DOCSLIB.ORG

Supplemental Figure and Table Legends

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Supplemental Figure and Table Legends Supplemental figure and table legends Supplementary Figure 1: KIAA1841 is well conserved among vertebrates. NCBI HomoloGene pairwise alignment scores of human KIAA1841 sequence compared to other vertebrate orthologs. Supplementary Figure 2: µ-germline transcripts (GLT) and AID mRNA expression are not affected by overexpression of KIAA1841. Splenic B cells were isolated from wild-type mice, and transduced with retroviral vector control (pMIG) or a vector expressing KIAA1841. Levels of µ-GLT and AID mRNA were determined at 72h post-infection by RT-qPCR, and normalized to -actin mRNA and the pMIG control. The mean of three independent experiments +/- SD is shown. NS, p = not significant, p 0.05, two-tailed paired student’s t-test. Supplementary Figure 3: Overexpression of untagged and Xpress-tagged KIAA1841 does not affect cell proliferation. Splenic B cells were isolated from wild-type mice, stimulated with LPS+IL4, and transduced with retroviral vector control (pMIG) or a vector expressing KIAA1841 or Xpress (Xp)-tagged KIAA1841. Cells are labeled with seminaphthorhodafluor (SNARF) cell tracking dye and SNARF intensity was measured at 0h, 24h, and 48h after retroviral infection. Histograms of transduced cells (GFP+) for pMIG control, KIAA1841 and Xp-KIAA1841 were superimposed at each time point. Three independent retroviral infection experiments are shown. Supplementary Figure 4: Sequence alignment of the putative SANT domain of KIAA1841 with the SANT domain of SWI3. Alignment was performed using ClustalOmega; *, conserved residue, :, strongly similar residues, ., weakly similar residues. Numbers indicate amino acid residues in each sequence. Helix 3, which has been reported to be important for the chromatin remodeling function of SWI3 (Boyer et. al., 2002), is well conserved in KIAA1841. Supplementary Table 1: Negative regulators of CSR recovered by the shRNA screen. Genes with shRNAs showing at least 2-fold enrichment in IgA+ compared to IgA- samples, i.e. log2(Cy3/Cy5)>1, and FDR less than 10 were identified as negative regulators. The novel gene of interest, NM_027860, which encodes for the protein KIAA1841, is highlighted in yellow. Supplementary Table 2: Positive regulators of CSR recovered by the shRNA screen. Genes with shRNAs showing at least 2-fold enrichment in IgA- compared to IgA+ samples, i.e. log2(Cy3/Cy5)<-1, and FDR less than 10, were identified as positive regulators. Known positive regulator, activation-induced cytidine deaminase (Aicda), is highlighted in green. Supplementary Figure 1 2.5 NS NS 2 pMIG KIAA1841 expression 1.5 1 0.5 Relative mRNA mRNA Relative 0 µ-GLT AID Supplementary Figure 2 GFP+ gated Exp 1 Exp 2 Exp 3 pMIG KIAA1841 Xp-KIAA1841 0 hr 24 hr 48 hr SNARF Supplementary Figure 3 KIAA1841 MVLDMILYPLIGI-PQTINWETVARLVPGLTPKECVKRFDELKS------ 60 SWI3 WSKEDLQKLLKGIQEFGADWYKVAKNVGNKSPEQCILRFLQLPIEDKFLY 576 : : * ** :* .