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Article ; Online: Noise stability of synchronization and optimal network structures.

Katoh, Yuriko / Kori, Hiroshi

2020 Volume 30, Issue 1, Page(s) 13148

Abstract: We provide a theoretical framework for quantifying the expected level of synchronization in a network of noisy oscillators. Through linearization around the synchronized state, we derive the following quantities as functions of the eigenvalues and ... ...

Abstract	We provide a theoretical framework for quantifying the expected level of synchronization in a network of noisy oscillators. Through linearization around the synchronized state, we derive the following quantities as functions of the eigenvalues and eigenfunctions of the network Laplacian using a standard technique for dealing with multivariate Ornstein-Uhlenbeck processes: the magnitude of the fluctuations around a synchronized state and the disturbance coefficients α
Language	English
Publishing date	2020-02-07
Publishing country	United States
Document type	Journal Article
ZDB-ID	1472677-4
ISSN	1089-7682 ; 1054-1500
ISSN (online)	1089-7682
ISSN	1054-1500
DOI	10.1063/1.5121341
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Article: [Relapsed/refractory Philadelphia chromosome-positive acute lymphoblastic leukemia responding to retreatment with inotuzumab ozogamicin].

Hashimoto, Hiroshi / Tamura, Yuhei / Yamada, Kaori / Katoh, Yuriko / Shimada, Takahiro / Fujiwara, Ryosuke / Hanamoto, Hitoshi

Rinsho ketsueki] The Japanese journal of clinical hematology

2023 Volume 64, Issue 8, Page(s) 746–750

Abstract: A 72-year-old man with Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ALL) was treated with dasatinib (week1: 50 mg/day, week2: 70 mg/day, week3-: 100 mg/day) and prednisolone from June 2017. However, in January 2018, it relapsed with ... ...

Abstract	A 72-year-old man with Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ALL) was treated with dasatinib (week1: 50 mg/day, week2: 70 mg/day, week3-: 100 mg/day) and prednisolone from June 2017. However, in January 2018, it relapsed with the T315I mutation. Although the treatment was changed to ponatinib 30 mg/day, he experienced a second relapse in June 2018. Following confirmation of CD22 positivity, he was treated with three cycles of inotuzumab ozogamicin (InO), resulting in CR. He was CR for 2.9 years before relapsing for the third time in May 2021. Because the patient was still CD22-positive, InO was given again, and the patient achieved CR at the end of the second cycle. We had a case where re-administering InO was effective as a salvage therapy for relapsed/refractory Ph+ALL (r/r Ph+ALL) in an elderly patient.
MeSH term(s)	Aged ; Male ; Humans ; Inotuzumab Ozogamicin/therapeutic use ; Philadelphia Chromosome ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/drug therapy ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/genetics ; Retreatment ; Dasatinib
Chemical Substances	Inotuzumab Ozogamicin (P93RUU11P7) ; Dasatinib (RBZ1571X5H)
Language	Japanese
Publishing date	2023-08-10
Publishing country	Japan
Document type	Case Reports ; English Abstract ; Journal Article
ZDB-ID	390900-1
ISSN	0485-1439
ISSN	0485-1439
DOI	10.11406/rinketsu.64.746
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Article ; Online: Performance Evaluation of Real-Time RT-PCR Assays for the Detection of Severe Acute Respiratory Syndrome Coronavirus-2 Developed by the National Institute of Infectious Diseases, Japan.

Shirato, Kazuya / Tomita, Yuriko / Katoh, Hiroshi / Yamada, Souichi / Fukushi, Shuetsu / Matsuyama, Shutoku / Takeda, Makoto

Japanese journal of infectious diseases

2021 Volume 74, Issue 5, Page(s) 465–472

Abstract: Soon after the 2019 outbreak of coronavirus disease 2019 in Wuhan, China, a protocol for real-time RT-PCR assay detection of severe acute respiratory syndrome coronavirus (SARS-CoV-2) was established by the National Institute of Infectious Diseases (NIID) ...

