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1. Full Text Clinical spectrum of early onset epileptic encephalopathies caused by KCNQ2 mutation
by Kato, Mitsuhiro and Yamagata, Takanori and Kubota, Masaya and Arai, Hiroshi and Yamashita, Sumimasa and Nakagawa, Taku and FujII, Takanari and Sugai, Kenji and Imai, Kaoru and Uster, Tami and Chitayat, David and Weiss, Shelly and Kashii, Hirofumi and Kusano, Ryosuke and Matsumoto, Ayumi and Nakamura, Kazuyuki and Oyazato, Yoshinobu and Maeno, Mari and Nishiyama, Kiyomi and Kodera, Hirofumi and Nakashima, Mitsuko and Tsurusaki, Yoshinori and Miyake, Noriko and Saito, Kayoko and Hayasaka, Kiyoshi and Matsumoto, Naomichi and Saitsu, Hirotomo
Epilepsia, ISSN 0013-9580, 07/2013, Volume 54, Issue 7, pp. 1282 - 1287
Summary Purpose KCNQ2 mutations have been found in patients with benign familial neonatal seizures, myokymia, or early onset epileptic encephalopathy (EOEE).... 
Ohtahara syndrome | Early onset epileptic encephalopathy | Ion channel | Mosaic | KCNQ2 | MENTAL-RETARDATION | CLINICAL NEUROLOGY | FAMILIAL NEONATAL CONVULSIONS | MYOCLONIC EPILEPSY | SEIZURES | DE-NOVO MUTATIONS | BENIGN | EXPANSION | SEQUENCING DATA | CHANNEL GENE | OHTAHARA-SYNDROME | Genetic Predisposition to Disease - genetics | Genetic Testing | Humans | Exons - genetics | Infant | Male | Tomography, X-Ray Computed | Electroencephalography | Epilepsy - physiopathology | Mutation - genetics | Magnetic Resonance Imaging | DNA Mutational Analysis | KCNQ2 Potassium Channel - genetics | Epilepsy - genetics | Female | Infant, Newborn | Anticonvulsants | Genetic aspects | Seizures (Medicine) | Invisibility | EEG
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2. Full Text De novo SOX11 mutations cause Coffin-Siris syndrome
by Tsurusaki, Yoshinori and Koshimizu, Eriko and Ohashi, Hirofumi and Phadke, Shubha and Kou, Ikuyo and Shiina, Masaaki and Suzuki, Toshifumi and Okamoto, Nobuhiko and Imamura, Shintaro and Yamashita, Michiaki and Watanabe, Satoshi and Yoshiura, Koh-Ichiro and Kodera, Hirofumi and Miyatake, Satoko and Nakashima, Mitsuko and Saitsu, Hirotomo and Ogata, Kazuhiro and Ikegawa, Shiro and Miyake, Noriko and Matsumoto, Naomichi
Nature Communications, ISSN 2041-1723, 06/2014, Volume 5, Issue 1, p. 4011
Coffin-Siris syndrome (CSS) is a congenital disorder characterized by growth deficiency, intellectual disability, microcephaly, characteristic facial features... 
EXPRESSION PATTERNS | PROGENITORS | COMPLEX | CHROMATIN | STABILITY | MULTIDISCIPLINARY SCIENCES | COMPONENTS | SUGGESTS | SOXC Transcription Factors - genetics | Face - abnormalities | Humans | Micrognathism - genetics | Child, Preschool | Zebrafish | Neck - abnormalities | Gene Knockdown Techniques | Intellectual Disability - genetics | Animals | Hand Deformities, Congenital - genetics | Adolescent | Female | SOX Transcription Factors - genetics | Mice | Mutation | Zebrafish Proteins - genetics | Abnormalities, Multiple - genetics | Cohort Studies
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3. Full Text De novo mutations in the autophagy gene WDR45 cause static encephalopathy of childhood with neurodegeneration in adulthood
by Saitsu, Hirotomo and Nishimura, Taki and Muramatsu, Kazuhiro and Kodera, Hirofumi and Kumada, Satoko and Sugai, Kenji and Kasai-Yoshida, Emi and Sawaura, Noriko and Nishida, Hiroya and Hoshino, Ai and Ryujin, Fukiko and Yoshioka, Seiichiro and Nishiyama, Kiyomi and Kondo, Yukiko and Tsurusaki, Yoshinori and Nakashima, Mitsuko and Miyake, Noriko and Arakawa, Hirokazu and Kato, Mitsuhiro and Mizushima, Noboru and Matsumoto, Naomichi
Nature Genetics, ISSN 1061-4036, 04/2013, Volume 45, Issue 4, pp. 445 - 449
Static encephalopathy of childhood with neurodegeneration in adulthood (SENDA) is a recently established subtype of neurodegeneration with brain iron... 
