DOCSLIB.ORG

Mouse Icam2 Conditional Knockout Project (CRISPR/Cas9)

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Mouse Icam2 Conditional Knockout Project (CRISPR/Cas9) https://www.alphaknockout.com Mouse Icam2 Conditional Knockout Project (CRISPR/Cas9) Objective: To create a Icam2 conditional knockout Mouse model (C57BL/6J) by CRISPR/Cas-mediated genome engineering. Strategy summary: The Icam2 gene (NCBI Reference Sequence: NM_010494 ; Ensembl: ENSMUSG00000001029 ) is located on Mouse chromosome 11. 4 exons are identified, with the ATG start codon in exon 1 and the TGA stop codon in exon 4 (Transcript: ENSMUST00000001055). Exon 2~3 will be selected as conditional knockout region (cKO region). Deletion of this region should result in the loss of function of the Mouse Icam2 gene. To engineer the targeting vector, homologous arms and cKO region will be generated by PCR using BAC clone RP24-141A4 as template. Cas9, gRNA and targeting vector will be co-injected into fertilized eggs for cKO Mouse production. The pups will be genotyped by PCR followed by sequencing analysis. Note: Homozygous inactivation of this gene results in increased respiratory responsiveness due to an increased accumulation of eosinophils in the lung interstitium and a concomittant delay in the increase of eosinophils in the airway lumen during the development of an allergic inflammatory response. Exon 2~3 is not frameshift exon, and covers 71.12% of the coding region. The size of intron 1 for 5'-loxP site insertion: 1490 bp, and the size of intron 3 for 3'-loxP site insertion: 651 bp. The size of effective cKO region: ~2794 bp. The cKO region does not have any other known gene. Page 1 of 8 https://www.alphaknockout.com Overview of the Targeting Strategy Wildtype allele 5' gRNA region gRNA region 3' 1 2 3 4 5 4 Targeting vector Targeted allele Constitutive KO allele (After Cre recombination) Legends Homology arm Exon of mouse Icam2 cKO region Exon of mouse Prr29 loxP site Page 2 of 8 https://www.alphaknockout.com Overview of the Dot Plot Window size: 10 bp Forward Reverse Complement Sequence 12 Note: The sequence of homologous arms and cKO region is aligned with itself to determine if there are tandem repeats. Tandem repeats are found in the dot plot matrix. It may be difficult to construct this targeting vector. Overview of the GC Content Distribution Window size: 300 bp Sequence 12 Summary: Full Length(9294bp) | A(22.79% 2118) | C(27.34% 2541) | T(24.88% 2312) | G(24.99% 2323) Note: The sequence of homologous arms and cKO region is analyzed to determine the GC content. No significant high GC-content region is found. So this region is suitable for PCR screening or sequencing analysis. Page 3 of 8 https://www.alphaknockout.com BLAT Search Results (up) QUERY SCORE START END QSIZE IDENTITY CHROM STRAND START END SPAN ----------------------------------------------------------------------------------------------- browser details YourSeq 3000 1 3000 3000 100.0% chr11 - 106381190 106384189 3000 browser details YourSeq 39 363 414 3000 83.8% chr1 + 12691290 12691338 49 browser details YourSeq 38 225 264 3000 92.4% chr8 + 38075823 38075861 39 browser details YourSeq 33 405 443 3000 83.8% chr6 - 62632046 62632082 37 browser details YourSeq 33 363 397 3000 91.2% chr6 - 54849685 54849718 34 browser details YourSeq 32 383 419 3000 97.2% chr4 - 36236787 36236833 47 browser details YourSeq 32 233 264 3000 100.0% chr11 - 104121016 104121047 32 browser details