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1. Full Text Liver-specific expression of dominant- negative transcription factor 7-like 2 causes progressive impairment in glucose homeostasis
by Ip, Wilfred and Shao, Weijuan and Song, Zhuolun and Chen, Zonglan and Wheeler, Michael B and Jin, Tianru
Diabetes, ISSN 0012-1797, 06/2015, Volume 64, Issue 6, pp. 1923 - 1932
Investigations on the metabolic role of the Wnt signaling pathway and hepatic transcription factor 7-like 2 (TCF7L2) have generated opposing views. While some... 
TCF7L2 | OXIDATIVE STRESS | ACTIVATION | PANCREATIC-ISLETS | METABOLISM | ENDOCRINOLOGY & METABOLISM | CATENIN SIGNALING PROTECTS | GENE-EXPRESSION | MICE | BETA-CELL MASS | GENOME-WIDE ASSOCIATION | Transcription Factor 7-Like 2 Protein - genetics | Signal Transduction | Humans | Liver - metabolism | Mice, Inbred C57BL | Male | Mice, Transgenic | Transcription Factor 7-Like 2 Protein - metabolism | beta Catenin - metabolism | Animals | Forkhead Transcription Factors - metabolism | Homeostasis - physiology | Glucose - metabolism | Female | Forkhead Box Protein O1 | Mice | Homeostasis - genetics | Genetically modified mice | Transcription factors | Research | Biological control systems | Gluconeogenesis
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2. Full Text Chromatin occupancy of transcription factor 7-like 2 (TCF7L2) and its role in hepatic glucose metabolism
by Norton, L and Fourcaudot, M and Abdul-Ghani, M A and Winnier, D and Mehta, F F and Jenkinson, C P and DeFronzo, R A
Diabetologia, ISSN 0012-186X, 12/2011, Volume 54, Issue 12, pp. 3132 - 3142
The mechanisms by which transcription factor 7-like 2 (TCF7L2) regulates the pathways that are important in the pathogenesis of type 2 diabetes are unknown. We... 
Type 2 diabetes | TCF7L2 | Medicine & Public Health | Human Physiology | Metabolic Diseases | Internal Medicine | Hepatic glucose metabolism | HUMAN PANCREATIC-ISLETS | HOMEOSTASIS | CANCER CELLS | MOUSE-LIVER | INSULIN | SKELETAL-MUSCLE | ENDOCRINOLOGY & METABOLISM | GENE-EXPRESSION | GLUTAMINE-SYNTHETASE | H4IIE CELLS | TYPE-2 DIABETES-MELLITUS | Cell Line | Chromatin - metabolism | Glucose-6-Phosphatase - genetics | Insulin - pharmacology | Transcription Factor 7-Like 2 Protein - genetics | Diabetes Mellitus, Type 2 - genetics | Metformin - pharmacology | Gene Expression Regulation | Gene Silencing | Molecular Sequence Data | Rats | Diabetes Mellitus, Type 2 - metabolism | Hepatocytes - metabolism | Transcription Factor 7-Like 2 Protein - metabolism | Hypoglycemic Agents - pharmacology | Animals | Chromatin Immunoprecipitation | Glucose-6-Phosphatase - biosynthesis | Base Sequence | Glucose - metabolism | Gluconeogenesis | Chromatin | Genes | Glucose | Insulin | Dextrose | Glucose metabolism | Anopheles | Hyperglycemia | Multiprocessing | Analysis | DNA | Physiological aspects | Genomics | Nucleotide sequencing | DNA-ligand interactions | DNA sequencing | Transcription factors | Fasting | Diabetes mellitus | Liver | AKT2 protein | Data processing | Genomes | Gene polymorphism | Hepatocytes | Metformin
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3. Full Text The Transcription Factor 7‐Like 2–Peroxisome Proliferator‐Activated Receptor Gamma Coactivator‐1 Alpha Axis Connects Mitochondrial Biogenesis and Metabolic Shift with Stem Cell Commitment to Hepatic Differentiation
by Wanet, Anaïs and Caruso, Marino and Domelevo Entfellner, Jean‐Baka and Najar, Mehdi and Fattaccioli, Antoine and Demazy, Catherine and Evraerts, Jonathan and El‐Kehdy, Hoda and Pourcher, Guillaume and Sokal, Etienne and Arnould, Thierry and Tiffin, Nicki and Najimi, Mustapha and Renard, Patricia
STEM CELLS, ISSN 1066-5099, 10/2017, Volume 35, Issue 10, pp. 2184 - 2197
Increasing evidence supports that modifications in the mitochondrial content, oxidative phosphorylation (OXPHOS) activity, and cell metabolism influence the... 