PROTEIN FAMILY | ATG PROTEINS | BRAIN IRON ACCUMULATION | DISTINCT | DISEASE | GENETICS & HEREDITY | PROPPINS | MICE | MECHANISMS | MITOPHAGY | BINDING-SITES | Spasms, Infantile - etiology | Neurodegenerative Diseases - etiology | Humans | Mutation - genetics | Autophagy | Iron - metabolism | Carrier Proteins - genetics | Magnetic Resonance Imaging | Exome - genetics | Phenotype | Lennox Gastaut Syndrome | Adult | Female | High-Throughput Nucleotide Sequencing | Intellectual Disability - etiology | Child | Autophagy (Cytology) | Nervous system | Genetic aspects | Degeneration | Encephalopathy | Patient outcomes | Proteins | Brain research | Neurodegeneration | Science | Mutation | Grants | Mammals
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4. Full Text The Glucose-lowering Efficacy of Sitagliptin in Obese Japanese Patients with Type 2 Diabetes
by Kodera, Ryo and Shikata, Kenichi and Nakamura, Akihiko and Okazaki, Satoru and Nagase, Ryo and Nakatou, Tatsuaki and Haisa, Shigeru and Hida, Kazuyuki and Miyashita, Katsuhiro and Makino, Hirofumi
Internal Medicine, ISSN 0918-2918, 2017, Volume 56, Issue 6, pp. 605 - 613
Objective Dipeptidyl peptidase-4 (DPP-4) inhibitors are the most frequently prescribed oral hypoglycemic agents in Japan. Although a relationship between the... 
dipeptidyl peptidase-4 inhibitor | obesity | sitagliptin | Dipeptidyl peptidase-4 inhibitor | Obesity | Sitagliptin | METFORMIN | MEDICINE, GENERAL & INTERNAL | DIPEPTIDYL PEPTIDASE-4 INHIBITORS | MONOTHERAPY | SAFETY | TOLERANCE | INSULIN SENSITIVITY | BETA-CELL FUNCTION | Body Mass Index | Hypoglycemic Agents - therapeutic use | Prospective Studies | Dipeptidyl-Peptidase IV Inhibitors - therapeutic use | Glycated Hemoglobin A - metabolism | Humans | Japan | Middle Aged | Glycated Hemoglobin A - drug effects | Male | Diabetes Mellitus, Type 2 - epidemiology | Blood Glucose - drug effects | Obesity - epidemiology | Sitagliptin Phosphate - therapeutic use | Female | Aged | Blood Glucose - metabolism | Diabetes Mellitus, Type 2 - drug therapy | Peptidase | Effectiveness | Diabetes mellitus | Homeostasis | Regression analysis | Glucose | Metabolism | Glucose metabolism | Body mass index | Inhibitors | Body mass | Body size | Hemoglobin | Hypoglycemic agents | Diabetes | Diabetes mellitus (non-insulin dependent) | Original
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5. Full Text Mutations in the glutaminyl-tRNA synthetase gene cause early-onset epileptic encephalopathy
by Kodera, Hirofumi and Osaka, Hitoshi and Iai, Mizue and Aida, Noriko and Yamashita, Akio and Tsurusaki, Yoshinori and Nakashima, Mitsuko and Miyake, Noriko and Saitsu, Hirotomo and Matsumoto, Naomichi
Journal of Human Genetics, ISSN 1434-5161, 02/2015, Volume 60, Issue 2, pp. 97 - 101
Aminoacylation is the process of attaching amino acids to their cognate tRNA, and thus is essential for the translation of mRNA into protein. This direct... 