Abstract	Soon after the 2019 outbreak of coronavirus disease 2019 in Wuhan, China, a protocol for real-time RT-PCR assay detection of severe acute respiratory syndrome coronavirus (SARS-CoV-2) was established by the National Institute of Infectious Diseases (NIID) in Japan. The protocol used Charité's nucleocapsid (Sarbeco-N) and NIID nucleocapsid (NIID-N2) assays. During the following months, SARS-CoV-2 spread and caused a global pandemic, and various SARS-CoV-2 sequences were registered in public databases, such as the Global Initiative on Sharing All Influenza Data (GISAID). In this study, we evaluated the S2 assay (NIID-S2) that was newly developed to replace the Sarbeco-N assay and the performance of the NIID-N2 and NIID-S2 assays, referring to mismatches in the primer/probe targeted region. We found that the analytical sensitivity and specificity of the NIID-S2 set were comparable to those of the NIID-N2 assay, and the detection rate for clinical specimens was identical to that of the NIID-N2 assay. Furthermore, among the available sequences (approximately 192,000), the NIID-N2 and NIID-S2 sets had 2.6% and 1.2% mismatched sequences, respectively, although most of these mismatches did not affect the amplification efficiency, except the 3' end of the NIID-N2 forward primer. These findings indicate that the previously developed NIID-N2 assay is suitable for the detection of SARS-CoV-2 with support from the newly developed NIID-S2 set.
MeSH term(s)	COVID-19/diagnosis ; COVID-19 Nucleic Acid Testing/methods ; Coronavirus Nucleocapsid Proteins/genetics ; DNA Primers/genetics ; Humans ; Japan ; Phosphoproteins/genetics ; RNA, Viral/analysis ; RNA, Viral/genetics ; SARS-CoV-2/genetics ; SARS-CoV-2/isolation & purification ; Sensitivity and Specificity ; Spike Glycoprotein, Coronavirus/genetics
Chemical Substances	Coronavirus Nucleocapsid Proteins ; DNA Primers ; Phosphoproteins ; RNA, Viral ; Spike Glycoprotein, Coronavirus ; nucleocapsid phosphoprotein, SARS-CoV-2 ; spike protein, SARS-CoV-2
Language	English
Publishing date	2021-02-26
Publishing country	Japan
Document type	Evaluation Study ; Journal Article
ZDB-ID	1478383-6
ISSN	1884-2836 ; 1344-6304
ISSN (online)	1884-2836
ISSN	1344-6304
DOI	10.7883/yoken.JJID.2020.1079
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Article ; Online: Allergic contact dermatitis due to epsilon-aminocaproic acid: a case report and mini-review of the published work.

Yamamoto, Yuriko / Wada, Makoto / Nakai, Noriaki / Katoh, Norito

The Journal of dermatology

2013 Volume 40, Issue 4, Page(s) 301–303

MeSH term(s)	Aged ; Aminocaproic Acid/adverse effects ; Antifibrinolytic Agents/adverse effects ; Asian Continental Ancestry Group ; Conjunctivitis, Allergic/drug therapy ; Dermatitis, Allergic Contact/etiology ; Female ; Humans ; Ophthalmic Solutions/adverse effects ; Patch Tests
Chemical Substances	Antifibrinolytic Agents ; Ophthalmic Solutions ; Aminocaproic Acid (U6F3787206)
Language	English
Publishing date	2013-04
Publishing country	England
Document type	Case Reports ; Letter ; Review
ZDB-ID	800103-0
ISSN	1346-8138 ; 0385-2407
ISSN (online)	1346-8138
ISSN	0385-2407
DOI	10.1111/1346-8138.12092
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Article: FGFR2-related pathogenesis and FGFR2-targeted therapeutics (Review).

Katoh, Yuriko / Katoh, Masaru

International journal of molecular medicine

2009 Volume 23, Issue 3, Page(s) 307–311

Abstract: FGFR2 gene at human chromosome 10q26 encodes FGFR2b and FGFR2c isoforms functioning as FGF receptors with distinct expression domain and ligand specificity. FGFR2 plays oncogenic and anti-oncogenic roles in a context-dependent manner. Single nucleotide ... ...

