Gotowa bibliografia na temat „19p13.3”
Utwórz poprawne odniesienie w stylach APA, MLA, Chicago, Harvard i wielu innych
Spis treści
Zobacz listy aktualnych artykułów, książek, rozpraw, streszczeń i innych źródeł naukowych na temat „19p13.3”.
Przycisk „Dodaj do bibliografii” jest dostępny obok każdej pracy w bibliografii. Użyj go – a my automatycznie utworzymy odniesienie bibliograficzne do wybranej pracy w stylu cytowania, którego potrzebujesz: APA, MLA, Harvard, Chicago, Vancouver itp.
Możesz również pobrać pełny tekst publikacji naukowej w formacie „.pdf” i przeczytać adnotację do pracy online, jeśli odpowiednie parametry są dostępne w metadanych.
Artykuły w czasopismach na temat "19p13.3"
Swan, L., i D. Coman. "Ocular Manifestations of a Novel Proximal 19p13.3 Microdeletion". Case Reports in Genetics 2018 (2018): 1–5. http://dx.doi.org/10.1155/2018/2492437.
Pełny tekst źródłaIshikawa, Aki, Keisuke Enomoto, Makiko Tominaga, Toshiyuki Saito, Jun-ichi Nagai, Noritaka Furuya, Kentaro Ueno, Hideaki Ueda, Mitsuo Masuno i Kenji Kurosawa. "Pure duplication of 19p13.3". American Journal of Medical Genetics Part A 161, nr 9 (29.07.2013): 2300–2304. http://dx.doi.org/10.1002/ajmg.a.36041.
Pełny tekst źródłaSgardioli, Ilária C., Elaine Lustosa-Mendes, Ana P. dos Santos, Társis P. Vieira i Vera L. Gil-da-Silva-Lopes. "A Rare Case of Concomitant Deletions in 15q11.2 and 19p13.3". Cytogenetic and Genome Research 156, nr 2 (2018): 80–86. http://dx.doi.org/10.1159/000493283.
Pełny tekst źródłaRisheg, Hiba, Romela Pasion, Stephanie Sacharow, Virginia Proud, LaDonna Immken, Stuart Schwartz, Jim H. Tepperberg i in. "Clinical Comparison of Overlapping Deletions of 19p13.3". American Journal of Medical Genetics Part A 161, nr 5 (22.04.2013): 1110–16. http://dx.doi.org/10.1002/ajmg.a.35923.
Pełny tekst źródłaSingh, Vertika, Renu Bala, Arijit Chakraborty, Singh Rajender, Sameer Trivedi i Kiran Singh. "Duplications in 19p13.3 are associated with male infertility". Journal of Assisted Reproduction and Genetics 36, nr 10 (16.08.2019): 2171–79. http://dx.doi.org/10.1007/s10815-019-01547-1.
Pełny tekst źródłaAso, Teijiro, Peter Tsai, Tatsuo Kawaguchi, Joan C. Menninger, Shigetaka Kitajima, Yukio Yasukochi, David C. Ward i Sherman M. Weissman. "Assignment of the Human GTF2F1 Gene to Chromosome 19p13.3". Genomics 16, nr 1 (kwiecień 1993): 252–53. http://dx.doi.org/10.1006/geno.1993.1168.
Pełny tekst źródłaAl-Othman, Abdallah Ahmad, Mir Sadat-Ali, Ahmed Sh Amer i Dakheel A. Al-Dakheel. "Genetic Markers for Adolescent Idiopathic Scoliosis on Chromosome 19p13.3 among Saudi Arabian Girls". Asian Spine Journal 11, nr 2 (30.04.2017): 167–73. http://dx.doi.org/10.4184/asj.2017.11.2.167.
Pełny tekst źródłaLiaquat, S., R. Riley, G. Massey i W. T. Gunning. "Unique case of 19p13 syndrome with storage pool disease". American Journal of Clinical Pathology 156, Supplement_1 (1.10.2021): S104. http://dx.doi.org/10.1093/ajcp/aqab191.221.