LEUKOENCEPHALOPATHY | BRAIN-STEM | HUMAN-DISEASE | CAUSE HYPOMYELINATION | GENETICS & HEREDITY | SPINAL-CORD INVOLVEMENT | Amino Acyl-tRNA Synthetases - genetics | Brain Diseases - diagnosis | Humans | Brain Diseases - genetics | Family Health | Male | Electroencephalography | Epilepsy - diagnosis | Magnetic Resonance Imaging | Exome - genetics | DNA Mutational Analysis | Adolescent | Age of Onset | Epilepsy - genetics | Mutation | Child | Siblings
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6. Full Text De novo GABRA1 mutations in Ohtahara and West syndromes
by Kodera, Hirofumi and Ohba, Chihiro and Kato, Mitsuhiro and Maeda, Toshiyuki and Araki, Kaoru and Tajima, Daisuke and Matsuo, Muneaki and Hino‐Fukuyo, Naomi and Kohashi, Kosuke and Ishiyama, Akihiko and Takeshita, Saoko and Motoi, Hirotaka and Kitamura, Taro and Kikuchi, Atsuo and Tsurusaki, Yoshinori and Nakashima, Mitsuko and Miyake, Noriko and Sasaki, Masayuki and Kure, Shigeo and Haginoya, Kazuhiro and Saitsu, Hirotomo and Matsumoto, Naomichi
Epilepsia, ISSN 0013-9580, 04/2016, Volume 57, Issue 4, pp. 566 - 573
Summary Objective GABRA1 mutations have been identified in patients with familial juvenile myoclonic epilepsy, sporadic childhood absence epilepsy, and... 
Infantile epilepsy | GABRA1 | Early onset epileptic encephalopathy | GABAA receptor | De novo mutation | GABA | receptor | SUSCEPTIBILITY | GAMMA-2-SUBUNIT | GAMMA-2 SUBUNIT | CLINICAL NEUROLOGY | CHILDHOOD ABSENCE EPILEPSY | ENCEPHALOPATHY | RECEPTOR SUBUNIT MUTATIONS | FEBRILE SEIZURES PLUS | GABA(A) receptor | GENES | GABA(A) RECEPTORS | GENERALIZED EPILEPSY | Amino Acid Sequence | Spasms, Infantile - physiopathology | Humans | Child, Preschool | Molecular Sequence Data | Infant | Male | Electroencephalography | Spasms, Infantile - genetics | Mutation, Missense - genetics | Receptors, GABA-A - genetics | Female | Spasms, Infantile - diagnosis | Child | Genetic aspects | Epilepsy | Analysis | Convulsions & seizures | Mutation | Patients
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7. Full Text De Novo Mutations in SLC35A2 Encoding a UDP‐Galactose Transporter Cause Early‐Onset Epileptic Encephalopathy
by Kodera, Hirofumi and Nakamura, Kazuyuki and Osaka, Hitoshi and Maegaki, Yoshihiro and Haginoya, Kazuhiro and Mizumoto, Shuji and Kato, Mitsuhiro and Okamoto, Nobuhiko and Iai, Mizue and Kondo, Yukiko and Nishiyama, Kiyomi and Tsurusaki, Yoshinori and Nakashima, Mitsuko and Miyake, Noriko and Hayasaka, Kiyoshi and Sugahara, Kazuyuki and Yuasa, Isao and Wada, Yoshinao and Matsumoto, Naomichi and Saitsu, Hirotomo
Human Mutation, ISSN 1059-7794, 12/2013, Volume 34, Issue 12, pp. 1708 - 1714
ABSTRACT Early‐onset epileptic encephalopathies (EOEE) are severe neurological disorders characterized by frequent seizures accompanied by developmental... 
SLC35A2 | early‐onset epileptic encephalopathy | congenital disorders of glycosylation | Early-onset epileptic encephalopathy | Congenital disorders of glycosylation | MENTAL-RETARDATION | SUPPRESSION-BURST PATTERN | CUTIS LAXA | GDP-FUCOSE TRANSPORTER | MYOCLONIC EPILEPSY | GENE | GENETICS & HEREDITY | CONGENITAL DISORDERS | early-onset epileptic encephalopathy | SEQUENCING DATA | GLYCOSYLATION DISORDERS | OHTAHARA-SYNDROME | RNA Isoforms | Humans | Infant | Electroencephalography | Spasms, Infantile - genetics | Exome | DNA Mutational Analysis | Facies | Female | Spasms, Infantile - diagnosis | Child | Gene Order | Infant, Newborn | Monosaccharide Transport Proteins - genetics | Cell Line | Gene Expression | Brain - physiopathology | Protein Transport | Magnetic Resonance Imaging | Phenotype | Animals | Age of Onset | Brain - pathology | High-Throughput Nucleotide Sequencing | Mice | Monosaccharide Transport Proteins - chemistry | Mutation | Galactose | Genetic aspects
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8. Full Text De novo KCNT1 mutations in early‐onset epileptic encephalopathy
by Ohba, Chihiro and Kato, Mitsuhiro and Takahashi, Nobuya and Osaka, Hitoshi and Shiihara, Takashi and Tohyama, Jun and Nabatame, Shin and Azuma, Junji and Fujii, Yuji and Hara, Munetsugu and Tsurusawa, Reimi and Inoue, Takahito and Ogata, Reina and Watanabe, Yoriko and Togashi, Noriko and Kodera, Hirofumi and Nakashima, Mitsuko and Tsurusaki, Yoshinori and Miyake, Noriko and Tanaka, Fumiaki and Saitsu, Hirotomo and Matsumoto, Naomichi
Epilepsia, ISSN 0013-9580, 09/2015, Volume 56, Issue 9, pp. e121 - e128
Summary KCNT1 mutations have been found in epilepsy of infancy with migrating focal seizures (EIMFS; also known as migrating partial seizures in infancy),... 