**: * . :*::*: ** :* Helix 3 Supplementary Figure 4 Supplementary Table 1: Negative regulators of CSR recovered by the shRNA screen Gene.Name log2.ratio q.value... Hit? Codex_hai Codex_97mCodex_19mCodex_Accession Codex_gene.name Codex_gene.symbol OB_ReleasOB_Plate OB_Well_ROB_Well_C 092308m1_V2MM_141890 3.829646 3.004939 TRUE HP_36260 TGCTGTTGGCTTTATC XM_157111 Mus musculus LOC212310 (LOC212310), mR. 2.4 SM2050 h 12 mPool2_V2MM_133332 3.684535 3.004939 TRUE HP_35407 TGCTGTTGGATTCTCT XM_149195 RIKEN cDNA E230025N21 gene E230025N21Rik 2.11 SM2373 e 7 mPool2_V2MM_2305 3.67322 2.205692 TRUE HP_22592 TGCTGTTGCTCCTAAAXM_132611 similar to variable region of immunoglobulin kappa light chain 2.11 SM2381 h 4 mPool7_V2MM_141895 3.615101 3.004939 TRUE HP_36260 TGCTGTTGCGCTTTAT XM_157111 Mus musculus LOC212310 (LOC212310), mRNA. 2.1 SM2329 a 8 mPool7_V2MM_88676 3.592123 2.205692 TRUE HP_31011 TGCTGTTGGTACAGATNM_175463 RIKEN cDNA A930012O16 gene A930012O16Rik 2.9 SM2257 e 8 mPool7_V2MM_88676 3.592123 2.205692 TRUE HP_31011 TGCTGTTGGTACAGATNM_175463 RIKEN cD A930012O16 gene A930012O16Rik 2.9 SM2257 e 8 mPool2_V2MM_145554 3.486776 3.004939 TRUE HP_36626 TGCTGTTGCATTCTTATXM_161053 Mus musculus LOC230170 (LOC230170), mR. 2.4 SM2040 e 9 mPool2_V2MM_145554 3.486776 3.004939 TRUE HP_36626 TGCTGTTGCATTCTTATXM_161053 Mus musculus LOC230170 (LOC230170), mRNA. 2.4 SM2040 e 9 mPool2_V2MM_92494 3.390594 3.004939 TRUE HP_31384 TGCTGTTGGTTGGAATNM_178720 RIKEN cDNA 9430016A21 gene 9430016A21Rik 2.6 SM2137 a 5 mPool2_V2MM_138848 3.381957 2.205692 TRUE HP_35956 TGCTGTTGGACATTAAXM_154566 Mus musculus LOC238925 (LOC238925), mR. 2.4 SM2030 d 11 mPool2_V2MM_138848 3.381957 2.205692 TRUE HP_35956 TGCTGTTGGACATTAAXM_154566 Mus musculus LOC238925 (LOC238925), mRNA. 2.4 SM2030 d 11 mPool2_V2MM_134275 3.329965 2.205692 TRUE HP_35500 TGCTGTTGGGCTAGTTXM_357654 hypothetical LOC384452 2.11 SM2368 f 8 mPool7_V2MM_199459 3.328607 2.205692 TRUE HP_41750 TGCTGTTGCCATTTAA XM_289192 Mus musculus LOC332813 (LOC332813), mRNA. 2.9 SM2276 c 3 mPool2_V2MM_17530 3.318772 2.205692 TRUE HP_240804TGCTGTTGGATACTTT NM_134054 RIKEN cDNA 1110002B05 gene 1110002B05Rik 2.11 SM2378 g 1 092308m1_V2MM_171708 3.314424 1.959154 TRUE HP_39219 TGCTGTTGCATGTTAGXM_286679 Mus musculus hypothetical gene supported by AK039985 (LOC328540), mR. 2.5 SM2074 b 9 mPool2_V2MM_36734 3.311664 3.004939 TRUE HP_25950 TGCTGTTGCTTGTACANM_023816 RIKEN cDNA 1700012M14 gene 1700012M14Rik 2.11 SM2392 a 9 mPool2_V2MM_84705 3.309396 3.004939 TRUE HP_14696 TGCTGTTGCTAATCAT NM_028930 transmembrane channel‐like gene family 5 Tmc5 2.6 SM2137 b 10 092308m1_V2MM_121144 3.273188 3.004939 TRUE HP_34202 TGCTGTTGCGGCATCTXM_141454 Mus musculus similar to lactate dehydrogese [Mus musculus] (LOC228430), mR. 2.6 SM2106 g 6 092308m1_V2MM_124008 3.268085 2.205692 TRUE HP_34486 TGCTGTTGGTCTGGAAXM_143251 Mus musculus similar to hypothetical protein [Macaca fascicularis] (LOC242043), 2.6 SM2102 b 7 mPool7_V2MM_113184 3.252594 2.205692 TRUE HP_334174TGCTGTTGCTACATTC XM_136853 Mus musculus LOC241181 (LOC241181), mRNA. 2.1 SM2304 d 4 mPool2_V2MM_120733 3.242869 2.205692 TRUE HP_34162 TGCTGTTGGAAATTTCXM_141156 Mus musculus similar to olfactory receptor MOR264‐19 [Mus musculus] (LOC228 2.11 SM2359 f 5 mPool7_V2MM_79723 3.198836 3.004939 TRUE HP_30137 TGCTGTTGGCCAGGATNM_009828 cyclin A2 Ccna2 2.8 SM2227 d 7 092308m1_V2MM_159994 3.196066 2.205692 TRUE HP_38058 TGCTGTTGCATCTAACAK048916 cD sequence BC052055 BC052055 2.6 SM2115 f 1 mPool2_V2MM_14135 3.188079 2.205692 TRUE HP_23748 TGCTGTTGCCCTGAAANM_007672 cerebellar degeneration‐related 2 Cdr2 2.11 SM2379 d 10 mPool2_V2MM_212177 3.187273 1.959154 TRUE HP_42985 TGCTGTTGCTTCTATCCXM_148779 RIKEN cDNA 4930541O19 gene 4930541O19Rik 2.11 SM2365 f 7 mPool2_V2MM_17214 