Pełny tekst źródłaDi Blasi, Claudia, Behzad Moghadaszadeh, Claudia Ciano, Tiziana Negri, Alessio Giavazzi, Ferdinando Cornelio, Lucia Morandi i Marina Mora. "Abnormal lysosomal and ubiquitin-proteasome pathways in 19p13.3 distal myopathy". Annals of Neurology 56, nr 1 (2004): 133–38. http://dx.doi.org/10.1002/ana.20158.
Pełny tekst źródłaCapela de Matos, Roberto R., Daniela R. Ney Garcia, Moneeb A. K. Othman, Gerson Moura Ferreira, Joana B. Melo, Isabel M. Carreira, Claus Meyer i in. "A New Complex Karyotype Involving a KMT2A-r Variant Three-Way Translocation in a Rare Clinical Presentation of a Pediatric Patient with Acute Myeloid Leukemia". Cytogenetic and Genome Research 157, nr 4 (2019): 213–19. http://dx.doi.org/10.1159/000499640.
Pełny tekst źródłaRozprawy doktorskie na temat "19p13.3"
Curtain, Robert, i n/a. "Candidate Gene Analysis of Migraine Susceptibility Regions on Chromosome 1q and 19p". Griffith University. School of Medical Science, 2006. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20070810.132610.
Pełny tekst źródłaCurtain, Robert. "Candidate Gene Analysis of Migraine Susceptibility Regions on Chromosome 1q and 19p". Thesis, Griffith University, 2006. http://hdl.handle.net/10072/365960.
Pełny tekst źródłaThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Full Text
Mogk, Rhonda L. "Molecular analysis of a rare folate-sensitive fragile site located at 19p13.1, FRA19B". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ45099.pdf.
Pełny tekst źródłaSu, YenJui, i 蘇彥睿. "High Frequency of Loss of Heterozygosity on Chromosome 19p13.2-13.3 Suggests Multiple Putative Tumor Suppressor Genes of Breast Cancer". Thesis, 2002. http://ndltd.ncl.edu.tw/handle/02277612628959845503.
Pełny tekst źródła國立臺灣大學
流行病學研究所
90
Cancer is believed to arise from a series of genetic alterations, including activation of proto-oncogenes and/or inactivation of tumor suppressor genes. The two-hit hypothesis proposed by Knudson, indicating that two mutational events are necessary to inactivate both alleles of a tumor suppressor gene, and, more importantly, the same tumor suppressor genes are responsible for both inherited and sporadic forms of the same cancer. Because one of the two hits is commonly involved genetic loss of the locus harboring tumor suppressor gene, the identification of a high frequency of genomic deletion detected by allelic loss or loss of heterozygosity(LOH) in specific genomic regions is widely used to provide critical evidence about the location and importance of putative tumor suppressor genes. Germ-line mutations in the STK11/LKB1 gene on chromosome 19p13 are found to be the causes of the Peutz-Jeghers syndrome(PJS), in which intestinal hamartomas are associated with elevated risks of several cancer types, including breast cancer. However, subsequent studies failed to identify STK11/LKB1 mutation, which is seemingly inconsistent to the importance of this gene in breast cancer defined in PJS patients and high LOH frequency found in 19p13 in breast cancer. One common explanation for this inconsistent result suggests other breast cancer-associated genes may be located at the loci adjacent to STK11/LKB1, and are responsible for the high frequency of LOH observed at 19p. In order to know whether other genes are at the neighboring loci of STK11/LKB1, and to define the importance of STK11/LKB1, the present study performed high-resolution allelotyping for loss of heterozygosity (LOH) on 19p13.3-13.2, based on laser-capture-microdissected tumor tissues from 140 breast cancers patients. A total of 24 microsatellite markers at these loci were employed to define the contribution of 19p13.3-13.2 in breast cancer development. The results show that:(1)Five commonly deleted regions(CDRs) are identified on chromosome 19p13.3-13.2, including D19S814-D19S565 (the STK11/LKB1 gene locus), and D19S894-D19S884 (the SAFB gene locus). These suggest STK11/LKB1 gene and SAFB gene may play an important role in breast cancer development. (2)Frequent allele loss we found in other three CDRs of chromosome 19p13.3-13.2 may harbor unknown tumor suppressor genes. (3)High LOH frequency in these CDRs supports the importance of allelic loss on chromosome 19p13.3-13.2 during breast tumorigenesis. (4)The frequency of the fractional allele loss(FAL) of chromosome 19p13.3-13.2 is found to be significantly associated with increasing grade of breast cancer differentiation (p=0.01).(5) Multiple genes on 19p13.3-13.2 may synergitically contribute to breast cancer progression.
