NKX2-8 Antibody (Pab)

Total Page：16

File Type：pdf, Size：1020Kb

21.10.2014NKX2-8 antibody (pAb) Rabbit Anti -Human/Mouse/Rat NK2 homeobox 8 (NKXH, NKX2 -9) Instruction Manual Catalog Number PK-AB718-6753 Synonyms NKX2-8 Antibody: NK2 homeobox 8, NKXH, NKX2-9 Description NKX2-8 (NK2 homeobox 8) is a member of a family of transcription factors that are involved in embryonic development and cell fate. It is expressed in the ventral foregut, the developing heart, the epithelial layers of the branchial arches and in the dorsal mesoderm. In conjunction with related protein, NKX2-5, NKX2-8 may play a role in cardiac embryonic development. NKX2-8 is also thought to be involved in lung development and is suspected of being an oncogene in lung cancer that is activated by way of gene amplification at chromosome 14q13. Quantity 100 µg Source / Host Rabbit Immunogen NKX2-8 antibody was raised against a 19 amino acid synthetic peptide near the center of human NKX2-8. Purification Method Affinity chromatography purified via peptide column. Clone / IgG Subtype Polyclonal antibody Species Reactivity Human, Mouse, Rat Specificity NKX2-8 antibody is predicted to not cross-react with other NK2 homeobox family members. Formulation Antibody is supplied in PBS containing 0.02% sodium azide. Reconstitution During shipment, small volumes of antibody will occasionally become entrapped in the seal of the product vial. For products with volumes of 200 μl or less, we recommend gently tapping the vial on a hard surface or briefly centrifuging the vial in a tabletop centrifuge to dislodge any liquid in the container’s cap. Storage & Stability Antibody can be stored at 4ºC for three months and at -20°C for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures. Applications E, WB, IHC, IF |Note: Antibody might be suitable for other applications not tested so far. Optimal concentrations for each application have to be determined indivudually. NKX2-8 antibody can be used for detection of NKX2-8 by Western blot at 1 µg/mL. Antibody can also be used for immunohistochemistry starting at 2.5 µg/mL. For immunofluorescence start at 2.5 µg/mL. Images Available upon request. References Boettger T, Stein S, and Kessel M. The chicken NKX2.8 homeobox gene: A novel member of the NK-2 gene family. Dev. Genes Evol. 1997; 207:65-70. Kendall J, Liu Q, Bakleh A, et al. Oncogenic ccooperation and coamplification of developmental transcription factor genes in lung cancer. Proc. Natl. Acad. Sci. USA 2007; 104:16663-8. Hsu DS, Acharya CR, Balakumaran BS, et al. Characterizing the developmental pathways TTF-1, NKX2-8, and PAX9 in lung cancer. Proc. Natl. Acad. Sci. USA 2009; 106:5312-7. Images Available upon request. Related Products Cat. No. PK-AB718-6753P - NKX2 8 Peptide Cat. No. PK-AB718-1464 - Rat Liver Tissue Lysate FOR IN VITRO RESEARCH USE ONLY. NOT FOR DIAGNOSTIC OR THERAPEUTIC PROCEDURES. PromoCell GmbH North America 1 – 866 – 251 – 2860 (toll free) Email: [email protected] Sickingenstr. 63/65 Deutschland 0800 – 776 66 23 (gebührenfrei) www.promokine.info 69126 Heidelberg France 0800 90 93 32 (ligne verte) Germany United Kingdom 0800 – 96 03 33 (toll free) Other Countries +49 6221 – 649 34 0 09/2014 .

Copy Link

Recommended publications

A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated.