Abstract	FGFR2 gene at human chromosome 10q26 encodes FGFR2b and FGFR2c isoforms functioning as FGF receptors with distinct expression domain and ligand specificity. FGFR2 plays oncogenic and anti-oncogenic roles in a context-dependent manner. Single nucleotide polymorphisms (SNPs) within intron 2 of FGFR2 gene are associated with breast cancer through allelic FGFR2 upregulation. Missense mutations or copy number gains of FGFR2 gene occur in breast cancer and gastric cancer to activate FGFR2 signaling. Aberrant FGFR2 signaling activation induces proliferation and survival of tumor cells. The class switch from FGFR2b to FGFR2c occurs during progression of prostate cancer and bladder cancer because of spliceosome dysregulation. In addition, epidermal Fgfr2b knockout mice show increased sensitivity to chemical carcinogenesis partly due to the failure of Nfe2l2 (Nrf2)-mediated detoxification of reactive oxygen species (ROS). Loss of FGFR2b signaling induces epithelial-to-mesenchymal transition (EMT) and unruly ROS. FGFR2 signaling dysregulation due to the accumulation of epigenetic modifications and genetic alterations during chronic inflammation, smoking, increased caloric uptake, and decreased exercise leads to carcinogenesis. PD173074, SU5402, AZD2171, and Ki23057 are small-molecule FGFR inhibitors. Human antibody, peptide mimetic, RNA aptamer, siRNA, and synthetic microRNA (miRNA) are emerging technologies to be applied for cancer therapeutics targeted to FGFR2. Because novel sequence technology and peta-scale super-computer are opening up the sequence era following the genome era, personalized medicine prescribing targeted drugs based on germline and/or somatic genomic information is coming reality. Application of FGFR2 inhibitors for cancer treatment in patients with FGFR2 mutation or gene amplification is beneficial; however, that for cancer prevention in people with FGFR2 risk allele might be disadvantageous due to the impediment of a cytoprotective mechanism against oxidative stress.
MeSH term(s)	Alleles ; Animals ; Chromosomes, Human, Pair 10/genetics ; Chromosomes, Human, Pair 10/metabolism ; Enzyme Inhibitors/therapeutic use ; Female ; Gene Dosage/drug effects ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Isoenzymes/genetics ; Isoenzymes/metabolism ; Male ; Mice ; Mice, Knockout ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/metabolism ; Oxidative Stress/drug effects ; Oxidative Stress/genetics ; Polymorphism, Single Nucleotide ; Reactive Oxygen Species/metabolism ; Receptor, Fibroblast Growth Factor, Type 2/antagonists & inhibitors ; Receptor, Fibroblast Growth Factor, Type 2/genetics ; Receptor, Fibroblast Growth Factor, Type 2/metabolism ; Risk Factors ; Signal Transduction/drug effects ; Signal Transduction/genetics ; Spliceosomes/genetics ; Spliceosomes/metabolism ; Up-Regulation/drug effects
Chemical Substances	Enzyme Inhibitors ; Isoenzymes ; Reactive Oxygen Species ; FGFR2 protein, human (EC 2.7.10.1) ; Receptor, Fibroblast Growth Factor, Type 2 (EC 2.7.10.1)
Language	English
Publishing date	2009-01-08
Publishing country	Greece
Document type	Journal Article ; Review
ZDB-ID	1444428-8
ISSN	1107-3756
ISSN	1107-3756
DOI	10.3892/ijmm_00000132
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Article: Integrative genomic analyses on GLI1: positive regulation of GLI1 by Hedgehog-GLI, TGFbeta-Smads, and RTK-PI3K-AKT signals, and negative regulation of GLI1 by Notch-CSL-HES/HEY, and GPCR-Gs-PKA signals.

Katoh, Yuriko / Katoh, Masaru

International journal of oncology

2009 Volume 35, Issue 1, Page(s) 187–192

Abstract: GLI family members are zinc-finger transcription factors, which are involved in embryogenesis and carcinogenesis through transcription regulation of GLI1, CCND1, CCND2, FOXA2, FOXC2, RUNX2, SFRP1, and JAG2. GLI1 transcription is upregulated in a variety ... ...