Early onset epileptic encephalopathies | Epilepsy of infancy with migrating focal seizures | KCNT1 | De novo mutation | SLACK | MIGRATING PARTIAL SEIZURES | GENES | INFANCY | GAIN | CLINICAL NEUROLOGY | Magnetic Resonance Imaging | DNA Mutational Analysis | Humans | Brain - pathology | Child, Preschool | Infant | Electroencephalography | Spasms, Infantile - genetics | Mutation - genetics | Child | Nerve Tissue Proteins - genetics | Potassium Channels - genetics | Genetic research | Genetic aspects | Seizures (Medicine) | Epilepsy
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9. Full Text GRIN1 mutations cause encephalopathy with infantile‐onset epilepsy, and hyperkinetic and stereotyped movement disorders
by Ohba, Chihiro and Shiina, Masaaki and Tohyama, Jun and Haginoya, Kazuhiro and Lerman‐Sagie, Tally and Okamoto, Nobuhiko and Blumkin, Lubov and Lev, Dorit and Mukaida, Souichi and Nozaki, Fumihito and Uematsu, Mitsugu and Onuma, Akira and Kodera, Hirofumi and Nakashima, Mitsuko and Tsurusaki, Yoshinori and Miyake, Noriko and Tanaka, Fumiaki and Kato, Mitsuhiro and Ogata, Kazuhiro and Saitsu, Hirotomo and Matsumoto, Naomichi
Epilepsia, ISSN 0013-9580, 06/2015, Volume 56, Issue 6, pp. 841 - 848
Summary Objective Recently, de novo mutations in GRIN1 have been identified in patients with nonsyndromic intellectual disability and epileptic encephalopathy.... 
Seizure | Neurotransmitter disorders | Encephalopathy | Movement disorders | GRIN1 | NMDA RECEPTOR | AUTISM | D-ASPARTATE RECEPTORS | MONOAMINE NEUROTRANSMITTER DISORDERS | SYNAPTIC PLASTICITY | CHILDHOOD | CLINICAL NEUROLOGY | DE-NOVO MUTATIONS | ION-CHANNEL | DOPAMINE D1 RECEPTOR | MICE | Genetic Predisposition to Disease - genetics | Hyperkinesis - genetics | Hyperkinesis - complications | Humans | Brain Diseases - genetics | Child, Preschool | Male | Electroencephalography | Nerve Tissue Proteins - genetics | Mutation, Missense - genetics | Epilepsy - complications | Receptors, N-Methyl-D-Aspartate - genetics | Stereotypic Movement Disorder - complications | Magnetic Resonance Imaging | DNA Mutational Analysis | Brain Diseases - complications | Adolescent | Stereotypic Movement Disorder - genetics | Epilepsy - genetics | Female | Child | Methyl aspartate | Gene mutations | Analysis | Epilepsy | Genetic aspects | Seizures (Medicine)
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10. Full Text Development of a novel estimation method for hemoglobin A1c using glycated albumin in type 2 diabetes mellitus patients with end-stage renal disease
by Nakamura, Akihiko and Kodera, Ryo and Sakamoto, Noriko and Ujike, Haruyo and Wada, Jun and Shikata, Kenichi and Makino, Hirofumi
Diabetology International, ISSN 2190-1678, 7/2018, Volume 9, Issue 3, pp. 179 - 188
We developed a novel estimation method for hemoglobin A1c (HbA1c) in type 2 diabetes (T2D) patients with end-stage renal disease (ESRD). This method is based... 