[Show full text]
BMP Signaling Orchestrates a Transcriptional Network to Control the Fate of Mesenchymal Stem Cells (Mscs)
bioRxiv preprint doi: https://doi.org/10.1101/104927; this version posted February 1, 2017. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. BMP signaling orchestrates a transcriptional network to control the fate of mesenchymal stem cells (MSCs) Jifan Feng1, Junjun Jing1,2, Jingyuan Li1, Hu Zhao1, Vasu Punj3, Tingwei Zhang1,2, Jian Xu1 and Yang Chai1,* 1Center for Craniofacial Molecular Biology, University of Southern California, Los Angeles, CA 90033, USA 2State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China 3Department of Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA 90089, USA *Corresponding author: Yang Chai 2250 Alcazar Street – CSA 103 Center for Craniofacial Molecular Biology University of Southern California Los Angeles, CA Phone number: 323-442-3480 [email protected] Running Title: BMP regulates cell fate of MSCs Key Words: BMP, mesenchymal stem cells (MSCs), odontogenesis, Gli1 Summary Statement: BMP signaling activity is required for the lineage commitment of MSCs and transcription factors downstream of BMP signaling may determine distinct cellular identities within the dental mesenchyme. 1 bioRxiv preprint doi: https://doi.org/10.1101/104927; this version posted February 1, 2017. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license.
[Show full text]
Genome-Wide DNA Methylation Analysis of KRAS Mutant Cell Lines Ben Yi Tew1,5, Joel K
www.nature.com/scientificreports OPEN Genome-wide DNA methylation analysis of KRAS mutant cell lines Ben Yi Tew1,5, Joel K. Durand2,5, Kirsten L. Bryant2, Tikvah K. Hayes2, Sen Peng3, Nhan L. Tran4, Gerald C. Gooden1, David N. Buckley1, Channing J. Der2, Albert S. Baldwin2 ✉ & Bodour Salhia1 ✉ Oncogenic RAS mutations are associated with DNA methylation changes that alter gene expression to drive cancer. Recent studies suggest that DNA methylation changes may be stochastic in nature, while other groups propose distinct signaling pathways responsible for aberrant methylation. Better understanding of DNA methylation events associated with oncogenic KRAS expression could enhance therapeutic approaches. Here we analyzed the basal CpG methylation of 11 KRAS-mutant and dependent pancreatic cancer cell lines and observed strikingly similar methylation patterns. KRAS knockdown resulted in unique methylation changes with limited overlap between each cell line. In KRAS-mutant Pa16C pancreatic cancer cells, while KRAS knockdown resulted in over 8,000 diferentially methylated (DM) CpGs, treatment with the ERK1/2-selective inhibitor SCH772984 showed less than 40 DM CpGs, suggesting that ERK is not a broadly active driver of KRAS-associated DNA methylation. KRAS G12V overexpression in an isogenic lung model reveals >50,600 DM CpGs compared to non-transformed controls. In lung and pancreatic cells, gene ontology analyses of DM promoters show an enrichment for genes involved in diferentiation and development. Taken all together, KRAS-mediated DNA methylation are stochastic and independent of canonical downstream efector signaling. These epigenetically altered genes associated with KRAS expression could represent potential therapeutic targets in KRAS-driven cancer. Activating KRAS mutations can be found in nearly 25 percent of all cancers1.
[Show full text]
The Regulation of Lunatic Fringe During Somitogenesis
THE REGULATION OF LUNATIC FRINGE DURING SOMITOGENESIS DISSERTATION Presented in Partial Fulfillment of the Requirements for the Degree Doctor of Philosophy in the Graduate School of The Ohio State University By Emily T. Shifley ***** The Ohio State University 2009 Dissertation Committee: Approved by Professor Susan Cole, Advisor Professor Christine Beattie _________________________________ Professor Mark Seeger Advisor Graduate Program in Molecular Genetics Professor Michael Weinstein ABSTRACT Somitogenesis is the morphological hallmark of vertebrate segmentation. Somites bud from the presomitic mesoderm (PSM) in a sequential, periodic fashion and give rise to the rib cage, vertebrae, and dermis and muscles of the back. The regulation of somitogenesis is complex. In the posterior region of the PSM, a segmentation clock operates to organize cohorts of cells into presomites, while in the anterior region of the PSM the presomites are patterned into rostral and caudal compartments (R/C patterning). Both of these stages of somitogenesis are controlled, at least in part, by the Notch pathway and Lunatic fringe (Lfng), a glycosyltransferase that modifies the Notch receptor. To dissect the roles played by Lfng during somitogenesis, we created a novel allele that lacks cyclic Lfng expression within the segmentation clock, but that maintains expression during R/C somite patterning (Lfng∆FCE1). Lfng∆FCE1/∆FCE1 mice have severe defects in their anterior vertebrae and rib cages, but relatively normal sacral and tail vertebrae, unlike Lfng knockouts. Segmentation clock function is differentially affected by the ∆FCE1 deletion; during anterior somitogenesis the expression patterns of many clock genes are disrupted, while during posterior somitogenesis, certain clock components have recovered. R/C patterning occurs relatively normally in Lfng∆FCE1/∆FCE1 embryos, likely contributing to the partial phenotype rescue, and confirming that Lfng ii plays separate roles in the two regions of the PSM.