Abstract	GLI family members are zinc-finger transcription factors, which are involved in embryogenesis and carcinogenesis through transcription regulation of GLI1, CCND1, CCND2, FOXA2, FOXC2, RUNX2, SFRP1, and JAG2. GLI1 transcription is upregulated in a variety of human tumors, such as basal cell carcinoma, lung cancer, breast cancer, gastric cancer, pancreatic cancer, and esophageal cancer. Hedgehog signaling via Smoothened cascade and receptor tyrosine kinase (RTK) signaling via PI3K-AKT cascade induce stabilization of GLI1 protein, whereas G-protein coupled receptor (GPCR) signaling via Gs-PKA cascade induces degradation of GLI1 protein. Here we report integrative genomic analyses of the GLI1 gene. The GLI1 and ARHGAP9 genes are located in a tail-to-tail manner with overlapping 3'-ends. ARHGAP9 was expressed in bone marrow, spleen, thymus, monocytes, and macrophages, whereas GLI1 was almost undetectable in normal tissues or cells with predominant ARHGAP9 expression. Because overlapping sense and anti-sense transcripts are annealed to each other to give rise to double-stranded RNAs functioning as endogenous RNAi, GLI1 expression might be negatively regulated by ARHGAP9 transcripts. GLI-binding element with one base substitution at the +1589-bp position from the transcriptional start site (TSS) of the human GLI1 gene was completely conserved in chimpanzee GLI1, mouse Gli1, and rat Gli1 genes. Ten Smad-binding elements, double E-boxes for EMT regulators, and double N-boxes for HES/HEY family members within intron 1 of the human GLI1 gene were also conserved in mammalian GLI1 orthologs. GLI1 transcription is upregulated due to Hedgehog, and TGFbeta signaling activation, whereas GLI1 transcription is downregulated due to Snail/Slug, and Notch signaling activation. Together these facts indicate that Hedgehog, TGFbeta, and RTK signals positively regulate GLI1, and that Notch, and GsPCR signals negatively regulate the GLI1.
MeSH term(s)	Adaptor Proteins, Signal Transducing/genetics ; Animals ; Base Sequence ; Conserved Sequence ; Cyclic AMP-Dependent Protein Kinases/genetics ; Databases, Nucleic Acid ; GTP-Binding Protein alpha Subunits, Gs/genetics ; GTPase-Activating Proteins/genetics ; Gene Regulatory Networks ; Hedgehog Proteins/genetics ; Humans ; Immunoglobulin J Recombination Signal Sequence-Binding Protein/genetics ; Molecular Sequence Data ; Phosphatidylinositol 3-Kinases/genetics ; Proto-Oncogene Proteins c-akt/genetics ; Receptors, G-Protein-Coupled/genetics ; Receptors, Notch/genetics ; Signal Transduction/genetics ; Smad Proteins/genetics ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Transforming Growth Factor beta/genetics ; Zinc Finger Protein GLI1
Chemical Substances	ARHGAP9 protein, human ; Adaptor Proteins, Signal Transducing ; GLI1 protein, human ; GTPase-Activating Proteins ; Hedgehog Proteins ; Immunoglobulin J Recombination Signal Sequence-Binding Protein ; RBPJ protein, human ; Receptors, G-Protein-Coupled ; Receptors, Notch ; Smad Proteins ; Transcription Factors ; Transforming Growth Factor beta ; Zinc Finger Protein GLI1 ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Cyclic AMP-Dependent Protein Kinases (EC 2.7.11.11) ; GTP-Binding Protein alpha Subunits, Gs (EC 3.6.5.1)
Language	English
Publishing date	2009-06-05
Publishing country	Greece
Document type	Journal Article
ZDB-ID	1154403-x
ISSN	1019-6439
ISSN	1019-6439
DOI	10.3892/ijo_00000328
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Article: Hedgehog signaling, epithelial-to-mesenchymal transition and miRNA (review).

Katoh, Yuriko / Katoh, Masaru

International journal of molecular medicine

2008 Volume 22, Issue 3, Page(s) 271–275

Abstract: SHH, IHH, and DHH are lipid-modified secreted proteins binding to Patched receptors, and CDON, BOC or GAS1 co-receptors. In the absence of Hedgehog signaling, GLI1 is transcriptionally repressed, GLI2 is phosphorylated by GSK3 and CK1 for the FBXW11 ( ... ...

