2005): 1574–80. http://dx.doi.org/10.1038/sj.bjc.6602478.

Full text

APA, Harvard, Vancouver, ISO, and other styles

48

TAKAHASHI, Nozomi, Eito YAMAGUCHI, Yukiko KAWABATA, and Tomohiro KONO. "Deleting maternal Gtl2 leads to growth enhancement and decreased expression of stem cell markers in teratoma." Journal of Reproduction and Development 61, no. 1 (2015): 7–12. http://dx.doi.org/10.1262/jrd.2014-089.

Full text

APA, Harvard, Vancouver, ISO, and other styles

49

Berghmans, Stéphane, Karin Segers, Tracy Shay, Michel Georges, Noelle Cockett, and Carole Charlier. "Breakpoint mapping positions the callipyge gene within a 450-kilobase chromosome segment containing the DLK1 and GTL2 genes." Mammalian Genome 12, no. 2 (February 1, 2001): 183–85. http://dx.doi.org/10.1007/s003350010246.

Full text

APA, Harvard, Vancouver, ISO, and other styles

50

Li, Zhikun, Libin Wang, Yukai Wang, Lei Liu, Liu Wang, Wei Li, and Qi Zhou. "Generation of an LncRNA Gtl2-GFP Reporter for Rapid Assessment of Pluripotency in Mouse Induced Pluripotent Stem Cells." Journal of Genetics and Genomics 42, no. 3 (March 2015): 125–28. http://dx.doi.org/10.1016/j.jgg.2015.02.004.

Full text

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!