3.164486 2.205692 TRUE HP_240494TGCTGTTGGAGCTAAANM_011623 topoisomerase (DNA) II alpha Top2a 2.11 SM2387 h 6 mPool7_V2MM_67258 3.157407 2.205692 TRUE HP_28924 TGCTGTTGCCGTTTGCNM_021546 amyloid beta (A4) precursor protein‐binding, family A, m Apba2bp 2.8 SM2237 d 7 mPool2_V2MM_208999 3.152098 3.004939 TRUE HP_42677 TGCTGTTGCTCAGGAAXM_157672 similar to Suppressor of G2 allele of SKP1 homolog (Sgt1) (Putative 40‐6‐3 protein 2.1 SM2338 a 5 mPool2_V2MM_94467 3.148552 2.205692 TRUE HP_31575 TGCTGTTGCAGCATGTBC052532 cDNA sequence BC006779 BC006779 2.6 SM2142 a 7 mPool7_V2MM_202647 3.143102 2.205692 TRUE HP_42064 TGCTGTTGGTATGATTAK045028 histone deacetylase 10 Hdac10 2.1 SM2317 h 10 mPool2_V2MM_1433 3.143072 2.205692 TRUE HP_225074TGCTGTTGCCGCATACNM_007855 twist homolog 2 (Drosophila) Twist2 2.11 SM2386 g 12 mPool2_V2MM_134121 3.135473 3.004939 TRUE HP_35484 TGCTGTTGCTGTCTTTANM_177582 hypothetical protein B930074I24 2.1 SM2349 h 4 092308m1_V2MM_180277 3.099315 2.205692 TRUE HP_40075 TGCTGTTGCTTTAGAT XM_288480 Mus musculus LOC331828 (LOC331828), mRNA. 2.5 SM2072 h 3 092308m1_V2MM_180277 3.099315 2.205692 TRUE HP_40075 TGCTGTTGCTTTAGAT XM_288480 Mus musculus LOC331828 (LOC331828), mR. 2.5 SM2072 h 3 092308m1_V2MM_156420 3.091247 2.205692 TRUE HP_37705 TGCTGTTGCTGCTTTA NM_027860 RIKEN cD 0610010F05 gene 0610010F05Rik 2.6 SM2115 e 4 092308m1_V2MM_70303 3.088266 3.004939 TRUE HP_29221 TGCTGTTGCAACCAATNM_028911 RIKEN cD 4933414I15 gene 4933414I15Rik 2.3 SM2006 e 3 mPool7_V2MM_197834 3.086251 2.205692 TRUE HP_41589 TGCTGTTGGATGATAAXM_111554 similar to Aspartate aminotransferase, mitochondrial precursor (Transamise A) (G 2.9 SM2266 b 12 mPool7_V2MM_197834 3.086251 2.205692 TRUE HP_41589 TGCTGTTGGATGATAAXM_111554 similar to Aspartate aminotransferase, mitochondrial precursor (Transaminase A) 2.9 SM2266 b 12 mPool7_V2MM_205300 3.075308 2.205692 TRUE HP_42316 TGCTGTTGCAAAGTTCXM_138746 Mus musculus similar to thymine D glycosylase [Mus musculus] (LOC238743), mR 2.1 SM2306 d 1 mPool7_V2MM_205300 3.075308 2.205692 TRUE HP_42316 TGCTGTTGCAAAGTTCXM_138746 Mus musculus similar to thymine DNA glycosylase [Mus musculus] (LOC238743), 2.1 SM2306 d 1 092308m1_V2MM_135215 3.072112 1.959154 TRUE HP_35593 TGCTGTTGCTTTATTTCXM_489372 similar to RIKEN cD 6720401G13 gene 2.5 SM2057 a 3 mPool2_V2MM_212145 3.039733 3.004939 TRUE HP_42982 TGCTGTTGCCCTTTAA AK017143 RIKEN cDNA 5031425E22 gene 5031425E22Rik 2.11 SM2362 d 9 mPool7_V2MM_144853 3.031093 2.205692 TRUE HP_365564TGCTGTTGGAGCTTATXM_160377 Mus musculus LOC229769 (LOC229769), mRNA. 2.1 SM2331 f 2 092308m1_V2MM_155240 3.030417 2.205692 TRUE HP_37588 TGCTGTTGGCCTGAAAXM_197286 Mus musculus LOC271407 (LOC271407), mR. 2.6 SM2114 g 7 mPool2_V2MM_106531 3.008607 3.004939 TRUE HP_32763 TGCTGTTGGAAACATCNM_001002927 preproenkephalin 1 Penk1 2.1 SM2316 h 4 mPool2_V2MM_210729 3.001055 2.205692 TRUE HP_42846 TGCTGTTGCGCAGTTAXM_359191 gene model 1773, (NCBI) Gm1773 2.11 SM2363 b 5 mPool2_V2MM_123973
Load more

Recommended publications
  • Old Data and Friends Improve with Age: Advancements with the Updated Tools of Genenetwork