Abstract	SHH, IHH, and DHH are lipid-modified secreted proteins binding to Patched receptors, and CDON, BOC or GAS1 co-receptors. In the absence of Hedgehog signaling, GLI1 is transcriptionally repressed, GLI2 is phosphorylated by GSK3 and CK1 for the FBXW11 (betaTRCP2)-mediated degradation, and GLI3 is processed to a cleaved repressor. In the presence of Hedgehog signaling, Smoothened is relieved from Patched-mediated suppression due to the Hedgehog-dependent internalization of Patched, which leads to MAP3K10 (MST) activation and SUFU inactivation for the stabilization and nuclear accumulation of GLI family members. GLI activators then upregulate CCND1, CCND2 for cell cycle acceleration, FOXA2, FOXC2, FOXE1, FOXF1, FOXL1, FOXP3, POU3F1, RUNX2, SOX13, TBX2 for cell fate determination, JAG2, INHBC, and INHBE for stem cell signaling regulation. Hedgehog signals also upregulate SFRP1 in mesenchymal cells for WNT signaling regulation. Epithelial-to-mesenchymal transition (EMT) during embryogenesis, adult tissue homeostasis and carcinogenesis is characterized by class switch from E-cadherin to N-cadherin. SNAI1 (Snail), SNAI2 (Slug), SNAI3, ZEB1, ZEB2 (SIP1), KLF8, TWIST1, and TWIST2 are EMT regulators repressing CDH1 gene encoding E-cadherin. Hedgehog signals induce JAG2 upregulation for Notch-CSL-mediated SNAI1 upregulation, and also induce TGFbeta1 secretion for ZEB1 and ZEB2 upregulation via TGFbeta receptor and NF-kappaB. TGFbeta-mediated downregulation of miR-141, miR-200a, miR-200b, miR-200c, miR-205, and miR-429 results in upregulation of ZEB1 and ZEB2 proteins. Hedgehog signaling activation indirectly leads to EMT through FGF, Notch, TGFbeta signaling cascades, and miRNA regulatory networks. miRNAs targeted to stem cell signaling components or EMT regulators are potent drug targets; however, off-target effects should be strictly controlled before clinical application of synthetic miRNA. Peptide mimetic and RNA aptamer could also be utilized as Hedgehog signaling inhibitors or EMT suppressors.
MeSH term(s)	Animals ; Cell Differentiation ; Epithelial Cells/cytology ; Epithelial Cells/metabolism ; Hedgehog Proteins/metabolism ; Humans ; Mesoderm/cytology ; Mesoderm/metabolism ; MicroRNAs/genetics ; Signal Transduction
Chemical Substances	Hedgehog Proteins ; MicroRNAs
Language	English
Publishing date	2008-09
Publishing country	Greece
Document type	Journal Article ; Review
ZDB-ID	1444428-8
ISSN	1107-3756
ISSN	1107-3756
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Article: Integrative genomic analyses on GLI2: mechanism of Hedgehog priming through basal GLI2 expression, and interaction map of stem cell signaling network with P53.

Katoh, Yuriko / Katoh, Masaru

International journal of oncology

2008 Volume 33, Issue 4, Page(s) 881–886

Abstract: Hedgehog-binding to Patched family receptors results in Smoothened-mediated activation of MAP3K10 (MST) and inactivation of SUFU. MAP3K10-induced DYRK2 phosphorylation combined with SUFU inhibition results in the stabilization and nuclear accumulation of ...