YourSeq 30 363 400 3000 94.3% chr4 - 13590386 13590426 41 browser details YourSeq 28 2098 2143 3000 96.8% chr2 - 113766117 113766167 51 browser details YourSeq 27 365 396 3000 96.6% chr6 - 31089718 31089751 34 browser details YourSeq 25 369 399 3000 93.2% chr2 - 181844730 181844761 32 browser details YourSeq 25 1336 1364 3000 96.5% chr2 + 65935661 65935693 33 browser details YourSeq 22 369 394 3000 92.4% chr15 - 86138956 86138981 26 browser details YourSeq 21 1299 1322 3000 95.9% chr17 - 15702380 15702404 25 Note: The 3000 bp section upstream of Exon 2 is BLAT searched against the genome. No significant similarity is found. BLAT Search Results (down) QUERY SCORE START END QSIZE IDENTITY CHROM STRAND START END SPAN ----------------------------------------------------------------------------------------------- browser details YourSeq 3000 1 3000 3000 100.0% chr11 - 106375396 106378395 3000 browser details YourSeq 32 1608 1669 3000 94.3% chr7 + 104995146 104995209 64 browser details YourSeq 29 1977 2018 3000 88.3% chr12 + 55215951 55215991 41 browser details YourSeq 26 1777 1803 3000 100.0% chr11 + 24289899 24289942 44 Note: The 3000 bp section downstream of Exon 3 is BLAT searched against the genome. No significant similarity is found. Page 4 of 8 https://www.alphaknockout.com Gene and protein information: Icam2 intercellular adhesion molecule 2 [ Mus musculus (house mouse) ] Gene ID: 15896, updated on 12-Aug-2019 Gene summary Official Symbol Icam2 provided by MGI Official Full Name intercellular adhesion molecule 2 provided by MGI Primary source MGI:MGI:96394 See related Ensembl:ENSMUSG00000001029 Gene type protein coding RefSeq status VALIDATED Organism Mus musculus Lineage Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; Mammalia; Eutheria; Euarchontoglires; Glires; Rodentia; Myomorpha; Muroidea; Muridae; Murinae; Mus; Mus Also known as CD102; Ly-60; Icam-2 Expression Biased expression in lung adult (RPKM 101.8), thymus adult (RPKM 40.1) and 12 other tissues See more Orthologs human all Genomic context Location: 11 E1; 11 69.09 cM See Icam2 in Genome Data Viewer Exon count: 7 Annotation release Status Assembly Chr Location 108 current GRCm38.p6 (GCF_000001635.26) 11 NC_000077.6 (106377656..106388139, complement) Build 37.2 previous assembly MGSCv37 (GCF_000001635.18) 11 NC_000077.5 (106238970..106243955, complement) Chromosome 11 - NC_000077.6 Page 5 of 8 https://www.alphaknockout.com Transcript information: This gene has 5 transcripts Gene: Icam2 ENSMUSG00000001029 Description intercellular adhesion molecule 2 [Source:MGI Symbol;Acc:MGI:96394] Gene Synonyms CD102, Icam-2 Location Chromosome 11: 106,377,656-106,388,075 reverse strand. GRCm38:CM001004.2 About this gene This gene has 5 transcripts (splice variants), 99 orthologues, 4 paralogues, is a member of 1 Ensembl protein family and is associated with 3 phenotypes. Transcripts Name Transcript ID bp Protein Translation ID Biotype CCDS UniProt Flags Icam2-201 ENSMUST00000001055.14 1282 277aa ENSMUSP00000001055.8 Protein coding CCDS25555 P35330 TSL:1 GENCODE basic APPRIS P1 Icam2-203 ENSMUST00000106813.8 574 162aa ENSMUSP00000102426.2 Protein coding - G5E8M9 CDS 3' incomplete TSL:2 Icam2-205 ENSMUST00000173795.1 539 180aa ENSMUSP00000133315.1 Protein coding - G3UWJ5 CDS 5' and 3' incomplete TSL:2 Icam2-204 ENSMUST00000141146.1 506 138aa ENSMUSP00000118043.1 Protein coding - B1ARJ2 CDS 3' incomplete TSL:3 Icam2-202 ENSMUST00000106809.2 624 No protein - Retained