    bioRxiv preprint doi: https://doi.org/10.1101/2021.05.24.445383; this version posted May 25, 2021. 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. Old data and friends improve with age: Advancements with the updated tools of GeneNetwork Alisha Chunduri1, David G. Ashbrook2 1Department of Biotechnology, Chaitanya Bharathi Institute of Technology, Hyderabad 500075, India 2Department of Genetics, Genomics and Informatics, University of Tennessee Health Science Center, Memphis, TN 38163, USA Abstract Understanding gene-by-environment interactions is important across biology, particularly behaviour. Families of isogenic strains are excellently placed, as the same genome can be tested in multiple environments. The BXD’s recent expansion to 140 strains makes them the largest family of murine isogenic genomes, and therefore give great power to detect QTL. Indefinite reproducible genometypes can be leveraged; old data can be reanalysed with emerging tools to produce novel biological insights. To highlight the importance of reanalyses, we obtained drug- and behavioural-phenotypes from Philip et al. 2010, and reanalysed their data with new genotypes from sequencing, and new models (GEMMA and R/qtl2). We discover QTL on chromosomes 3, 5, 9, 11, and 14, not found in the original study. We narrowed down the candidate genes based on their ability to alter gene expression and/or protein function, using cis-eQTL analysis, and variants predicted to be deleterious. Co-expression analysis (‘gene friends’) and human PheWAS were used to further narrow candidates.
    [Show full text]
  • Whole-Genome Microarray Detects Deletions and Loss of Heterozygosity of Chromosome 3 Occurring Exclusively in Metastasizing Uveal Melanoma
    Anatomy and Pathology Whole-Genome Microarray Detects Deletions and Loss of Heterozygosity of Chromosome 3 Occurring Exclusively in Metastasizing Uveal Melanoma Sarah L. Lake,1 Sarah E. Coupland,1 Azzam F. G. Taktak,2 and Bertil E. Damato3 PURPOSE. To detect deletions and loss of heterozygosity of disease is fatal in 92% of patients within 2 years of diagnosis. chromosome 3 in a rare subset of fatal, disomy 3 uveal mela- Clinical and histopathologic risk factors for UM metastasis noma (UM), undetectable by fluorescence in situ hybridization include large basal tumor diameter (LBD), ciliary body involve- (FISH). ment, epithelioid cytomorphology, extracellular matrix peri- ϩ ETHODS odic acid-Schiff-positive (PAS ) loops, and high mitotic M . Multiplex ligation-dependent probe amplification 3,4 5 (MLPA) with the P027 UM assay was performed on formalin- count. Prescher et al. showed that a nonrandom genetic fixed, paraffin-embedded (FFPE) whole tumor sections from 19 change, monosomy 3, correlates strongly with metastatic death, and the correlation has since been confirmed by several disomy 3 metastasizing UMs. Whole-genome microarray analy- 3,6–10 ses using a single-nucleotide polymorphism microarray (aSNP) groups. Consequently, fluorescence in situ hybridization were performed on frozen tissue samples from four fatal dis- (FISH) detection of chromosome 3 using a centromeric probe omy 3 metastasizing UMs and three disomy 3 tumors with Ͼ5 became routine practice for UM prognostication; however, 5% years’ metastasis-free survival. to 20% of disomy 3 UM patients unexpectedly develop metas- tases.11 Attempts have therefore been made to identify the RESULTS. Two metastasizing UMs that had been classified as minimal region(s) of deletion on chromosome 3.12–15 Despite disomy 3 by FISH analysis of a small tumor sample were found these studies, little progress has been made in defining the key on MLPA analysis to show monosomy 3.