Type 2 diabetes | End-stage renal disease | Glycated albumin | Medicine & Public Health | Hemoglobin A1c | Metabolic Diseases | Diabetes | Endocrinology
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11. Full Text PIGO mutations in intractable epilepsy and severe developmental delay with mild elevation of alkaline phosphatase levels
by Nakamura, Kazuyuki and Osaka, Hitoshi and Murakami, Yoshiko and Anzai, Rie and Nishiyama, Kiyomi and Kodera, Hirofumi and Nakashima, Mitsuko and Tsurusaki, Yoshinori and Miyake, Noriko and Kinoshita, Taroh and Matsumoto, Naomichi and Saitsu, Hirotomo
Epilepsia, ISSN 0013-9580, 02/2014, Volume 55, Issue 2, pp. e13 - e17
Summary Aberrations in the glycosylphosphatidylinositol (GPI)–anchor biosynthesis pathway constitute a subclass of congenital disorders of glycosylation, and... 
Epileptic encephalopathy | Glycosylphosphatidylinositol anchors | Congenital disorders of glycosylation | PIGO | DE-NOVO MUTATIONS | PGAP2 | ANCHOR-SYNTHESIS PATHWAY | CAUSE HYPERPHOSPHATASIA | CLINICAL NEUROLOGY | Developmental Disabilities - blood | Humans | Infant | Male | Developmental Disabilities - genetics | Intellectual Disability - genetics | Intellectual Disability - blood | Phosphorus Metabolism Disorders - genetics | Fatal Outcome | Epilepsy - genetics | Female | Hemoglobinuria, Paroxysmal - blood | Hemoglobinuria, Paroxysmal - diagnosis | Membrane Proteins - blood | Child | Developmental Disabilities - diagnosis | Abnormalities, Multiple - genetics | Alkaline Phosphatase - blood | Abnormalities, Multiple - blood | Severity of Illness Index | Glycosylphosphatidylinositols - blood | Phosphorus Metabolism Disorders - diagnosis | Membrane Proteins - genetics | Mutation - genetics | Phosphorus Metabolism Disorders - blood | Epilepsy - diagnosis | Pedigree | Abnormalities, Multiple - diagnosis | Intellectual Disability - diagnosis | Glycosylphosphatidylinositols - deficiency | Epilepsy - blood | Proteins | Fc receptors | Genetic disorders | Phosphatases | Epilepsy | Physiological aspects | Genetic aspects | Mental illness | Mutation
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12. Full Text Targeted capture and sequencing for detection of mutations causing early onset epileptic encephalopathy
by Kodera, Hirofumi and Kato, Mitsuhiro and Nord, Alex S and Walsh, Tom and Lee, Ming and Yamanaka, Gaku and Tohyama, Jun and Nakamura, Kazuyuki and Nakagawa, Eiji and Ikeda, Tae and Ben‐Zeev, Bruria and Lev, Dorit and Lerman‐Sagie, Tally and Straussberg, Rachel and Tanabe, Saori and Ueda, Kazutoshi and Amamoto, Masano and Ohta, Sayaka and Nonoda, Yutaka and Nishiyama, Kiyomi and Tsurusaki, Yoshinori and Nakashima, Mitsuko and Miyake, Noriko and Hayasaka, Kiyoshi and King, Mary‐Claire and Matsumoto, Naomichi and Saitsu, Hirotomo
Epilepsia, ISSN 0013-9580, 07/2013, Volume 54, Issue 7, pp. 1262 - 1269
Summary Purpose Early onset epileptic encephalopathies (EOEEs) are heterogeneous epileptic disorders caused by various abnormalities in causative genes... 