intron - - TSL:2 Page 6 of 8 https://www.alphaknockout.com 30.42 kb Forward strand 106.37Mb 106.38Mb 106.39Mb Genes Prr29-201 >protein coding (Comprehensive set... Prr29-202 >protein coding Prr29-205 >protein coding Prr29-203 >protein coding Prr29-206 >protein coding Prr29-204 >protein coding Contigs AL604045.7 > Genes < Icam2-201protein coding < Ern1-201protein coding (Comprehensive set... < Icam2-205protein coding < Ern1-205lncRNA < Icam2-203protein coding < Icam2-204protein coding < Icam2-202retained intron Regulatory Build 106.37Mb 106.38Mb 106.39Mb Reverse strand 30.42 kb Regulation Legend CTCF Open Chromatin Promoter Promoter Flank Gene Legend Protein Coding Ensembl protein coding merged Ensembl/Havana Non-Protein Coding RNA gene processed transcript Page 7 of 8 https://www.alphaknockout.com Transcript: ENSMUST00000001055 < Icam2-201protein coding Reverse strand 5.13 kb ENSMUSP00000001... Transmembrane heli... PDB-ENSP mappings Low complexity (Seg) Cleavage site (Sign... Superfamily Immunoglobulin-like domain superfamily Prints Intercellular adhesion molecule/vascular cell adhesion molecule, N-terminal Pfam Intercellular adhesion molecule, N-terminal PANTHER Intercellular adhesion molecule 2 PTHR13771 Gene3D Immunoglobulin-like fold All sequence SNPs/i... Sequence variants (dbSNP and all other sources) Variant Legend missense variant synonymous variant Scale bar 0 40 80 120 160 200 277 We wish to acknowledge the following valuable scientific information resources: Ensembl, MGI, NCBI, UCSC. Page 8 of 8.
Load more

Recommended publications
  • Ejercicio Físico En La Patogenia De La Artritis Inducida Por Proteoglicano En Ratón
    UNIVERSIDAD AUTÓNOMA DE CHIHUAHUA FACULTAD DE CIENCIAS DE LA CULTURA FÍSICA SECRETARÍA DE INVESTIGACIÓN Y POSGRADO EJERCICIO FÍSICO EN LA PATOGENIA DE LA ARTRITIS INDUCIDA POR PROTEOGLICANO EN RATÓN TESIS QUE PARA OBTENER EL GRADO DE: DOCTORA EN CIENCIAS DE LA CULTURA FÍSICA PRESENTA: M. EN C. SUSANA AIDEÉ GONZÁLEZ CHÁVEZ DIRECTOR DE TESIS: DR. CÉSAR FRANCISCO PACHECO TENA CHIHUAHUA, CHIH., MÉXICO, SEPTIEMBRE DE 2017 UNIVERSIDAD AUTÓNOMA DE CHIHUAHUA FACULTAD DE CIENCIAS DE LA CULTURA FÍSICA SECRETARÍA DE INVESTIGACIÓN Y POSGRADO El que suscribe, integrante del Núcleo Complementario del Programa de Doctorado Interinstitucional en Ciencias de la Cultura Física de la Facultad de Ciencias de la Cultura Física de la Universidad Autónoma de Chihuahua. CERTIFICA Que el presente trabajo titulado “Ejercicio físico en la patogenia de la artritis inducida por proteoglicano en ratón”, ha sido realizado bajo mi dirección en el Laboratorio de Investigación PABIOM de la Facultad de Medicina y Ciencias Biomédicas de la Universidad Autónoma de Chihuahua, por la M. en C. Susana Aideé González Chávez para optar por el grado de: DOCTORA EN CIENCIAS DE LA CULTURA FÍSICA Esta es una investigación original que ha sido realizada con rigor ético y científico, por lo que autorizo su presentación ante el grupo de sinodales correspondiente. Para los fines que haya lugar, se extiende la presente a los doce días del mes de Septiembre del dos mil diecisiete. Atentamente Dr. César Francisco Pacheco Tena Doctor en Ciencias Médicas Facultad de Medicina y Ciencias Biomédicas, UACH i UNIVERSIDAD AUTÓNOMA DE CHIHUAHUA FACULTAD DE CIENCIAS DE LA CULTURA FÍSICA SECRETARÍA DE INVESTIGACIÓN Y POSGRADO El presente trabajo “Ejercicio físico en la patogenia de la artritis inducida por proteoglicano en ratón” realizado por la M.
