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Supplemental Information to Mammadova-Bach Et Al., “Laminin Α1 Orchestrates VEGFA Functions in the Ecosystem of Colorectal Carcinogenesis”
Supplemental information to Mammadova-Bach et al., “Laminin α1 orchestrates VEGFA functions in the ecosystem of colorectal carcinogenesis” Supplemental material and methods Cloning of the villin-LMα1 vector The plasmid pBS-villin-promoter containing the 3.5 Kb of the murine villin promoter, the first non coding exon, 5.5 kb of the first intron and 15 nucleotides of the second villin exon, was generated by S. Robine (Institut Curie, Paris, France). The EcoRI site in the multi cloning site was destroyed by fill in ligation with T4 polymerase according to the manufacturer`s instructions (New England Biolabs, Ozyme, Saint Quentin en Yvelines, France). Site directed mutagenesis (GeneEditor in vitro Site-Directed Mutagenesis system, Promega, Charbonnières-les-Bains, France) was then used to introduce a BsiWI site before the start codon of the villin coding sequence using the 5’ phosphorylated primer: 5’CCTTCTCCTCTAGGCTCGCGTACGATGACGTCGGACTTGCGG3’. A double strand annealed oligonucleotide, 5’GGCCGGACGCGTGAATTCGTCGACGC3’ and 5’GGCCGCGTCGACGAATTCACGC GTCC3’ containing restriction site for MluI, EcoRI and SalI were inserted in the NotI site (present in the multi cloning site), generating the plasmid pBS-villin-promoter-MES. The SV40 polyA region of the pEGFP plasmid (Clontech, Ozyme, Saint Quentin Yvelines, France) was amplified by PCR using primers 5’GGCGCCTCTAGATCATAATCAGCCATA3’ and 5’GGCGCCCTTAAGATACATTGATGAGTT3’ before subcloning into the pGEMTeasy vector (Promega, Charbonnières-les-Bains, France). After EcoRI digestion, the SV40 polyA fragment was purified with the NucleoSpin Extract II kit (Machery-Nagel, Hoerdt, France) and then subcloned into the EcoRI site of the plasmid pBS-villin-promoter-MES. Site directed mutagenesis was used to introduce a BsiWI site (5’ phosphorylated AGCGCAGGGAGCGGCGGCCGTACGATGCGCGGCAGCGGCACG3’) before the initiation codon and a MluI site (5’ phosphorylated 1 CCCGGGCCTGAGCCCTAAACGCGTGCCAGCCTCTGCCCTTGG3’) after the stop codon in the full length cDNA coding for the mouse LMα1 in the pCIS vector (kindly provided by P. -
Electronic Supplementary Material (ESI) for Molecular Biosystems
Electronic Supplementary Material (ESI) for Molecular BioSystems. This journal is © The Royal Society of Chemistry 2015 Table S5 Mass data of proteins identified with label free shotgun proteomics a #Alt. Proteins; b Scores; c #Peptides; d SC [%]; e RMS90 [ppm]; f Rank; g Median(Controls:GLP1); h #(Controls:GLP1); i CV [%](Controls:GLP1); l Median(Controls:Palmitate); m #(Controls:Palmitate) ; n CV [%](Controls:Palmitate); o Median(Controls:GLP1 + Palmitate); p #(Controls:GLP1 + Palmitate); q CV [%](Controls:GLP1 + Palmitate) MW OK Accession Protein pI a b c d e f g h i l m n o p q [kDa] 78 kDa glucose-regulated protein OS=Rattus 1672.6 true GRP78_RAT 72.3 4.9 1 22 39 1.48 1 1.16 6 20.53 1.18 9 9.56 1.24 10 13.52 norvegicus GN=Hspa5 PE=1 SV=1 (M:1672.6) Endoplasmin OS=Rattus norvegicus 1253.0 true ENPL_RAT 92.7 4.6 1 23 29 3.34 2 0.85 8 33.34 1.19 6 39.58 1.18 10 28.11 GN=Hsp90b1 PE=1 SV=2 (M:1253.0) Stress-70 protein, mitochondrial OS=Rattus 1138.8 true GRP75_RAT 73.8 5.9 1 17 28.7 1.18 3 1.21 5 7.62 0.78 1 1.1 8 8.04 norvegicus GN=Hspa9 PE=1 SV=3 (M:1138.8) Protein disulfide-isomerase A3 OS=Rattus 1035.4 true PDIA3_RAT 56.6 5.8 1 16 35.2 2.84 4 0.94 3 17.22 1.15 4 26.62 1.25 4 7.86 norvegicus GN=Pdia3 PE=1 SV=2 (M:1035.4) Aconitate hydratase, mitochondrial 983.8 true ACON_RAT OS=Rattus norvegicus GN=Aco2 PE=1 85.4 8.7 1 19 31.4 2.72 5 0.89 2 23.6 1.21 2 9.25 0.89 3 32.87 (M:983.8) SV=2 60 kDa heat shock protein, mitochondrial 906.9 true CH60_RAT OS=Rattus norvegicus GN=Hspd1 PE=1 60.9 5.8 1 13 32.5 3.26 6 1.05 5 13.15 1.01 2 32.54 1.01 -