[Show full text]
Genome-Wide DNA Methylation Analysis Reveals Molecular Subtypes of Pancreatic Cancer
www.impactjournals.com/oncotarget/ Oncotarget, 2017, Vol. 8, (No. 17), pp: 28990-29012 Research Paper Genome-wide DNA methylation analysis reveals molecular subtypes of pancreatic cancer Nitish Kumar Mishra1 and Chittibabu Guda1,2,3,4 1Department of Genetics, Cell Biology and Anatomy, University of Nebraska Medical Center, Omaha, NE, 68198, USA 2Bioinformatics and Systems Biology Core, University of Nebraska Medical Center, Omaha, NE, 68198, USA 3Department of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE, 68198, USA 4Fred and Pamela Buffet Cancer Center, University of Nebraska Medical Center, Omaha, NE, 68198, USA Correspondence to: Chittibabu Guda, email: [email protected] Keywords: TCGA, pancreatic cancer, differential methylation, integrative analysis, molecular subtypes Received: October 20, 2016 Accepted: February 12, 2017 Published: March 07, 2017 Copyright: Mishra et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC-BY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. ABSTRACT Pancreatic cancer (PC) is the fourth leading cause of cancer deaths in the United States with a five-year patient survival rate of only 6%. Early detection and treatment of this disease is hampered due to lack of reliable diagnostic and prognostic markers. Recent studies have shown that dynamic changes in the global DNA methylation and gene expression patterns play key roles in the PC development; hence, provide valuable insights for better understanding the initiation and progression of PC. In the current study, we used DNA methylation, gene expression, copy number, mutational and clinical data from pancreatic patients.
[Show full text]
An OTX2-PAX3 Signaling Axis Regulates Group 3 Medulloblastoma Cell Fate
ARTICLE https://doi.org/10.1038/s41467-020-17357-4 OPEN An OTX2-PAX3 signaling axis regulates Group 3 medulloblastoma cell fate Jamie Zagozewski1, Ghazaleh M. Shahriary 1, Ludivine Coudière Morrison1, Olivier Saulnier 2,3, Margaret Stromecki1, Agnes Fresnoza4, Gareth Palidwor5, Christopher J. Porter 5, Antoine Forget6,7, Olivier Ayrault 6,7, Cynthia Hawkins2,8,9, Jennifer A. Chan10, Maria C. Vladoiu2,3,9, Lakshmikirupa Sundaresan2,3, Janilyn Arsenio11,12, Michael D. Taylor 2,3,9,13, Vijay Ramaswamy 2,3,14,15 & ✉ Tamra E. Werbowetski-Ogilvie 1 1234567890():,; OTX2 is a potent oncogene that promotes tumor growth in Group 3 medulloblastoma. However, the mechanisms by which OTX2 represses neural differentiation are not well characterized. Here, we perform extensive multiomic analyses to identify an OTX2 regulatory network that controls Group 3 medulloblastoma cell fate. OTX2 silencing modulates the repressive chromatin landscape, decreases levels of PRC2 complex genes and increases the expression of neurodevelopmental transcription factors including PAX3 and PAX6. Expression of PAX3 and PAX6 is signiﬁcantly lower in Group 3 medulloblastoma patients and is cor- related with reduced survival, yet only PAX3 inhibits self-renewal in vitro and increases survival in vivo. Single cell RNA sequencing of Group 3 medulloblastoma tumorspheres demonstrates expression of an undifferentiated progenitor program observed in primary tumors and characterized by translation/elongation factor genes. Identiﬁcation of mTORC1 signaling as a downstream effector of OTX2-PAX3 reveals roles for protein synthesis pathways in regulating Group 3 medulloblastoma pathogenesis. 1 Regenerative Medicine Program, Department of Biochemistry and Medical Genetics, University of Manitoba, Winnipeg, MB, Canada. 2 The Arthur and Sonia Labatt Brain Tumour Research Center, The Hospital for Sick Children, Toronto, ON, Canada.