    [Show full text]
  • Cellular and Molecular Signatures in the Disease Tissue of Early
    Cellular and Molecular Signatures in the Disease Tissue of Early Rheumatoid Arthritis Stratify Clinical Response to csDMARD-Therapy and Predict Radiographic Progression Frances Humby1,* Myles Lewis1,* Nandhini Ramamoorthi2, Jason Hackney3, Michael Barnes1, Michele Bombardieri1, Francesca Setiadi2, Stephen Kelly1, Fabiola Bene1, Maria di Cicco1, Sudeh Riahi1, Vidalba Rocher-Ros1, Nora Ng1, Ilias Lazorou1, Rebecca E. Hands1, Desiree van der Heijde4, Robert Landewé5, Annette van der Helm-van Mil4, Alberto Cauli6, Iain B. McInnes7, Christopher D. Buckley8, Ernest Choy9, Peter Taylor10, Michael J. Townsend2 & Costantino Pitzalis1 1Centre for Experimental Medicine and Rheumatology, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK. Departments of 2Biomarker Discovery OMNI, 3Bioinformatics and Computational Biology, Genentech Research and Early Development, South San Francisco, California 94080 USA 4Department of Rheumatology, Leiden University Medical Center, The Netherlands 5Department of Clinical Immunology & Rheumatology, Amsterdam Rheumatology & Immunology Center, Amsterdam, The Netherlands 6Rheumatology Unit, Department of Medical Sciences, Policlinico of the University of Cagliari, Cagliari, Italy 7Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow G12 8TA, UK 8Rheumatology Research Group, Institute of Inflammation and Ageing (IIA), University of Birmingham, Birmingham B15 2WB, UK 9Institute of
    [Show full text]
  • Molecular Analyses of Malignant Pleural Mesothelioma
    Molecular Analyses of Malignant Pleural Mesothelioma Shir Kiong Lo National Heart and Lung Institute Imperial College Dovehouse Street London SW3 6LY A thesis submitted for MD (Res) Faculty of Medicine, Imperial College London 2016 1 Abstract Malignant pleural mesothelioma (MPM) is an aggressive cancer that is strongly associated with asbestos exposure. Majority of patients with MPM present with advanced disease and the treatment paradigm mainly involves palliative chemotherapy and best supportive care. The current chemotherapy options are limited and ineffective hence there is an urgent need to improve patient outcomes. This requires better understanding of the genetic alterations driving MPM to improve diagnostic, prognostic and therapeutic strategies. This research aims to gain further insights in the pathogenesis of MPM by exploring the tumour transcriptional and mutational profiles. We compared gene expression profiles of 25 MPM tumours and 5 non-malignant pleura. This revealed differentially expressed genes involved in cell migration, invasion, cell cycle and the immune system that contribute to the malignant phenotype of MPM. We then constructed MPM-associated co-expression networks using weighted gene correlation network analysis to identify clusters of highly correlated genes. These identified three distinct molecular subtypes of MPM associated with genes involved in WNT and TGF-ß signalling pathways. Our results also revealed genes involved in cell cycle control especially the mitotic phase correlated significantly with poor prognosis. Through exome analysis of seven paired tumour/blood and 29 tumour samples, we identified frequent mutations in BAP1 and NF2. Additionally, the mutational profile of MPM is enriched with genes encoding FAK, MAPK and WNT signalling pathways.
    [Show full text]
  • Identification of Key Pathways and Genes in Dementia Via Integrated Bioinformatics Analysis
    bioRxiv preprint doi: https://doi.org/10.1101/2021.04.18.440371; this version posted July 19, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Identification of Key Pathways and Genes in Dementia via Integrated Bioinformatics Analysis Basavaraj Vastrad1, Chanabasayya Vastrad*2 1. Department of Biochemistry, Basaveshwar College of Pharmacy, Gadag, Karnataka 582103, India. 2. Biostatistics and Bioinformatics, Chanabasava Nilaya, Bharthinagar, Dharwad 580001, Karnataka, India. * Chanabasayya Vastrad [email protected] Ph: +919480073398 Chanabasava Nilaya, Bharthinagar, Dharwad 580001 , Karanataka, India bioRxiv preprint doi: https://doi.org/10.1101/2021.04.18.440371; this version posted July 19, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Abstract To provide a better understanding of dementia at the molecular level, this study aimed to identify the genes and key pathways associated with dementia by using integrated bioinformatics analysis. Based on the expression profiling by high throughput sequencing dataset GSE153960 derived from the Gene Expression Omnibus (GEO), the differentially expressed genes (DEGs) between patients with dementia and healthy controls were identified. With DEGs, we performed a series of functional enrichment analyses. Then, a protein–protein interaction (PPI) network, modules, miRNA-hub gene regulatory network and TF-hub gene regulatory network was constructed, analyzed and visualized, with which the hub genes miRNAs and TFs nodes were screened out. Finally, validation of hub genes was performed by using receiver operating characteristic curve (ROC) analysis.