    [Show full text]
  • Methods Mouse Strains and Housing Male Wild-Type Mice
    Methods Mouse strains and housing Male wild-type mice (C57BL/6J background) and B6.Cg-Tg (APPSwFlLon, PSEN1*M146L*L286V) 6799Vas/Mmjax (5xFAD, JAX 008730) were purchased from the Jackson Laboratory. μMT-/- mice which are deficient in B cells were purchased from Shanghai Model Organisms Center, Inc. Both B6.Cg-Tg and μMT-/- mice were bred on a C57BL/6J background. 5xFAD mice and μMT-/- mice were crossed to generate μMT-/-/5xFAD mice. The mice were used at different ages that are indicated throughout the manuscript. Mice of all strains were specific pathogen free environment with controlled temperature and humidity, on 12 h light: dark cycles (lights on at 7:00), and fed with regular rodent’s chow and sterilized tap water ad libitum. All experiments were approved by the Institutional Animal Care and Use Committee of the Nanjing Medical University. Human samples Frontal cortex tissues were obtained from 4 cases within 4-6 h of death, via informed donation for the Medical Education and Research of Nanjing Medical University, with corresponding written consents prepared by the donors and their families. Cases that were died from brain associated diseases were excluded from this study. The utilization of human tissues was approved by the Ethics Committee of Nanjing Medical University. All obtained samples were fixed in a 4% formalin solution and kept in paraffin blocks until further sectioning. Animal surgery DcLN ligation: The procedure of surgical ligation of the lymphatics afferent to the dcLNs was according to published literature (3, 30). In brief, mice were anaesthetized by i.p. injection with ketamine and xylazine in saline, and fixed on a stereotaxic apparatus in a supine position.
    [Show full text]
  • The Popeye Domain Containing Protein Family E a Novel Class of Camp Effectors with Important Functions in Multiple Tissues
    Progress in Biophysics and Molecular Biology xxx (2016) 1e9 Contents lists available at ScienceDirect Progress in Biophysics and Molecular Biology journal homepage: www.elsevier.com/locate/pbiomolbio The Popeye domain containing protein family e A novel class of cAMP effectors with important functions in multiple tissues * Roland F.R. Schindler, Thomas Brand Heart Science Centre, National Heart and Lung Institute (NHLI), Imperial College London, United Kingdom article info abstract Article history: Popeye domain containing (Popdc) proteins are a unique family, which combine several different Received 16 September 2015 properties and functions in a surprisingly complex fashion. They are expressed in multiple tissues and Received in revised form cell types, present in several subcellular compartments, interact with different classes of proteins, and 3 December 2015 are associated with a variety of physiological and pathophysiological processes. Moreover, Popdc proteins Accepted 4 January 2016 bind the second messenger cAMP with high affinity and it is thought that they act as a novel class of Available online xxx cAMP effector proteins. Here, we will review the most important findings about the Popdc family, which accumulated since its discovery about 15 years ago. We will be focussing on Popdc protein interaction Keywords: Popeye domain containing genes and function in striated muscle tissue. However, as a full picture only emerges if all aspects are taken into cAMP account, we will also describe what is currently known about the role of Popdc proteins in epithelial cells Proteineprotein interaction and in various types of cancer, and discuss these findings with regard to their relevance for cardiac and Ion channel skeletal muscle.