Abstract	Hedgehog-binding to Patched family receptors results in Smoothened-mediated activation of MAP3K10 (MST) and inactivation of SUFU. MAP3K10-induced DYRK2 phosphorylation combined with SUFU inhibition results in the stabilization and nuclear accumulation of GLI2 for transcriptional activation of GLI1, CCND1, CCND2, FOXA2, FOXC2, FOXP3, FOXQ1, RUNX2, and JAG2. Here, integrative genomic analyses on GLI2 orthologs were carried out. Rat Gli2 complete coding sequence was determined by assembling nucleotide sequences of exons 1, 2, and 5'-truncated rat Gli2 RefSeq (NM_001107169.1). GLI2 orthologs were more related to GLI3 orthologs than to GLI1 orthologs lacking the N-terminal repressor domain. betaTRCP1 (FBXW1)-binding DSYxxxS motif was conserved in GLI2 and GLI3 orthologs, while betaTRCP2 (FBXW11)-binding DSGxxxxxxxxxS motif in GLI2 and GLI1 orthologs. Human GLI2 mRNA was expressed in ES cells, NT2 cells, fetal lung, fetal heart, regenerating liver, gastric cancer, and other tumors. Mouse Gli2 mRNA was expressed in unfertilized egg, ES cells, and EG cells. Tandem RRRCWWGYYY motifs for P53, P63 or P73, and also four conserved bHLH-binding sites were identified within GLI2 proximal promoter region. Interaction map of P53 and stem cell signaling network were then constructed. P53-induced NOTCH1 upregulation leads to HES1, HES5, HEY1, HEY2 or HEYL upregulation for the repression of tissue specific bHLH transcriptional activators. DYRK2 functions as a positive regulator of P53-mediated apoptosis, and also as a negative regulator of the Hedgehog signaling cascade. GLI2 expression is regulated based on the balance of P53, Notch, and TGF-beta signaling, and Hedgehog signaling activation results in cell survival and proliferation due to transcriptional activation of Hedgehog-target genes, and also partly due to perturbation of P53-mediated transcriptional regulation.
MeSH term(s)	Amino Acid Sequence ; Animals ; Cell Line, Tumor ; Cell Proliferation ; Cell Survival ; Genomics/methods ; Hedgehog Proteins/metabolism ; Humans ; Kruppel-Like Transcription Factors/metabolism ; Molecular Sequence Data ; Nuclear Proteins/metabolism ; Rats ; Sequence Homology, Amino Acid ; Signal Transduction ; Stem Cells/cytology ; Tumor Suppressor Protein p53/metabolism ; Zinc Finger Protein Gli2
Chemical Substances	GLI2 protein, human ; Hedgehog Proteins ; Kruppel-Like Transcription Factors ; Nuclear Proteins ; TP53 protein, human ; Tumor Suppressor Protein p53 ; Zinc Finger Protein Gli2
Language	English
Publishing date	2008-09-22
Publishing country	Greece
Document type	Journal Article
ZDB-ID	1154403-x
ISSN	1019-6439
ISSN	1019-6439
DOI	10.3892/ijo_00000076
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Article: Comparative genomics on PROM1 gene encoding stem cell marker CD133.

Katoh, Yuriko / Katoh, Masaru

International journal of molecular medicine

2007 Volume 19, Issue 6, Page(s) 967–970

Abstract: Stem cells are characterized by self-renewal and multipotency to produce multiple lineages of progenitor and differentiated cells. PROM1 gene encodes CD133 protein, which is a cell surface marker of hematopoietic stem cells, prostatic epithelial stem ... ...

Abstract	Stem cells are characterized by self-renewal and multipotency to produce multiple lineages of progenitor and differentiated cells. PROM1 gene encodes CD133 protein, which is a cell surface marker of hematopoietic stem cells, prostatic epithelial stem cells, pancreatic stem cells, leukemic stem cells, liver cancer stem cells, and colorectal cancer stem cells. Here, comparative integromics analyses on PROM1 orthologs were performed. Human PROM1 RefSeq NM_006017.1 was a truncated transcript, while AK027422.1 was the representative human PROM1 cDNA. Chimpanzee PROM1 gene, consisting of 27 exons, was identified within NW_001234057.1 genome sequence. Chimpanzee 5-transmembrane protein CD133 showed 99.2% and 60.9% total-amino-acid identity with human and mouse CD133 orthologs, respectively. Only 2 of 8 Asn-linked glycosylation sites in primate CD133 orthologs were conserved in rodent CD133 orthologs. Comparative proteomics revealed that CD133 orthologs were relatively divergent between primates and rodents. PROM1 mRNA was expressed in human embryonic stem (ES) cells, trachea, small intestine, NT2 cells, diffuse-type gastric cancer, and colorectal cancer. Human PROM1 mRNA transcribed from exon 1A was the major transcript. Comparative genomics revealed that the region around exon 1A corresponding to 5'-UTR of human PROM1 mRNA was not conserved in mouse and rat. Intron 2 of PROM1 orthologs was relatively well conserved among mammals. Tandem TCF/LEF-binding sites with 7-bp spacing within intron 2 were conserved among human, chimpanzee, mouse, and rat PROM1 orthologs. Together these facts indicate that canonical WNT signaling activation is implicated in CD133 expression in ES cells, adult stem cells, and cancer stem cells.
MeSH term(s)	AC133 Antigen ; Animals ; Antigens, CD/genetics ; Base Sequence ; Gene Expression ; Genetic Markers ; Genomics ; Glycoproteins/genetics ; Humans ; Mice ; Molecular Sequence Data ; Pan troglodytes/genetics ; Peptides/genetics ; Rats ; Sequence Homology, Nucleic Acid ; Stem Cells/metabolism
Chemical Substances	AC133 Antigen ; Antigens, CD ; Genetic Markers ; Glycoproteins ; PROM1 protein, human ; Peptides ; Prom1 protein, mouse ; Prom1 protein, rat
Language	English
Publishing date	2007-06
Publishing country	Greece
Document type	Comparative Study ; Journal Article
ZDB-ID	1444428-8
ISSN	1107-3756
ISSN	1107-3756
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Article: Comparative integromics on JMJD2A, JMJD2B and JMJD2C: preferential expression of JMJD2C in undifferentiated ES cells.