CYB5R3 Gene Cytochrome B5 Reductase 3
CYB5R3 gene cytochrome b5 reductase 3 Normal Function The CYB5R3 gene provides instruction for making an enzyme called cytochrome b5 reductase 3. This enzyme is involved in transferring negatively charged particles called electrons from one molecule to another. Two versions (isoforms) of this enzyme are produced from the CYB5R3 gene. The soluble isoform is present only in red blood cells, and the membrane-bound isoform is found in all other cell types. Normal red blood cells contain molecules of iron-containing hemoglobin, which deliver oxygen to the body's tissues. The iron in hemoglobin is ferrous (Fe2+), but it can spontaneously become ferric (Fe3+). Hemoglobin that contains ferric iron is called methemoglobin, and it cannot deliver oxygen. The soluble isoform of cytochrome b5 reductase 3 changes ferric iron back to ferrous iron so hemoglobin can function. Normally, red blood cells contain less than 2 percent methemoglobin. The membrane-bound isoform is embedded in the membranes of various cellular compartments and is widely used in the body. This isoform is necessary for many chemical reactions, including the breakdown and formation of fatty acids, the formation of cholesterol, and the breakdown of various molecules and drugs. Health Conditions Related to Genetic Changes Autosomal recessive congenital methemoglobinemia More than 65 mutations in the CYB5R3 gene have been found to cause autosomal recessive congenital methemoglobinemia types I and II. Most of these CYB5R3 gene mutations cause autosomal recessive congenital methemoglobinemia type I, which is characterized by a lack of oxygen in the body's tissues and bluish appearance of the skin, lips, and nails (cyanosis). -
Murine Neonatal Ketogenesis Preserves Mitochondrial Energetics by Preventing Protein Hyperacetylation
ARTICLES https://doi.org/10.1038/s42255-021-00342-6 Murine neonatal ketogenesis preserves mitochondrial energetics by preventing protein hyperacetylation Yuichiro Arima 1,2,13 ✉ , Yoshiko Nakagawa3,13, Toru Takeo 3,13, Toshifumi Ishida 1, Toshihiro Yamada1, Shinjiro Hino4, Mitsuyoshi Nakao4, Sanshiro Hanada 2, Terumasa Umemoto 2, Toshio Suda2, Tetsushi Sakuma 5, Takashi Yamamoto5, Takehisa Watanabe6, Katsuya Nagaoka6, Yasuhito Tanaka6, Yumiko K. Kawamura7,8, Kazuo Tonami7, Hiroki Kurihara7, Yoshifumi Sato9, Kazuya Yamagata9,10, Taishi Nakamura 1,11, Satoshi Araki1, Eiichiro Yamamoto1, Yasuhiro Izumiya1,12, Kenji Sakamoto1, Koichi Kaikita1, Kenichi Matsushita 1, Koichi Nishiyama2, Naomi Nakagata3 and Kenichi Tsujita1,10 Ketone bodies are generated in the liver and allow for the maintenance of systemic caloric and energy homeostasis during fasting and caloric restriction. It has previously been demonstrated that neonatal ketogenesis is activated independently of starvation. However, the role of ketogenesis during the perinatal period remains unclear. Here, we show that neonatal ketogen- esis plays a protective role in mitochondrial function. We generated a mouse model of insufficient ketogenesis by disrupting the rate-limiting hydroxymethylglutaryl-CoA synthase 2 enzyme gene (Hmgcs2). Hmgcs2 knockout (KO) neonates develop microvesicular steatosis within a few days of birth. Electron microscopic analysis and metabolite profiling indicate a restricted energy production capacity and accumulation of acetyl-CoA in Hmgcs2 KO mice. Furthermore, -
FKBP52 Regulates TRPC3-Dependent Ca<Sup>