    [Show full text]
  • Meta-Analysis of Nasopharyngeal Carcinoma
    BMC Genomics BioMed Central Research article Open Access Meta-analysis of nasopharyngeal carcinoma microarray data explores mechanism of EBV-regulated neoplastic transformation Xia Chen†1,2, Shuang Liang†1, WenLing Zheng1,3, ZhiJun Liao1, Tao Shang1 and WenLi Ma*1 Address: 1Institute of Genetic Engineering, Southern Medical University, Guangzhou, PR China, 2Xiangya Pingkuang associated hospital, Pingxiang, Jiangxi, PR China and 3Southern Genomics Research Center, Guangzhou, Guangdong, PR China Email: Xia Chen - [email protected]; Shuang Liang - [email protected]; WenLing Zheng - [email protected]; ZhiJun Liao - [email protected]; Tao Shang - [email protected]; WenLi Ma* - [email protected] * Corresponding author †Equal contributors Published: 7 July 2008 Received: 16 February 2008 Accepted: 7 July 2008 BMC Genomics 2008, 9:322 doi:10.1186/1471-2164-9-322 This article is available from: http://www.biomedcentral.com/1471-2164/9/322 © 2008 Chen et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Background: Epstein-Barr virus (EBV) presumably plays an important role in the pathogenesis of nasopharyngeal carcinoma (NPC), but the molecular mechanism of EBV-dependent neoplastic transformation is not well understood. The combination of bioinformatics with evidences from biological experiments paved a new way to gain more insights into the molecular mechanism of cancer. Results: We profiled gene expression using a meta-analysis approach. Two sets of meta-genes were obtained. Meta-A genes were identified by finding those commonly activated/deactivated upon EBV infection/reactivation.
    [Show full text]
  • Environmental Influences on Endothelial Gene Expression
    ENDOTHELIAL CELL GENE EXPRESSION John Matthew Jeff Herbert Supervisors: Prof. Roy Bicknell and Dr. Victoria Heath PhD thesis University of Birmingham August 2012 University of Birmingham Research Archive e-theses repository This unpublished thesis/dissertation is copyright of the author and/or third parties. The intellectual property rights of the author or third parties in respect of this work are as defined by The Copyright Designs and Patents Act 1988 or as modified by any successor legislation. Any use made of information contained in this thesis/dissertation must be in accordance with that legislation and must be properly acknowledged. Further distribution or reproduction in any format is prohibited without the permission of the copyright holder. ABSTRACT Tumour angiogenesis is a vital process in the pathology of tumour development and metastasis. Targeting markers of tumour endothelium provide a means of targeted destruction of a tumours oxygen and nutrient supply via destruction of tumour vasculature, which in turn ultimately leads to beneficial consequences to patients. Although current anti -angiogenic and vascular targeting strategies help patients, more potently in combination with chemo therapy, there is still a need for more tumour endothelial marker discoveries as current treatments have cardiovascular and other side effects. For the first time, the analyses of in-vivo biotinylation of an embryonic system is performed to obtain putative vascular targets. Also for the first time, deep sequencing is applied to freshly isolated tumour and normal endothelial cells from lung, colon and bladder tissues for the identification of pan-vascular-targets. Integration of the proteomic, deep sequencing, public cDNA libraries and microarrays, delivers 5,892 putative vascular targets to the science community.
    [Show full text]
  • Genetic and Genomic Analysis of Hyperlipidemia, Obesity and Diabetes Using (C57BL/6J × TALLYHO/Jngj) F2 Mice
    University of Tennessee, Knoxville TRACE: Tennessee Research and Creative Exchange Nutrition Publications and Other Works Nutrition 12-19-2010 Genetic and genomic analysis of hyperlipidemia, obesity and diabetes using (C57BL/6J × TALLYHO/JngJ) F2 mice Taryn P. Stewart Marshall University Hyoung Y. Kim University of Tennessee - Knoxville, [email protected] Arnold M. Saxton University of Tennessee - Knoxville, [email protected] Jung H. Kim Marshall University Follow this and additional works at: https://trace.tennessee.edu/utk_nutrpubs Part of the Animal Sciences Commons, and the Nutrition Commons Recommended Citation BMC Genomics 2010, 11:713 doi:10.1186/1471-2164-11-713 This Article is brought to you for free and open access by the Nutrition at TRACE: Tennessee Research and Creative Exchange. It has been accepted for inclusion in Nutrition Publications and Other Works by an authorized administrator of TRACE: Tennessee Research and Creative Exchange. For more information, please contact [email protected]. Stewart et al. BMC Genomics 2010, 11:713 http://www.biomedcentral.com/1471-2164/11/713 RESEARCH ARTICLE Open Access Genetic and genomic analysis of hyperlipidemia, obesity and diabetes using (C57BL/6J × TALLYHO/JngJ) F2 mice Taryn P Stewart1, Hyoung Yon Kim2, Arnold M Saxton3, Jung Han Kim1* Abstract Background: Type 2 diabetes (T2D) is the most common form of diabetes in humans and is closely associated with dyslipidemia and obesity that magnifies the mortality and morbidity related to T2D. The genetic contribution to human T2D and related metabolic disorders is evident, and mostly follows polygenic inheritance. The TALLYHO/ JngJ (TH) mice are a polygenic model for T2D characterized by obesity, hyperinsulinemia, impaired glucose uptake and tolerance, hyperlipidemia, and hyperglycemia.