    [Show full text]
  • Faculty of Graduate Studies and Scientific Research Molecular
    Republic of Sudan Ministry of Higher Education and Scientific Research Shendi University Faculty of Graduate Studies and Scientific Research Molecular Identification of Genetic Markers of Susceptibility to Essential Hypertension Using Whole Exome Sequencing among Sudanese Patients from Afro- Asiatic and Nilo-Saharan ethnic groups A Thesis Submitted in Fulfillment for the Requirements of PhD Degree in Biochemistry By: Wesal Ahmed ELHanbli Babiker MBBS- MSc Medical Biochemistry Supervisor: Dr: Dina Ahmed Hassan Associate professor of Biochemistry (2020) سورة الفاتحة I Bibliographic Entry Author: Wesal Ahmed ELHanbli Babiker Thesis: Molecular Identification of Genetic Markers of Susceptibility to Essential Hypertension Using Whole Exome Sequencing among Sudanese Patients from Afro-asiatic and Nilo-Saharan ethnic groups Degree program: PhD Faculty: Faculty of Medicine Field of study: Biochemistry Supervisor: Dr: Dina Ahmed Hassan Duration: (from 2015 to 2020) Key words: Essential hypertension, whole exome sequencing, bioinformatics tools, GPCR, MTHFR, ADM, Real-time PCR. II PhD Examination Committee Members Thesis Title: Molecular Identification of Genetic Markers of Susceptibility to Essential Hypertension Using Whole Exome Sequencing among Sudanese Patients from Afro-asiatic and Nilo-Saharan ethnic groups Supervisor: Dr: Dina Ahmed Hassan Signature …………………………… date ……………………………. Internal Examiner: Prof. Rashid Eltayeb Abdalla Signature …………………………….. date …………………………… External Examiner: Prof. Mamoun Makki EL Manna Signature …………………………….. date ……………………………. III Statement I Wesal Ahmed ELHanbli Babiker, declare that the study of Molecular Identification of Genetic Markers of Susceptibility to Essential Hypertension Using Whole Exome Sequencing among Sudanese Patients from Afro-asiatic and Nilo- Saharan ethnic groups, is my own original work and submitted in fulfillment for the requirements of PhD degree in biochemistry. I have followed all ethical and technical principles in the preparation, data collection, data analysis and compilation of this study.
    [Show full text]
  • Investigating the Effect of Chronic Activation of AMP-Activated Protein
    Investigating the effect of chronic activation of AMP-activated protein kinase in vivo Alice Pollard CASE Studentship Award A thesis submitted to Imperial College London for the degree of Doctor of Philosophy September 2017 Cellular Stress Group Medical Research Council London Institute of Medical Sciences Imperial College London 1 Declaration I declare that the work presented in this thesis is my own, and that where information has been derived from the published or unpublished work of others it has been acknowledged in the text and in the list of references. This work has not been submitted to any other university or institute of tertiary education in any form. Alice Pollard The copyright of this thesis rests with the author and is made available under a Creative Commons Attribution Non-Commercial No Derivatives license. Researchers are free to copy, distribute or transmit the thesis on the condition that they attribute it, that they do not use it for commercial purposes and that they do not alter, transform or build upon it. For any reuse or redistribution, researchers must make clear to others the license terms of this work. 2 Abstract The prevalence of obesity and associated diseases has increased significantly in the last decade, and is now a major public health concern. It is a significant risk factor for many diseases, including cardiovascular disease (CVD) and type 2 diabetes. Characterised by excess lipid accumulation in the white adipose tissue, which drives many associated pathologies, obesity is caused by chronic, whole-organism energy imbalance; when caloric intake exceeds energy expenditure. Whilst lifestyle changes remain the most effective treatment for obesity and the associated metabolic syndrome, incidence continues to rise, particularly amongst children, placing significant strain on healthcare systems, as well as financial burden.