[Show full text]
Mutational Analysis of AXIN2, MSX1, and PAX9 in Two Mexican Oligodontia Families
Mutational analysis of AXIN2, MSX1, and PAX9 in two Mexican oligodontia families Y.D. Mu1,2, Z. Xu1, C.I. Contreras1, J.S. McDaniel1, K.J. Donly1 and S. Chen1 1Department of Developmental Dentistry, Dental School, University of Texas Health Science Center, San Antonio, Texas, USA 2Stomotology Department, Sichuan Provincial People’s Hospital, Chengdu, Sichuan, China Corresponding author: S. Chen E-mail: [email protected] Genet. Mol. Res. 12 (4): 4446-4458 (2013) Received July 4, 2012 Accepted May 15, 2013 Published October 10, 2013 DOI http://dx.doi.org/10.4238/2013.October.10.10 ABSTRACT. The genes for axin inhibition protein 2 (AXIN2), msh homeobox 1 (MSX1), and paired box gene 9 (PAX9) are involved in tooth root formation and tooth development. Mutations of the AXIN2, MSX1, and PAX9 genes are associated with non-syndromic oligodontia. In this study, we investigated phenotype and AXIN2, MSX1, and PAX9 gene variations in two Mexican families with non-syndromic oligodontia. Individuals from two families underwent clinical examinations, including an intra-oral examination and panoramic radiograph. Retrospective data were reviewed, and peripheral blood samples were collected. The exons and exon-intronic boundaries of the AXIN2, MSX1, and PAX9 genes were sequenced and analyzed. Protein and messenger RNA structures were predicted using bioinformative software programs. Clinical and oral examinations revealed isolated non-syndromic oligodontia in the two Mexican families. The average number of missing teeth was 12. The sequence analysis of exons and exon-intronic regions of AXIN2, MSX1, and PAX9 revealed 11 single- nucleotide polymorphisms (SNPs), including seven in AXIN2, two Genetics and Molecular Research 12 (4): 4446-4458 (2013) ©FUNPEC-RP www.funpecrp.com.br AXIN2, MSX1, and PAX9 SNPs and oligodontia 4447 in MSX1, and three in PAX9.
[Show full text]
Figure S1. Basic Information of RNA-Seq Results. (A) Bar Plot of Reads Component for Each Sample
Figure S1. Basic information of RNA-seq results. (A) Bar plot of reads component for each sample. (B) Dot plot shows the principal component analysis (PCA) of each sample. (C) Venn diagram of DEGs for three time points, the overlap part of the circles represents common differentially expressed genes between combinations. Figure S2. Scatter plot of DEGs for each time point. The X and Y axes represent the logarithmic value of gene expression. Red represents up-regulated DEG, blue represents down-regulated DEG, and gray represents non-DEG. Table S1. Primers used for quantitative real-time PCR analysis of DEGs. Gene Primer Sequence Forward 5’-CTACGAGTGGATGGTCAAGAGC-3’ FOXO1 Reverse 5’-CCAGTTCCTTCATTCTGCACACG-3’ Forward 5’-GACGTCCGGCATCAGAGAAA-3’ IRS2 Reverse 5’-TCCACGGCTAATCGTCACAG-3’ Forward 5’-CACAACCAGGACCTCACACC-3’ IRS1 Reverse 5’-CTTGGCACGATAGAGAGCGT-3’ Forward 5’-AGGATACCACTCCCAACAGACCT-3’ IL6 Reverse 5’-CAAGTGCATCATCGTTGTTCATAC-3’ Forward 5’-TCACGTTGTACGCAGCTACC-3’ CCL5 Reverse 5’-CAGTCCTCTTACAGCCTTTGG-3’ Forward 5’-CTGTGCAGCCGCAGTGCCTACC-3’ BMP7 Reverse 5’-ATCCCTCCCCACCCCACCATCT-3’ Forward 5’-CTCTCCCCCTCGACTTCTGA-3’ BCL2 Reverse 5’-AGTCACGCGGAACACTTGAT-3’ Forward 5’-CTGTCGAACACAGTGGTACCTG-3’ FGF7 Reverse 5’-CCAACTGCCACTGTCCTGATTTC-3’ Forward 5’-GGGAGCCAAAAGGGTCATCA-3’ GAPDH Reverse 5’-CGTGGACTGTGGTCATGAGT-3’ Supplementary material: Differentially expressed genes log2(SADS-CoV_12h/ Qvalue (SADS-CoV _12h/ Gene Symbol Control_12h) Control_12h) PTGER4 -1.03693 6.79E-04 TMEM72 -3.08132 3.66E-04 IFIT2 -1.02918 2.11E-07 FRAT2 -1.09282 4.66E-05
[Show full text]