    [Show full text]
  • Silkworm Z Chromosome Is Enriched in Testis-Specific Genes
    Supporting Information http://www.genetics.org/cgi/content/full/genetics.108.099994/DC1 Silkworm Z Chromosome is Enriched in Testis-Specific Genes K. P. Arunkumar, Kazuei Mita and J. Nagaraju Copyright © 2009 by the Genetics Society of America DOI: 10.1534/genetics.108.099994 2 SI K. Arunkumar et al. File S1 Gene Ontology annotation GO annotation generates a dynamic controlled vocabulary that can be applied to all organisms, even while knowledge of gene and protein roles in cells is still accumulating and changing. To this end, the Seqdblite FASTA sequence flat file was downloaded from the GO database. By running BLAST against Seqdblite, closest homologue was identified. From BLAST output, molecular functions, biological processes and cellular localisation were parsed by building an in-house GO database in MySQL from the GO-term-database flat file, downloaded from Gene Ontology Database Downloads (http://www.godatabase.org/dev/). The Perl-DBI was used to interface with MySQL, to extract the parent terms of each individual GO term that are obtained by parsing BLAST output. The output was then represented graphically. All ESTs were assigned a biological process, molecular function and cellular component using Gene Ontology (GO) database. The closest annotated homologue in the GO database was used for assigning these categories. The results of the GO annotation are graphically represented in Figures S1-3. Many of the gene products were found to be localized in cell (42%). In cell, gene products were predominant in intracellular region (78%) which comprised of localizations in intracellular organelle (38%) and cytoplasm (29%). The other localizations were organelle (29%) followed by protein complex (18%) (Figure S1).
    [Show full text]
  • 1 Supporting Information for a Microrna Network Regulates
    Supporting Information for A microRNA Network Regulates Expression and Biosynthesis of CFTR and CFTR-ΔF508 Shyam Ramachandrana,b, Philip H. Karpc, Peng Jiangc, Lynda S. Ostedgaardc, Amy E. Walza, John T. Fishere, Shaf Keshavjeeh, Kim A. Lennoxi, Ashley M. Jacobii, Scott D. Rosei, Mark A. Behlkei, Michael J. Welshb,c,d,g, Yi Xingb,c,f, Paul B. McCray Jr.a,b,c Author Affiliations: Department of Pediatricsa, Interdisciplinary Program in Geneticsb, Departments of Internal Medicinec, Molecular Physiology and Biophysicsd, Anatomy and Cell Biologye, Biomedical Engineeringf, Howard Hughes Medical Instituteg, Carver College of Medicine, University of Iowa, Iowa City, IA-52242 Division of Thoracic Surgeryh, Toronto General Hospital, University Health Network, University of Toronto, Toronto, Canada-M5G 2C4 Integrated DNA Technologiesi, Coralville, IA-52241 To whom correspondence should be addressed: Email: [email protected] (M.J.W.); yi- [email protected] (Y.X.); Email: [email protected] (P.B.M.) This PDF file includes: Materials and Methods References Fig. S1. miR-138 regulates SIN3A in a dose-dependent and site-specific manner. Fig. S2. miR-138 regulates endogenous SIN3A protein expression. Fig. S3. miR-138 regulates endogenous CFTR protein expression in Calu-3 cells. Fig. S4. miR-138 regulates endogenous CFTR protein expression in primary human airway epithelia. Fig. S5. miR-138 regulates CFTR expression in HeLa cells. Fig. S6. miR-138 regulates CFTR expression in HEK293T cells. Fig. S7. HeLa cells exhibit CFTR channel activity. Fig. S8. miR-138 improves CFTR processing. Fig. S9. miR-138 improves CFTR-ΔF508 processing. Fig. S10. SIN3A inhibition yields partial rescue of Cl- transport in CF epithelia.