    [Show full text]
  • The Pdx1 Bound Swi/Snf Chromatin Remodeling Complex Regulates Pancreatic Progenitor Cell Proliferation and Mature Islet Β Cell
    Page 1 of 125 Diabetes The Pdx1 bound Swi/Snf chromatin remodeling complex regulates pancreatic progenitor cell proliferation and mature islet β cell function Jason M. Spaeth1,2, Jin-Hua Liu1, Daniel Peters3, Min Guo1, Anna B. Osipovich1, Fardin Mohammadi3, Nilotpal Roy4, Anil Bhushan4, Mark A. Magnuson1, Matthias Hebrok4, Christopher V. E. Wright3, Roland Stein1,5 1 Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN 2 Present address: Department of Pediatrics, Indiana University School of Medicine, Indianapolis, IN 3 Department of Cell and Developmental Biology, Vanderbilt University, Nashville, TN 4 Diabetes Center, Department of Medicine, UCSF, San Francisco, California 5 Corresponding author: [email protected]; (615)322-7026 1 Diabetes Publish Ahead of Print, published online June 14, 2019 Diabetes Page 2 of 125 Abstract Transcription factors positively and/or negatively impact gene expression by recruiting coregulatory factors, which interact through protein-protein binding. Here we demonstrate that mouse pancreas size and islet β cell function are controlled by the ATP-dependent Swi/Snf chromatin remodeling coregulatory complex that physically associates with Pdx1, a diabetes- linked transcription factor essential to pancreatic morphogenesis and adult islet-cell function and maintenance. Early embryonic deletion of just the Swi/Snf Brg1 ATPase subunit reduced multipotent pancreatic progenitor cell proliferation and resulted in pancreas hypoplasia. In contrast, removal of both Swi/Snf ATPase subunits, Brg1 and Brm, was necessary to compromise adult islet β cell activity, which included whole animal glucose intolerance, hyperglycemia and impaired insulin secretion. Notably, lineage-tracing analysis revealed Swi/Snf-deficient β cells lost the ability to produce the mRNAs for insulin and other key metabolic genes without effecting the expression of many essential islet-enriched transcription factors.
    [Show full text]
  • Mks1p Is a Regulator of Nitrogen Catabolism Upstream of Ure2p in Saccharomyces Cerevisiae
    Copyright 1999 by the Genetics Society of America Mks1p Is a Regulator of Nitrogen Catabolism Upstream of Ure2p in Saccharomyces cerevisiae Herman K. Edskes,* John A. Hanover² and Reed B. Wickner* *Laboratory of Biochemistry and Genetics and ²Laboratory of Cell Biochemistry and Biology, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892-0830 Manuscript received April 14, 1999 Accepted for publication June 4, 1999 ABSTRACT The supply of nitrogen regulates yeast genes affecting nitrogen catabolism, pseudohyphal growth, and meiotic sporulation. Ure2p of Saccharomyces cerevisiae is a negative regulator of nitrogen catabolism that inhibits Gln3p, a positive regulator of DAL5, and other genes of nitrogen assimilation. Dal5p, the allantoate permease, allows ureidosuccinate uptake (Usa1) when cells grow on a poor nitrogen source such as proline. We ®nd that overproduction of Mks1p allows uptake of ureidosuccinate on ammonia and lack of Mks1p prevents uptake of ureidosuccinate or Dal5p expression on proline. Overexpression of Mks1p does not affect cellular levels of Ure2p. An mks1 ure2 double mutant can take up ureidosuccinate on either ammonia or proline. Moreover, overexpression of Ure2p suppresses the ability of Mks1p overexpression to allow ureidosuccinate uptake on ammonia. These results suggest that Mks1p is involved in nitrogen control upstream of Ure2p as follows: NH Mks1p Ure2p Gln3p DAL5. Either overproduction of Mks1p 3a a a ! or deletion of MKS1 interferes with pseudohyphal growth. OTH the abundance and the chemical nature of et al. 1996, 1997). Gln3p is a positively acting GATA B environmental nitrogen sources provide important transcription factor whose activity is negatively regulated cues regulating cellular events.