© 2019. Published by The Company of Biologists Ltd | Journal of Cell Science (2019) 132, jcs231506. doi:10.1242/jcs.231506 RESEARCH ARTICLE FKBP52 regulates TRPC3-dependent Ca2+ signals and the hypertrophic growth of cardiomyocyte cultures Sandra Bandleon1, Patrick P. Strunz1, Simone Pickel2, Oleksandra Tiapko3, Antonella Cellini1, Erick Miranda-Laferte2 and Petra Eder-Negrin1,* ABSTRACT A single TRPC subunit is composed of six transmembrane The transient receptor potential (TRP; C-classical, TRPC) channel domains with a pore-forming loop connecting the transmembrane ‘ ’ TRPC3 allows a cation (Na+/Ca2+) influx that is favored by the domains 5 and 6, a preserved 25 amino acid sequence called a TRP domain and two cytosolic domains, an N-terminal ankyrin repeat stimulation of Gq protein-coupled receptors (GPCRs). An enhanced TRPC3 activity is related to adverse effects, including pathological domain and a C-terminal coiled-coil domain (Eder et al., 2007; Fan hypertrophy in chronic cardiac disease states. In the present study, et al., 2018). The cytosolic domains mediate ion channel formation we identified FK506-binding protein 52 (FKBP52, also known as and are implicated in ion channel regulation and plasma membrane FKBP4) as a novel interaction partner of TRPC3 in the heart. FKBP52 targeting (Eder et al., 2007). Among several protein interaction sites, was recovered from a cardiac cDNA library by a C-terminal TRPC3 the C-terminus of all TRPC subunits harbors a highly conserved fragment (amino acids 742–848) in a yeast two-hybrid screen. proline-rich sequence that corresponds to the binding domain in the Drosophila Downregulation of FKBP52 promoted a TRPC3-dependent photoreceptor channel TRPL for the FK506-binding hypertrophic response in neonatal rat cardiomyocytes (NRCs). -
Genome-Wide Analysis of Epigenetic Silencing Identifies BEX1 and BEX2 As Candidate Tumor Suppressor Genes in Malignant Glioma
Research Article Genome-Wide Analysis of Epigenetic Silencing Identifies BEX1 and BEX2 as Candidate Tumor Suppressor Genes in Malignant Glioma Greg Foltz,1,3 Gi-Yung Ryu,1 Jae-Geun Yoon,1 Timothy Nelson,1 Jessica Fahey,1 Amanda Frakes,1 Hwahyung Lee,1 Lorie Field,1 Kaitlin Zander,1 Zita Sibenaller,1 Timothy C. Ryken,1 Rajeev Vibhakar,2 Leroy Hood,3 and Anup Madan1,3 1Neurogenomic Research Laboratory, Department of Neurosurgery; 2Department of Pediatrics, University of Iowa Carver College of Medicine, Iowa City, Iowa; and 3Institute for Systems Biology, Seattle, Washington Abstract common underlying epigenetic mechanisms, such as promoter hypermethylation, histone deacetylation, histone methylation, Promoter hypermethylation and histone deacetylation are and other histone modifications, which directly or indirectly common epigenetic mechanisms implicated in the transcrip- alter chromatin structure (3–5). When combined with microarray tional silencing of tumor suppressor genes in human cancer. analysis, the pharmacologic reversal of one or more of these We treated two immortalized glioma cell lines, T98 and U87, common underlying epigenetic mechanisms provides a powerful and 10patient-derived primary glioma cell lines with screening tool for the comprehensive identification of epigenet- trichostatin A (TSA), a histone deacetylase inhibitor, or 5- ically silenced genes on a global scale. Several recent studies aza-2¶-deoxycytidine (5-AzaC), a DNA methyltransferase in- have validated this large-scale approach using DNA methyltrans- hibitor, to comprehensively identify the cohort of genes ferase and histone deacetylase (HDAC) inhibitors, either alone or reactivated through the pharmacologic reversal of these in combination, in a variety of human cancers, including distinct but related epigenetic processes. -
KENNETH B. STOREY and ERNEST BAILEY Department of Biochemistry, University of Sheffield, Sheffield SI0 2TN, U.K