Mitochondria | Oxidative phosphorylation | Hepatic differentiation | Stem cells | Wnt/β‐catenin | Wnt/β-catenin | PGC-1-ALPHA | KINASE | CELL & TISSUE ENGINEERING | CELL BIOLOGY | GLUCONEOGENESIS | ONCOLOGY | BIOTECHNOLOGY & APPLIED MICROBIOLOGY | ENZYMES | Wnt/beta-catenin | COPY NUMBER | GENES | LIVER | PGC-1 | ADIPOCYTE DIFFERENTIATION | HEMATOLOGY | Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - genetics | Transcription Factor 7-Like 2 Protein - genetics | Signal Transduction | Mitochondria, Liver - metabolism | Humans | Liver - metabolism | Cells, Cultured | Oxidative Phosphorylation | Hepatocytes - metabolism | Liver - growth & development | Transcription Factor 7-Like 2 Protein - metabolism | beta Catenin - metabolism | Organelle Biogenesis | Hepatocytes - cytology | Transfection | Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - metabolism | Liver - cytology | Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - biosynthesis | Cell Differentiation - physiology | Physiological aspects | Biosynthesis | Cell differentiation | Phosphorylation | Regulators | Transcription factors | Wnt protein | Liver | Crosstalk | Differentiation (biology) | Abundance | Metabolism | Cell fate | Pluripotency
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4. Full Text Transcription Factor 7-like 2 Mediates Canonical Wnt/β-Catenin Signaling and c-Myc Upregulation in Heart Failure
by Hou, Ning and Ye, Bo and Li, Xiang and Margulies, Kenneth B and Xu, Haodong and Wang, Xuejun and Li, Faqian
Circulation: Heart Failure, ISSN 1941-3289, 06/2016, Volume 9, Issue 6
Background-How canonical Wnt/beta-catenin signals in adult hearts, especially in different diseased states, remains unclear. The proto-oncogene, c-Myc, is a... 
acetylation | heart failure | desmin | cell signaling/signal transduction | cardiomyopathy | PRESSURE-OVERLOAD | CARDIAC & CARDIOVASCULAR SYSTEMS | DOWN-REGULATION | BETA-CATENIN | INFARCT SIZE | MYOCYTE HYPERTROPHY | GENE-EXPRESSION | TUMOR-SUPPRESSOR | INDUCED CARDIAC-HYPERTROPHY | CELL-DIFFERENTIATION | TRANSGENIC MICE | Up-Regulation | Humans | Middle Aged | Male | Transcription Factor 7-Like 2 Protein - metabolism | Transfection | RNA Interference | Adult | Female | Transcription, Genetic | Binding Sites | Wnt Signaling Pathway | Disease Models, Animal | Cardiomyopathy, Dilated - genetics | Promoter Regions, Genetic | Cells, Cultured | Heart Failure - genetics | Heart Failure - metabolism | Cardiomyopathy, Dilated - metabolism | Proto-Oncogene Proteins c-myc - metabolism | Rats, Sprague-Dawley | beta Catenin - metabolism | Desmin - deficiency | Mice, Knockout | Animals | Desmin - genetics | Proto-Oncogene Proteins c-myc - genetics | signal transduction | cell signaling
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5. Full Text Transcription factor 7-like 2 controls matrix degradation through nuclear factor κB signaling and is repressed by microRNA-155 in nucleus pulposus cells
by Sun, Siguo and Sun, Jianchao and Hong, Junmin and Wang, Xiaofei and Peng, Yan and Zhou, Jie and Huang, Yingjie and Li, Shuangxing and Li, Chunhai and Chen, Weijian and Xu, Kang and Ye, Wei
Biomedicine & Pharmacotherapy, ISSN 0753-3322, 12/2018, Volume 108, pp. 646 - 655
TCF7L2, a key transcription factor in the canonical Wnt pathway, plays a vital role in the matrix degradation of chondrocytes. However, it is unknown whether... 