    [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]
  • Macropinocytosis Requires Gal-3 in a Subset of Patient-Derived Glioblastoma Stem Cells
    ARTICLE https://doi.org/10.1038/s42003-021-02258-z OPEN Macropinocytosis requires Gal-3 in a subset of patient-derived glioblastoma stem cells Laetitia Seguin1,8, Soline Odouard2,8, Francesca Corlazzoli 2,8, Sarah Al Haddad2, Laurine Moindrot2, Marta Calvo Tardón3, Mayra Yebra4, Alexey Koval5, Eliana Marinari2, Viviane Bes3, Alexandre Guérin 6, Mathilde Allard2, Sten Ilmjärv6, Vladimir L. Katanaev 5, Paul R. Walker3, Karl-Heinz Krause6, Valérie Dutoit2, ✉ Jann N. Sarkaria 7, Pierre-Yves Dietrich2 & Érika Cosset 2 Recently, we involved the carbohydrate-binding protein Galectin-3 (Gal-3) as a druggable target for KRAS-mutant-addicted lung and pancreatic cancers. Here, using glioblastoma patient-derived stem cells (GSCs), we identify and characterize a subset of Gal-3high glio- 1234567890():,; blastoma (GBM) tumors mainly within the mesenchymal subtype that are addicted to Gal-3- mediated macropinocytosis. Using both genetic and pharmacologic inhibition of Gal-3, we showed a significant decrease of GSC macropinocytosis activity, cell survival and invasion, in vitro and in vivo. Mechanistically, we demonstrate that Gal-3 binds to RAB10, a member of the RAS superfamily of small GTPases, and β1 integrin, which are both required for macro- pinocytosis activity and cell survival. Finally, by defining a Gal-3/macropinocytosis molecular signature, we could predict sensitivity to this dependency pathway and provide proof-of- principle for innovative therapeutic strategies to exploit this Achilles’ heel for a significant and unique subset of GBM patients. 1 University Côte d’Azur, CNRS UMR7284, INSERM U1081, Institute for Research on Cancer and Aging (IRCAN), Nice, France. 2 Laboratory of Tumor Immunology, Department of Oncology, Center for Translational Research in Onco-Hematology, Swiss Cancer Center Léman (SCCL), Geneva University Hospitals, University of Geneva, Geneva, Switzerland.
    [Show full text]
  • Análise Integrativa De Perfis Transcricionais De Pacientes Com
    UNIVERSIDADE DE SÃO PAULO FACULDADE DE MEDICINA DE RIBEIRÃO PRETO PROGRAMA DE PÓS-GRADUAÇÃO EM GENÉTICA ADRIANE FEIJÓ EVANGELISTA Análise integrativa de perfis transcricionais de pacientes com diabetes mellitus tipo 1, tipo 2 e gestacional, comparando-os com manifestações demográficas, clínicas, laboratoriais, fisiopatológicas e terapêuticas Ribeirão Preto – 2012 ADRIANE FEIJÓ EVANGELISTA Análise integrativa de perfis transcricionais de pacientes com diabetes mellitus tipo 1, tipo 2 e gestacional, comparando-os com manifestações demográficas, clínicas, laboratoriais, fisiopatológicas e terapêuticas Tese apresentada à Faculdade de Medicina de Ribeirão Preto da Universidade de São Paulo para obtenção do título de Doutor em Ciências. Área de Concentração: Genética Orientador: Prof. Dr. Eduardo Antonio Donadi Co-orientador: Prof. Dr. Geraldo A. S. Passos Ribeirão Preto – 2012 AUTORIZO A REPRODUÇÃO E DIVULGAÇÃO TOTAL OU PARCIAL DESTE TRABALHO, POR QUALQUER MEIO CONVENCIONAL OU ELETRÔNICO, PARA FINS DE ESTUDO E PESQUISA, DESDE QUE CITADA A FONTE. FICHA CATALOGRÁFICA Evangelista, Adriane Feijó Análise integrativa de perfis transcricionais de pacientes com diabetes mellitus tipo 1, tipo 2 e gestacional, comparando-os com manifestações demográficas, clínicas, laboratoriais, fisiopatológicas e terapêuticas. Ribeirão Preto, 2012 192p. Tese de Doutorado apresentada à Faculdade de Medicina de Ribeirão Preto da Universidade de São Paulo. Área de Concentração: Genética. Orientador: Donadi, Eduardo Antonio Co-orientador: Passos, Geraldo A. 1. Expressão gênica – microarrays 2. Análise bioinformática por module maps 3. Diabetes mellitus tipo 1 4. Diabetes mellitus tipo 2 5. Diabetes mellitus gestacional FOLHA DE APROVAÇÃO ADRIANE FEIJÓ EVANGELISTA Análise integrativa de perfis transcricionais de pacientes com diabetes mellitus tipo 1, tipo 2 e gestacional, comparando-os com manifestações demográficas, clínicas, laboratoriais, fisiopatológicas e terapêuticas.
    [Show full text]