Insect Biochem.,. 1978, Vol. 8, pp. 125 to 131. Peroamon Press. Printed in Great Britain INTRACELLULAR DISTRIBUTION OF ENZYMES ASSOCIATED WITH LIPOGENESIS AND GLUCONEOGENESIS IN FAT BODY OF THE ADULT COCKROACH, PERIPLANETA KENNETH B. STOREY and ERNEST BAILEY Department of Biochemistry, University of Sheffield, Sheffield SI0 2TN, U.K. (Received 30 April 1977) Abstract--The intracellular distribution and maximal activities of some enzymes associated with lipo- genesis, gluconeogenesis and fatty acid oxidation have been determined in the fat body of the adult male cockroach Periplaneta americana. Of the enzymes of lipogenesis, acetyl-CoA synthase, acetyl-CoA carboxylase, glucose 6-phosphate dehydrogenase, and ATP citrate lyase are located entirely in the cytosol. Of the other enzymes of citrate metabolism studied, citrate synthase and NAD-dependent isocitrate dehydrogenase are almost exclusively mitochondrial, whereas NADP-dependent isocitrate dehydrogenase and aconitase are predominantly cytosolic although significant mitochondrial activity is also present. The latter subeellular distribution is also observed for 'malic enzyme' and NAD and NADP dependent malate dehydrogenase. The enzyme of fatty acid oxidation studied, 3-hydroxyacyl- CoA dehydrogenase is entirely mitochondrial. Of the enzymes possibly involved in glueoneogenesis, glucose 6-phosphate is microsomal, fructose 1,6-diphosphatase cytosolic, pyruvate carboxylase mito- chondrial and phosphoenolpyruvate carboxykinase predominantly eytosolic. Of the enzymes of amino acid metabolism studied, glutamate dehydrogenase is NAD-dependent and located in the mitochondria whereas glutamate/oxalacetate and glutamate/pyruvate transaminases are predominantly cytosolic but with significant activity in the mitochondria. Glycerol kinase and sorbitol dehydrogenase are cytosolic and the glyoxylate cycle enzymes malate synthetase and isocitrate lyase are not detected in the fat body. -
Bioinformatics Analysis Based on Gene Expression Omnibus
ANTICANCER RESEARCH 39 : 1689-1698 (2019) doi:10.21873/anticanres.13274 Chemo-resistant Gastric Cancer Associated Gene Expression Signature: Bioinformatics Analysis Based on Gene Expression Omnibus JUN-BAO LIU 1* , TUNYU JIAN 2* , CHAO YUE 3, DAN CHEN 4, WEI CHEN 5, TING-TING BAO 6, HAI-XIA LIU 7, YUN CAO 8, WEI-BING LI 6, ZHIJIAN YANG 9, ROBERT M. HOFFMAN 9 and CHEN YU 6 1Traditional Chinese Medicine Department, People's Hospital of Henan Province, People's Hospital of Zhengzhou University, Zhengzhou, P.R. China; 2Institute of Botany, Jiangsu Province and Chinese Academy of Sciences, Nanjing, P.R. China; 3Department of general surgery, Jiangsu Cancer Hospital & Jiangsu Institute of Cancer Research & The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, P.R. China; 4Research Center of Clinical Oncology, Jiangsu Cancer Hospital & Jiangsu Institute of Cancer Research & The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, P.R. China; 5Department of Head and Neck Surgery, Jiangsu Cancer Hospital & Jiangsu Institute of Cancer Research & The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, P.R. China; 6Department of Integrated TCM & Western Medicine, Jiangsu Cancer Hospital & Jiangsu Institute of Cancer Research & The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, P.R. China; 7Emergency Department, The Second Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, P.R. China; 8Master candidate of Oncology, Nanjing University of Chinese Medicine, Nanjing, P.R. China; 9AntiCancer, Inc., San Diego, CA, U.S.A. Abstract. Background/Aim: This study aimed to identify identified, including 13 up-regulated and 1,473 down-regulated biomarkers for predicting the prognosis of advanced gastric genes. -
Candidate Genes Linked to QTL Regions Associated with Fatty Acid