    [Show full text]
  • Original Article Squamous Cell Carcinoma of the Lung: Gene Expression and Network Analysis During Carcinogenesis
    Int J Clin Exp Med 2019;12(6):6671-6683 www.ijcem.com /ISSN:1940-5901/IJCEM0088518 Original Article Squamous cell carcinoma of the lung: gene expression and network analysis during carcinogenesis Angel Juarez-Flores1,2, Marco V José2 1Posgrado en Ciencias Biológicas, Unidad de Posgrado, Circuito de Posgrados, Ciudad Universitaria, Universidad Nacional Autónoma de México, CP 04510, Mexico City, Mexico; 2Theoretical Biology Group, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, CP 04510, Mexico City, Mexico Received October 31, 2019; Accepted March 12, 2019; Epub June 15, 2019; Published June 30, 2019 Abstract: Lung cancer is one of the most common and deadliest types of cancer. Most often, diagnosis is made in the later stages of the disease, with few treatment options available. Squamous cell carcinoma of the lung (SCCL) is one of the most common types of lung cancer. Knowledge concerning its carcinogenic process lags behind that of other cancers of the lungs. Aiming to understand the biological phenomena underlying each stage of the disease and unveil the most significant genes, the current study carried out bioinformatic analysis of different samples that corresponded to the carcinogenic process. New relevant genes for early diagnosis and treatment are proposed and expression profiles for each stage are presented. Based on Protein-Protein interaction networks of these genes, this study proposes that they function as gatekeepers for a wide variety of processes. MYC, MCM2, AURKA, CUL3, and DDIT4L are proposed as a possible group for treatment of SCCL. This work provides a general panorama of the transcriptome profile of SCCL, with a plethora of information regarding its carcinogenesis.
    [Show full text]
  • SUPPLEMENTARY MATERIALS and METHODS PBMC Transcriptomics
    BMJ Publishing Group Limited (BMJ) disclaims all liability and responsibility arising from any reliance Supplemental material placed on this supplemental material which has been supplied by the author(s) Gut SUPPLEMENTARY MATERIALS AND METHODS PBMC transcriptomics identifies immune-metabolism disorder during the development of HBV-ACLF Contents l Supplementary methods l Supplementary Figure 1 l Supplementary Figure 2 l Supplementary Figure 3 l Supplementary Figure 4 l Supplementary Figure 5 l Supplementary Table 1 l Supplementary Table 2 l Supplementary Table 3 l Supplementary Table 4 l Supplementary Tables 5-14 l Supplementary Table 15 l Supplementary Table 16 l Supplementary Table 17 Li J, et al. Gut 2021;0:1–13. doi: 10.1136/gutjnl-2020-323395 BMJ Publishing Group Limited (BMJ) disclaims all liability and responsibility arising from any reliance Supplemental material placed on this supplemental material which has been supplied by the author(s) Gut SUPPLEMENTARY METHODS Test for HBV DNA The levels of HBV DNA were detected using real-time PCR with a COBAS® AmpliPrep/COBAS® TaqMan 48 System (Roche, Basel, Switzerland) and HBV Test v2.0. Criteria for diagnosing cirrhosis Pathology The gold standard for the diagnosis of cirrhosis is a liver biopsy obtained through a percutaneous or transjugular approach.1 Ultrasonography was performed 2-4 hours before biopsy. Liver biopsy specimens were obtained by experienced physicians. Percutaneous transthoracic puncture of the liver was performed according to the standard criteria. After biopsy, patients were monitored in the hospital with periodic analyses of haematocrit and other vital signs for 24 hours. Cirrhosis was diagnosed according to the globally agreed upon criteria.2 Cirrhosis is defined based on its pathological features under a microscope: (a) the presence of parenchymal nodules, (b) differences in liver cell size and appearance, (c) fragmentation of the biopsy specimen, (d) fibrous septa, and (d) an altered architecture and vascular relationships.