Katoh, Yuriko / Katoh, Masaru

International journal of molecular medicine

2007 Volume 20, Issue 2, Page(s) 269–273

Abstract: Fertilized egg or totipotent zygote undergoes cleavage divisions to form a blastocyst, consisting of outer trophoectoderm cells and inner cell mass with pluripotent primitive ectoderm cells. Epigenetic reprogramming, erasure and maintenance of epigenetic ...

Abstract	Fertilized egg or totipotent zygote undergoes cleavage divisions to form a blastocyst, consisting of outer trophoectoderm cells and inner cell mass with pluripotent primitive ectoderm cells. Epigenetic reprogramming, erasure and maintenance of epigenetic modification, occurs during early embryogenesis. In 2004, we identified and characterized JMJD2A/JHDM3A, JMJD2B, JMJD2C, JMJD2D, JMJD2E and JMJD2F. JMJD2A, JMJD2B and JMJD2C share the common domain architecture with JmjN, JmjC, two PHD, and two TUDOR domains. In 2006, other groups characterized JMJD2 family members as the H3K9 and/or H3K36 histone demethylases. Here, comparative integromics analyses on JMJD2A, JMJD2B and JMJD2C were carried out. Mouse Jmjd2a was expressed in fertilized egg and 2-cell embryos, while human JMJD2A was expressed in undifferentiated and differentiated ES cells. AP1-binding site and six bHLH-binding sites within intron 13 of human JMJD2A gene were conserved in mouse Jmjd2a gene. Mouse Jmjd2b was expressed in 8-cell embryos and undifferentiated ES cells, while human JMJD2B was expressed in undifferentiated and differentiated ES cells. Two GATA-binding sites within intron 6 of human JMJD2B gene were conserved in mouse Jmjd2b gene. Mouse Jmjd2c and human JMJD2C were preferentially expressed in undifferentiated ES cells. Four NANOG-binding sites, one TCF/ LEF-binding site, and one bHLH-binding site were located within evolutionary conserved region at the 3'-flanking region of human JMJD2C gene. NANOG- TCF/LEF-, and bHLH-binding sites within the 3'-flanking region of human JMJD2C gene were conserved in chimpanzee, cow, mouse and rat JMJD2C othologs. Together these facts indicate that JMJD2C is the evolutionarily conserved target of Homeo-domain transcription factor NANOG, and that JMJD2C is the histone demethylase implicated in the epigenetic reprogramming during the early embryogenesis.
MeSH term(s)	Base Sequence ; Cell Differentiation/genetics ; Computational Biology ; Conserved Sequence ; Embryonic Development/genetics ; Embryonic Stem Cells/cytology ; Embryonic Stem Cells/metabolism ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Genomics ; Humans ; Jumonji Domain-Containing Histone Demethylases ; Molecular Sequence Data ; Neoplasm Proteins/genetics ; Neoplasm Proteins/metabolism ; Oxidoreductases, N-Demethylating/genetics ; Oxidoreductases, N-Demethylating/metabolism ; Phylogeny ; Proteomics ; Sequence Homology, Nucleic Acid ; Transcription Factors/genetics ; Transcription Factors/metabolism
Chemical Substances	KDM4C protein, human ; Neoplasm Proteins ; Transcription Factors ; Jumonji Domain-Containing Histone Demethylases (EC 1.14.11.-) ; KDM4B protein, human (EC 1.14.11.-) ; KDM4A protein, human (EC 1.5.-) ; Oxidoreductases, N-Demethylating (EC 1.5.-)
Language	English
Publishing date	2007-08
Publishing country	Greece
Document type	Comparative Study ; Journal Article
ZDB-ID	1444428-8
ISSN	1107-3756
ISSN	1107-3756
Database	MEDical Literature Analysis and Retrieval System OnLINE

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