Copy number variation | Target capture | Mutation | Genetic testing | Sequencing | WEST SYNDROME | CDKL5 | HYPOMYELINATION | VARIANTS | PLATFORMS | STXBP1 MUTATIONS | CLINICAL NEUROLOGY | SEIZURES | GENE | OHTAHARA SYNDROME | MOSAICISM | Genetic Testing | Munc18 Proteins - genetics | Humans | NAV1.1 Voltage-Gated Sodium Channel - genetics | NAV1.2 Voltage-Gated Sodium Channel - genetics | Male | DNA Copy Number Variations - genetics | Electroencephalography | Spasms, Infantile - genetics | Mutation - genetics | Carrier Proteins - genetics | Microarray Analysis | Female | Microfilament Proteins - genetics | Sequence Analysis, DNA - methods | Gene mutations | Analysis | Genes | Genomics | Genetic research | Antisense RNA | Genetic aspects
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13. Full Text De Novo Mutations in GNAO1, Encoding a Gαo Subunit of Heterotrimeric G Proteins, Cause Epileptic Encephalopathy
by Nakamura, Shinichi and Nakamura, Kazuyuki and Kodera, Hirofumi and Akita, Tenpei and Shiina, Masaaki and Kato, Mitsuhiro and Hoshino, Hideki and Terashima, Hiroshi and Osaka, Hitoshi and Tohyama, Jun and Kumada, Tatsuro and Furukawa, Tomonori and Iwata, Satomi and Shiihara, Takashi and Kubota, Masaya and Miyatake, Satoko and Koshimizu, Eriko and Nishiyama, Kiyomi and Nakashima, Mitsuko and Tsurusaki, Yoshinori and Miyake, Noriko and Hayasaka, Kiyoshi and Ogata, Kazuhiro and Fukuda, Atsuo and Matsumoto, Naomichi and Saitsu, Hirotomo
The American Journal of Human Genetics, ISSN 0002-9297, 09/2013, Volume 93, Issue 3, pp. 496 - 505
Heterotrimeric G proteins, composed of α, β, and γ subunits, can transduce a variety of signals from seven-transmembrane-type receptors to intracellular... 
GTP-Binding Protein alpha Subunits, Gi-Go - genetics | Calcium - metabolism | Humans | Child, Preschool | Molecular Sequence Data | Infant | Electroencephalography | Epilepsy - physiopathology | GTP-Binding Protein alpha Subunits, Gi-Go - chemistry | Epilepsy - genetics | Female | Child | Amino Acid Sequence | Genetic Predisposition to Disease | Mutant Proteins - genetics | Models, Molecular | Mutant Proteins - metabolism | Signal Transduction - genetics | Mutation - genetics | Sequence Analysis, DNA | Protein Transport | Magnetic Resonance Imaging | Exome - genetics | Phenotype | Animals | Mutant Proteins - chemistry | Amino Acid Substitution - genetics | Mice | Epilepsy - pathology
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14. Full Text Cholecystokinin plays a novel protective role in diabetic kidney through anti-inflammatory actions on macrophage: Anti-inflammatory effect of cholecystokinin
by Miyamoto, Satoshi and Shikata, Kenichi and Miyasaka, Kyoko and Okada, Shinichi and Sasaki, Motofumi and Kodera, Ryo and Hirota, Daisho and Kajitani, Nobuo and Takatsuka, Tetsuharu and Kataoka, Hitomi Usui and Nishishita, Shingo and Sato, Chikage and Funakoshi, Akihiro and Nishimori, Hisakazu and Uchida, Haruhito Adam and Ogawa, Daisuke and Makino, Hirofumi
Diabetes, ISSN 0012-1797, 04/2012, Volume 61, Issue 4, pp. 897 - 907
Inflammatory process is involved in the pathogenesis of diabetic nephropathy. In this article, we show that cholecystokinin (CCK) is expressed in the kidney... 
CCK-A RECEPTOR | INTERCELLULAR-ADHESION MOLECULE-1 | RAT | ENDOCRINOLOGY & METABOLISM | PULMONARY INTERSTITIAL MACROPHAGES | ANGIOTENSIN-II | MICE | NF-KAPPA-B | EXPRESSION | NEPHROPATHY | MONOCYTE MIGRATION | Tumor Necrosis Factor-alpha - metabolism | Tumor Necrosis Factor-alpha - genetics | Sincalide - pharmacology | Receptor, Cholecystokinin B - metabolism | Male | NF-kappa B - metabolism | Chemokines, CC | Gene Expression Profiling | Cholecystokinin - metabolism | Inflammation - metabolism | Kidney - metabolism | Receptors, Cholecystokinin - genetics | Macrophages - physiology | Sincalide - analogs & derivatives | Diabetes Mellitus - metabolism | Gene Expression Regulation - physiology | Chemotaxis - drug effects | Receptor, Cholecystokinin B - genetics | Receptors, Cholecystokinin - metabolism | Mice, Knockout | Intercellular Adhesion Molecule-1 - metabolism | Animals | Cholecystokinin - genetics | NF-kappa B - genetics | Intercellular Adhesion Molecule-1 - genetics | Mice | Physiological aspects | Cholecystokinin | Research | Diabetic nephropathies | Complications
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