1 Candidate genes linked to QTL regions associated with fatty acid composition in oil palm 2 3 Abstract 4 5 The present study searched for candidate genes in five linkage groups (LGs) - T2, T3, OT4, OT6 and T9 hosting the QTLs 6 associated with iodine value (IV) and fatty acid composition (FAC) in an oil palm interspecific hybrid population. Each 7 of the five LGs was successfully anchored to its corresponding chromosomal segment where, a wider repertoire of 8 candidate genes was identified. This study further revealed a total of 19 candidate genes and four transcription factors 9 involved in biosynthesis of fatty acids, lipids (including triacylglycerol) and acetyl-CoA, glycosylation and degradation 10 of fatty acids. Their possible involvement in regulating the levels of saturation are discussed. In addition, 22 candidate 11 genes located outside the QTL intervals were also identified across the interspecific hybrid genome. A total of 92 SSR 12 markers were developed to tag the presence of these candidate genes and 50 were successfully mapped onto their 13 respective positions on the genome. The data obtained here complements the previous studies, and collectively, these 14 QTL-linked candidate gene markers could help breeders in more precisely selecting palms with the desired FAC. 15 16 Keywords 17 18 Elaeis guineensis, interspecific hybrid, fatty acid biosynthesis, triacylglycerol biosynthesis, transcription factors, genetic 19 linkage map 20 21 Abbreviations 22 23 4CLL1 4-coumarate--CoA ligase 1 24 AACT acetoacetyl-CoA thiolase 25 acbd4 acyl-CoA-binding domain-containing protein 4 26 ACX4 acyl-CoA oxidase 4 27 C14:0 myristic acid 28 C16:0 palmitic acid 29 C16:1 palmitoleic acid 30 C18:0 stearic acid 31 C18:1 oleic acid 32 C18:2 linoleic acid 33 CHR pseudo-chromosome 34 cM centiMorgan 35 CP cross pollinator 36 CPO crude palm oil 37 CTAB cetyltriammonium bromide 38 DNA deoxyribonucleic acid 39 EG5 E. -
Senescence Inhibits the Chaperone Response to Thermal Stress
SUPPLEMENTAL INFORMATION Senescence inhibits the chaperone response to thermal stress Jack Llewellyn1, 2, Venkatesh Mallikarjun1, 2, 3, Ellen Appleton1, 2, Maria Osipova1, 2, Hamish TJ Gilbert1, 2, Stephen M Richardson2, Simon J Hubbard4, 5 and Joe Swift1, 2, 5 (1) Wellcome Centre for Cell-Matrix Research, Oxford Road, Manchester, M13 9PT, UK. (2) Division of Cell Matrix Biology and Regenerative Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, M13 9PL, UK. (3) Current address: Department of Biomedical Engineering, University of Virginia, Box 800759, Health System, Charlottesville, VA, 22903, USA. (4) Division of Evolution and Genomic Sciences, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, M13 9PL, UK. (5) Correspondence to SJH ([email protected]) or JS ([email protected]). Page 1 of 11 Supplemental Information: Llewellyn et al. Chaperone stress response in senescence CONTENTS Supplemental figures S1 – S5 … … … … … … … … 3 Supplemental table S6 … … … … … … … … 10 Supplemental references … … … … … … … … 11 Page 2 of 11 Supplemental Information: Llewellyn et al. Chaperone stress response in senescence SUPPLEMENTAL FIGURES Figure S1. A EP (passage 3) LP (passage 16) 200 µm 200 µm 1.5 3 B Mass spectrometry proteomics (n = 4) C mRNA (n = 4) D 100k EP 1.0 2 p < 0.0001 p < 0.0001 LP p < 0.0001 p < 0.0001 ) 0.5 1 2 p < 0.0001 p < 0.0001 10k 0.0 0 -0.5 -1 Cell area (µm Cell area fold change vs. EP fold change vs. -
FABP7 Regulates Acetyl-Coa Metabolism Through the Interaction with ACLY in the Nucleus of Astrocytes