microRNA-155 | Intervertebral disc degeneration | Transcription factor 7-like 2 | Inflammatory cytokines | Nucleus pulposus | Nuclear factor κB signaling | MEDICINE, RESEARCH & EXPERIMENTAL | TCF7L2 | METALLOPROTEINASE | PROLIFERATION | BETA-CATENIN | GENE | WNT/BETA-CATENIN | PATHWAY | PHARMACOLOGY & PHARMACY | WNT | Nuclear factor kappa B signaling | EXPRESSION | Tumor Necrosis Factor-alpha - metabolism | Cell Line | Nucleus Pulposus - metabolism | Humans | Extracellular Matrix - metabolism | Rats | MicroRNAs - metabolism | NF-kappa B - metabolism | Rats, Sprague-Dawley | Transcription Factor 7-Like 2 Protein - metabolism | Animals | Transcription Factor RelA - metabolism | Interleukin-1beta - metabolism | HEK293 Cells | Signal Transduction - physiology
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6. Full Text Disease-associated loci are significantly over-represented among genes bound by transcription factor 7-like 2 (TCF7L2) in vivo
by Zhao, J and Schug, J and Li, M and Kaestner, K H and Grant, S F. A
Diabetologia, ISSN 0012-186X, 11/2010, Volume 53, Issue 11, pp. 2340 - 2346
Transcription factor 7-like 2 (TCF7L2) has been strongly implicated in type 2 diabetes and cancer. Our goal was to identify the DNA sequences bound by this... 
Type 2 diabetes | TCF7L2 | ChIP-sequencing | GWAS | Medicine & Public Health | Human Physiology | Metabolic Diseases | Internal Medicine | VARIANTS | BETA-CATENIN | CHROMATIN OCCUPANCY | RISK LOCI | POLYMORPHISMS | PATTERN | COLORECTAL-CANCER | ENDOCRINOLOGY & METABOLISM | RS6983267 | TYPE-2 | GENOME-WIDE ASSOCIATION | Transcription Factor 7-Like 2 Protein - genetics | Chromatin Immunoprecipitation | Neoplasms - genetics | Oligonucleotide Array Sequence Analysis | Diabetes Mellitus, Type 2 - genetics | HCT116 Cells | Humans | Protein Binding | RNA, Small Interfering | Binding Sites - genetics | Sequence Analysis, DNA | Transcription Factor 7-Like 2 Protein - metabolism | Chromatin | Anopheles | Nervous system diseases | Genetic disorders | Analysis | Genomics | DNA | Colorectal cancer | Genetic aspects | Universities and colleges | Coronary heart disease | Genes
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7. Full Text Clinical and non-targeted metabolomic profiling of homozygous carriers of Transcription Factor 7-like 2 variant rs7903146
by Wagner, Robert and Li, Jia and Kenar, Erhan and Kohlbacher, Oliver and Machicao, Fausto and Häring, Hans-Ulrich and Fritsche, Andreas and Xu, Guowang and Lehmann, Rainer
Scientific Reports, ISSN 2045-2322, 06/2014, Volume 4, Issue 1, p. 5296
An important role of the type 2 diabetes risk variant rs7903146 in TCF7L2 in metabolic actions of various tissues, in particular of the liver, has recently... 
ISLET FUNCTION | TCF7L2 | IMPACT | POLYMORPHISMS | GLUCOSE-METABOLISM | MULTIDISCIPLINARY SCIENCES | INSULIN-SECRETION | PREVENTION | MECHANISMS | DIABETES RISK GENES | MORPHOLOGY | C-Peptide - blood | Diabetes Mellitus, Type 2 - genetics | Humans | Middle Aged | Male | Diabetes Mellitus, Type 2 - metabolism | Insulin - blood | Transcription Factor 7-Like 2 Protein - metabolism | Insulin-Secreting Cells - metabolism | Adult | Fatty Acids, Nonesterified - blood | Female | Insulin Secretion | Genetic Predisposition to Disease - genetics | Glucose Tolerance Test | Transcription Factor 7-Like 2 Protein - genetics | Risk Factors | Metabolome | Genotype | Metabolomics - methods | Homozygote | Diabetes Mellitus, Type 2 - blood | Insulin - metabolism | Polymorphism, Single Nucleotide | Blood Glucose - metabolism | Beta cells | Secretion | Diabetes mellitus | Liver | Diabetes | Fatty acids | Insulin | Genotypes
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8. Full Text Genomic sequencing of colorectal adenocarcinomas identifies a recurrent VTI1A-TCF7L2 fusion
by Bass, Adam J and Lawrence, Michael S and Brace, Lear E and Ramos, Alex H and Drier, Yotam and Cibulskis, Kristian and Sougnez, Carrie and Voet, Douglas and Saksena, Gordon and Sivachenko, Andrey and Jing, Rui and Parkin, Melissa and Pugh, Trevor and Verhaak, Roel G and Stransky, Nicolas and Boutin, Adam T and Barretina, Jordi and Solit, David B and Vakiani, Evi and Shao, Wenlin and Mishina, Yuji and Warmuth, Markus and Jimenez, Jose and Chiang, Derek Y and Signoretti, Sabina and Kaelin Jr, William G and Spardy, Nicole and Hahn, William C and Hoshida, Yujin and Ogino, Shuji and Depinho, Ronald A and Chin, Lynda and Garraway, Levi A and Fuchs, Charles S and Baselga, Jose and Tabernero, Josep and Gabriel, Stacey and Lander, Eric S and Getz, Gad and Meyerson, Matthew
Nature Genetics, ISSN 1061-4036, 10/2011, Volume 43, Issue 10, pp. 964 - 970
Prior studies have identified recurrent oncogenic mutations in colorectal adenocarcinoma(1) and have surveyed exons of protein-coding genes for mutations in 11... 