Evaluation of the Role of Egfr, Sox2, and Pax9 in Oral
EVALUATION OF THE ROLE OF EGFR, SOX2, AND PAX9 IN ORAL CARCINOGENESIS Timothy John Bates A thesis submitted in partial fulfilment of the requirements for the degree of Doctor of Philosophy Northern Institute for Cancer Research Newcastle University August 2015 Acknowledgements I would like to acknowledge my three supervisors, Dr M. Robinson, Dr R. Kist, and Professor P. Sloan, without whom this project would not have been possible. Dr Kist and Dr Robinson shared the initial vision for this project and, in collaboration, designed and developed its overall structure. The project therefore arose from a unique collaboration between principle investigators with backgrounds in developmental oral biology and oral pathology. Professor Sloan’s experience and insight have proved invaluable to the analysis, interpretation, and presentation of our data. I would like to thank Miss A. Long and all members of the Research and Development Team, Department of Cellular Pathology, for their essential contribution to the processing, sectioning, and automated immunostaining of both human and mouse tissue during this project. Dr R. Mahsoub and Miss V. Rook contributed to the manual immunohistochemical staining of sections during this project, work which formed part of their Masters by Research projects. Mr M. Kennedy played a vital role in collecting clinical data for the group of early-stage oral squamous cell carcinoma patients, during a Master of Science project that he undertook at the University of Edinburgh. I would like to thank Miss M. Elias and all the team in the Dermatology Laboratory, Institute of Cellular Medicine. The generation of the tetracycline- inducible cell lines would not have been possible without the support of Martina and others in the Dermatology team: Carol, Keith, and Emma, to name just a few.
[Show full text]
Identifying the Risky SNP of Osteoporosis with ID3-PEP Decision Tree Algorithm
Hindawi Complexity Volume 2017, Article ID 9194801, 8 pages https://doi.org/10.1155/2017/9194801 Research Article Identifying the Risky SNP of Osteoporosis with ID3-PEP Decision Tree Algorithm Jincai Yang,1 Huichao Gu,1 Xingpeng Jiang,1 Qingyang Huang,2 Xiaohua Hu,1 and Xianjun Shen1 1 School of Computer Science, Central China Normal University, Wuhan 430079, China 2School of Life Science, Central China Normal University, Wuhan 430079, China Correspondence should be addressed to Jincai Yang; [email protected] Received 31 March 2017; Revised 26 May 2017; Accepted 8 June 2017; Published 7 August 2017 Academic Editor: Fang-Xiang Wu Copyright © 2017 Jincai Yang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. In the past 20 years, much progress has been made on the genetic analysis of osteoporosis. A number of genes and SNPs associated with osteoporosis have been found through GWAS method. In this paper, we intend to identify the suspected risky SNPs of osteoporosis with computational methods based on the known osteoporosis GWAS-associated SNPs. The process includes two steps. Firstly, we decided whether the genes associated with the suspected risky SNPs are associated with osteoporosis by using random walk algorithm on the PPI network of osteoporosis GWAS-associated genes and the genes associated with the suspected risky SNPs. In order to solve the overfitting problem in ID3 decision tree algorithm, we then classified the SNPs with positive results based on their features of position and function through a simplified classification decision tree which was constructed by ID3 decision tree algorithm with PEP (Pessimistic-Error Pruning).