Molecular Neurobiology (2020) 57:4891–4910 https://doi.org/10.1007/s12035-020-02057-3 FABP7 Regulates Acetyl-CoA Metabolism Through the Interaction with ACLY in the Nucleus of Astrocytes Yoshiteru Kagawa1 & Banlanjo Abdulaziz Umaru1 & Hiroki Shima2 & Ryo Ito3 & Ryo Zama1 & Ariful Islam1 & Shin-ichiro Kanno4 & Akira Yasui4 & Shun Sato5 & Kosuke Jozaki5 & Subrata Kumar Shil1 & Hirofumi Miyazaki1 & Shuhei Kobayashi1 & Yui Yamamoto1 & Hiroshi Kogo6 & Chie Shimamoto-Mitsuyama7 & Akira Sugawara3 & Norihiro Sugino5 & Masayuki Kanamori8 & Teiji Tominaga8 & Takeo Yoshikawa7 & Kohji Fukunaga9 & Kazuhiko Igarashi2 & Yuji Owada1 Received: 27 April 2020 /Accepted: 7 August 2020 / Published online: 19 August 2020 # The Author(s) 2020 Abstract Fatty acid binding protein 7 (FABP7) is an intracellular fatty acid chaperon that is highly expressed in astrocytes, oligodendrocyte-precursor cells, and malignant glioma. Previously, we reported that FABP7 regulates the response to extracel- lular stimuli by controlling the expression of caveolin-1, an important component of lipid raft. Here, we explored the detailed mechanisms underlying FABP7 regulation of caveolin-1 expression using primary cultured FABP7-KO astrocytes as a model of loss of function and NIH-3T3 cells as a model of gain of function. We discovered that FABP7 interacts with ATP-citrate lyase (ACLY) and is important for acetyl-CoA metabolism in the nucleus. This interaction leads to epigenetic regulation of several genes, including caveolin-1. Our novel findings suggest that FABP7-ACLY modulation of nuclear acetyl-CoA has more influence on histone acetylation than cytoplasmic acetyl-CoA. The changes to histone structure may modify caveolae-related cell activity in astrocytes and tumors, including malignant glioma. Keywords Fatty acid–binding protein (FABP) . -
Epigenetic Regulation of Developmental Expression of Cyp2d Genes in Mouse Liver
CORE Metadata, citation and similar papers at core.ac.uk Provided by Elsevier - Publisher Connector Acta Pharmaceutica Sinica B 2012;2(2):146–158 Institute of Materia Medica, Chinese Academy of Medical Sciences Chinese Pharmaceutical Association Acta Pharmaceutica Sinica B www.elsevier.com/locate/apsb www.sciencedirect.com ORIGINAL ARTICLE Epigenetic regulation of developmental expression of Cyp2d genes in mouse liver Ye Lia, Xiao-bo Zhongb,n aDepartment of Pharmacology, School of Chemical Biology and Pharmaceutical Sciences, Capital Medical University, Beijing 100069, China bDepartment of Pharmacology, Toxicology, and Therapeutics, University of Kansas Medical Center, Kansas City, KS 66160, USA Received 28 November 2011; revised 26 December 2011; accepted 10 January 2012 KEY WORDS Abstract CYP2D6 expression in liver is age-dependent. Because epigenetic mechanisms, such as DNA methylation and histone modifications, modulate age-related gene expression during develop- Cyp2d; ment, and are highly conserved among species, the current study examined the epigenetic regulation of DNA methylation; age-related expression of the Cyp2d genes in mouse liver. DNA methylation (DNAme), histone 3 Histone methylation; lysine 4 dimethylation (H3K4me2), and histone 3 lysine 27 trimethylation (H3K27me3) was Liver development established by ChIP-on-chip tiling microarrays from mouse livers at prenatal, neonatal, and adult stages. Levels of DNAme, H3K4me2, and H3K27me3 were analyzed in a genomic region containing the Cyp2d clustering genes and their surrounding genes. Gradually increased expression levels of the Cyp2d9, Cyp2d10, Cyp2d22,andCyp2d26 genes from prenatal, through neonatal, to adult are associated with gradually increased levels of H3K4me2 in the nucleosomes associated with these genes. Gene expression patterns during liver development in several Cyp2d surrounding genes, such as Srebf2, Sept3, Ndufa6, Tcf2, Nfam1,andCyb5r3, could be also explained by changes of DNA methylation, H3K4me2, or H3K27me3 in those genes.