Części książek na temat "19p13.3"
"CD54 (19p13.3-p13.2)". W Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 288. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_2505.
Pełny tekst źródła"Hypocalciuric Hypercalciuria (HHC2, 19p13.3)". W Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 945. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_8099.
Pełny tekst źródła"Hypogonadotropic Hypogonadism (19p13.3, 9q34.3)". W Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 946. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_8113.
Pełny tekst źródła"ICAM (CD54, intercellular adhesion molecule, 19p13.3-p13.2)". W Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 951–52. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_8166.
Pełny tekst źródła"Methyltransferase, DNA (dnmt1, dnmt1-b, 19p13.3-p13.2)". W Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 1201. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_10292.
Pełny tekst źródłaBabey, Muriel, i Dolores M. Shoback. "Familial Hypocalciuric Hypercalcaemia Types 1–3 and Neonatal Severe Primary Hyperparathyroidism". W Oxford Textbook of Endocrinology and Diabetes 3e, redaktorzy John A. H. Wass, Wiebke Arlt i Robert K. Semple, 673–84. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198870197.003.0084.
Pełny tekst źródła"Rabson-Mendenhall Syndrome (19p13.2)". W Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 1619. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_13978.
Pełny tekst źródła"Donohue Syndrome (Leprechaunism, 19p13.2)". W Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 550. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_4785.
Pełny tekst źródła"Polycystic Liver Disease; (PCLD, 19p13.2-p13.1)". W Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 1528. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_13177.
Pełny tekst źródła"Aicardi-Goutières Syndrome (AGS1 3p21; AGS2 13q14.3, AGS3 11q13.2, AGS4 19p13.13)". W Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 50. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_421.
Pełny tekst źródłaStreszczenia konferencji na temat "19p13.3"
Lawrenson, Kate, Siddhartha Kar, Karoline Kuckenbaeker, Stacey Edwards, Qiyuan Li, Jonathan Tyrer, Jonathan Beesley i in. "Abstract 2783: Common functional mechanisms underlying pleiotropy at the 19p13.1 breast and ovarian cancer cusceptibility locus". W Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-2783.
Pełny tekst źródłaXu, Z., H. Xing, L. Wang, H. Zhou i Y. Gu. "Abstract P4-04-11: Correlation study of gene polymorphisms on 19p13.1 with triple negative breast cancer". W Abstracts: Thirty-Sixth Annual CTRC-AACR San Antonio Breast Cancer Symposium - Dec 10-14, 2013; San Antonio, TX. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/0008-5472.sabcs13-p4-04-11.
Pełny tekst źródłaBolton, Kelly L., Jonathan Tyrer, Honglin Song, Susan Ramus, Chris Jones, Maria Notaridou, Stephen J. Chanock i in. "Abstract 4729: A genome-wide association study of ovarian cancer prognosis identifies a novel locus for aggressive serous cancer on 19p13". W Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-4729.
Pełny tekst źródłaRaporty organizacyjne na temat "19p13.3"
Oesterreich, Steffi. Rapid Screen for Tumor Suppressor Genes on Chromosome 19p13. Fort Belvoir, VA: Defense Technical Information Center, wrzesień 2001. http://dx.doi.org/10.21236/ada400057.
Pełny tekst źródłaOesterreich, Steffi. Rapid Screen for Tumor Suppressor Genes on Chromosome 19p13. Fort Belvoir, VA: Defense Technical Information Center, wrzesień 2002. http://dx.doi.org/10.21236/ada410864.
Pełny tekst źródła