[Show full text]
The Partial Role of KLF4 and KLF5 in Gastrointestinal Tumors
Hindawi Gastroenterology Research and Practice Volume 2021, Article ID 2425356, 13 pages https://doi.org/10.1155/2021/2425356 Review Article The Partial Role of KLF4 and KLF5 in Gastrointestinal Tumors Jun-Chen Li,1 Qiu-Han Chen,2 Rui Jian,3 Jiang-Rong Zhou,1 Yun Xu,4 Fang Lu,1 Jun-Qiao Li,5 and Hao Zhang 1 1Department of Gastroenterology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, China 2Blood Purification Center, University-Town Hospital of Chongqing Medical University, Chongqing 400000, China 3Department of Gastroenterology, People’s Hospital of Chongqing Banan District, Chongqing 401320, China 4Department of Gastroenterology, Chongqing Sixth People’s Hospital, Chongqing 400060, China 5Department of Gastroenterology, Chongqing North-Kuanren General Hospital, Chongqing 401147, China Correspondence should be addressed to Hao Zhang; [email protected] Received 30 April 2021; Revised 8 July 2021; Accepted 12 July 2021; Published 28 July 2021 Academic Editor: Fausto Rosa Copyright © 2021 Jun-Chen Li et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Background. KLF4 and KLF5 are members of the KLF transcription factor family, which play an important role in many gastrointestinal tumors. To gain a deeper insight into its function and role, bioinformatics was used to analyze the function and role of KLF4 and KLF5 in gastrointestinal tumors. Methods. Data were collected from several online databases. Gene Expression Profiling Interactive Analysis (GEPIA), UALCAN database analysis, Kaplan-Meier Plotter analysis, LOGpc system, the Pathology Atlas, and the STRING website were used to analyze the data.
[Show full text]
Deletion of the Sclerotome-Enriched Lncrna PEAT Augments Ribosomal Protein Expression
Deletion of the sclerotome-enriched lncRNA PEAT augments ribosomal protein expression David A. Stafforda, Darwin S. Dichmanna, Jessica K. Changb, and Richard M. Harlanda,1 aDepartment of Molecular and Cell Biology, University of California, Berkeley, CA 94720; and bDepartment of Genetics, Stanford University, Stanford, CA 94305-5120 Contributed by Richard M. Harland, September 23, 2016 (sent for review July 22, 2016; reviewed by Margaret Buckingham and Chen-Ming Fan) To define a complete catalog of the genes that are activated during developing sclerotome by dissection from early embryos at 8- to mouse sclerotome formation, we sequenced RNA from embryonic 9.5-d postconception is technically difficult. Although a model mouse tissue directed to form sclerotome in culture. In addition to for presomitic mesoderm culture from stem cells has been de- well-known early markers of sclerotome, such as Pax1, Pax9,andthe veloped (10), this has not been exploited as an in vitro model of Bapx2/Nkx3-2 homolog Nkx3-1, the long-noncoding RNA PEAT (Pax1 the sclerotome. To obtain sufficient sclerotomal transcripts for enhancer antisense transcript) was induced in sclerotome-directed RNA-seq, we chemically treated explants of embryonic tissue to samples. Strikingly, PEAT is located just upstream of the Pax1 gene. bias differentiation of fluorescently marked presomitic mesoderm Using CRISPR/Cas9, we generated a mouse line bearing a complete toward the sclerotome. Following FACS, we compared control deletion of the PEAT-transcribed unit. RNA-seq on PEAT mutant and induced cultures to define the sclerotome transcriptome. In embryos showed that loss of PEAT modestly increases bone mor- addition to the previously described transcription factors, we identi- phogenetic protein target gene expression and also elevates the fied an uncharacterized noncoding RNA transcript that we named expression of a large subset of ribosomal protein mRNAs.
[Show full text]