    [Show full text]
  • WO 2016/070129 Al 6 May 2016 (06.05.2016) W P O P C T
    (12) INTERNATIONAL APPLICATION PUBLISHED UNDER THE PATENT COOPERATION TREATY (PCT) (19) World Intellectual Property Organization International Bureau (10) International Publication Number (43) International Publication Date WO 2016/070129 Al 6 May 2016 (06.05.2016) W P O P C T (51) International Patent Classification: (74) Agent: BAKER, C , Hunter; Wolf, Greenfield & Sacks, A61K 9/00 (2006.01) C07K 14/435 (2006.01) P.C., 600 Atlantic Avenue, Boston, MA 02210-2206 (US). (21) International Application Number: (81) Designated States (unless otherwise indicated, for every PCT/US20 15/058479 kind of national protection available): AE, AG, AL, AM, AO, AT, AU, AZ, BA, BB, BG, BH, BN, BR, BW, BY, (22) International Filing Date: BZ, CA, CH, CL, CN, CO, CR, CU, CZ, DE, DK, DM, 30 October 2015 (30.10.201 5) DO, DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, (25) Filing Language: English HN, HR, HU, ID, IL, IN, IR, IS, JP, KE, KG, KN, KP, KR, KZ, LA, LC, LK, LR, LS, LU, LY, MA, MD, ME, MG, (26) Publication Language: English MK, MN, MW, MX, MY, MZ, NA, NG, NI, NO, NZ, OM, (30) Priority Data: PA, PE, PG, PH, PL, PT, QA, RO, RS, RU, RW, SA, SC, 14/529,010 30 October 2014 (30. 10.2014) US SD, SE, SG, SK, SL, SM, ST, SV, SY, TH, TJ, TM, TN, TR, TT, TZ, UA, UG, US, UZ, VC, VN, ZA, ZM, ZW. (71) Applicant: PRESIDENT AND FELLOWS OF HAR¬ VARD COLLEGE [US/US]; 17 Quincy Street, Cam (84) Designated States (unless otherwise indicated, for every bridge, MA 02138 (US).
    [Show full text]
  • Table S1. 103 Ferroptosis-Related Genes Retrieved from the Genecards
    Table S1. 103 ferroptosis-related genes retrieved from the GeneCards. Gene Symbol Description Category GPX4 Glutathione Peroxidase 4 Protein Coding AIFM2 Apoptosis Inducing Factor Mitochondria Associated 2 Protein Coding TP53 Tumor Protein P53 Protein Coding ACSL4 Acyl-CoA Synthetase Long Chain Family Member 4 Protein Coding SLC7A11 Solute Carrier Family 7 Member 11 Protein Coding VDAC2 Voltage Dependent Anion Channel 2 Protein Coding VDAC3 Voltage Dependent Anion Channel 3 Protein Coding ATG5 Autophagy Related 5 Protein Coding ATG7 Autophagy Related 7 Protein Coding NCOA4 Nuclear Receptor Coactivator 4 Protein Coding HMOX1 Heme Oxygenase 1 Protein Coding SLC3A2 Solute Carrier Family 3 Member 2 Protein Coding ALOX15 Arachidonate 15-Lipoxygenase Protein Coding BECN1 Beclin 1 Protein Coding PRKAA1 Protein Kinase AMP-Activated Catalytic Subunit Alpha 1 Protein Coding SAT1 Spermidine/Spermine N1-Acetyltransferase 1 Protein Coding NF2 Neurofibromin 2 Protein Coding YAP1 Yes1 Associated Transcriptional Regulator Protein Coding FTH1 Ferritin Heavy Chain 1 Protein Coding TF Transferrin Protein Coding TFRC Transferrin Receptor Protein Coding FTL Ferritin Light Chain Protein Coding CYBB Cytochrome B-245 Beta Chain Protein Coding GSS Glutathione Synthetase Protein Coding CP Ceruloplasmin Protein Coding PRNP Prion Protein Protein Coding SLC11A2 Solute Carrier Family 11 Member 2 Protein Coding SLC40A1 Solute Carrier Family 40 Member 1 Protein Coding STEAP3 STEAP3 Metalloreductase Protein Coding ACSL1 Acyl-CoA Synthetase Long Chain Family Member 1 Protein
    [Show full text]