REARRANGEMENT | LUNG-CANCER | COMPLEX | HUMAN BREAST | PROSTATE-CANCER | GENES | GENETICS & HEREDITY | TUMOR-SUPPRESSOR | RISK | CHROMOSOME-5Q21 | TUMORIGENESIS | Adenocarcinoma - pathology | Exons | Colorectal Neoplasms - genetics | Humans | Qb-SNARE Proteins - metabolism | Qb-SNARE Proteins - genetics | Transcription Factor 7-Like 2 Protein - metabolism | Gene Knockdown Techniques | Oncogene Proteins, Fusion | RNA Interference | Cell Transformation, Neoplastic - genetics | Gene Deletion | Adenocarcinoma - genetics | Transcription Factor 4 | Transcription Factor 7-Like 2 Protein - genetics | Gene Dosage | Transcription Factors - genetics | Sequence Analysis, DNA | beta Catenin - metabolism | beta Catenin - genetics | Transcription Factors - metabolism | Sequence Alignment | Gene Rearrangement | Basic Helix-Loop-Helix Leucine Zipper Transcription Factors - genetics | Cell Line, Tumor | Basic Helix-Loop-Helix Leucine Zipper Transcription Factors - metabolism | Colorectal Neoplasms - pathology | Genome, Human | Gene mutations | Colorectal cancer | Physiological aspects | Genetic aspects | Research | Binding proteins | Health aspects | Risk factors | Genomes | Mutation | Chromosomes | Deoxyribonucleic acid--DNA
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9. Full Text Differential transcriptional and posttranslational transcription factor 7-like regulation among nondiabetic individuals and type 2 diabetic patients
by Pradas-Juni, M and Nicod, N and Fernández-Rebollo, E and Gomis, R
Molecular endocrinology (Baltimore, Md.), ISSN 0888-8809, 09/2014, Volume 28, Issue 9, pp. 1558 - 1570
Human genetic studies have revealed that the T minor allele of single nucleotide polymorphism rs7903146 in the transcription factor 7-like 2 (TCF7L2) gene is... 
VARIANTS | TCF7L2 GENE | PATHWAY | METABOLIC MEMORY | ENDOCRINOLOGY & METABOLISM | RISK | MECHANISMS | EXPRESSION | ASSOCIATION | CONTRIBUTES | SPLICING FACTOR | Protein Biosynthesis | Receptors, Estrogen - metabolism | Transcription Factor 7-Like 2 Protein - genetics | Alternative Splicing | Exons | Diabetes Mellitus, Type 2 - genetics | Humans | Middle Aged | Gene Expression Regulation | Genotype | Male | Diabetes Mellitus, Type 2 - metabolism | Transcription Factor 7-Like 2 Protein - metabolism | Insulin - metabolism | Alleles | Glucose - metabolism | Female | Transcription, Genetic | Aged | Polymorphism, Single Nucleotide | Binding Sites
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10. Full Text Analysis of the interaction between transcription factor 7-like 2 genetic variants with nopal and wholegrain fibre intake: Effects on anthropometric and metabolic characteristics in type 2 diabetes patients
by López-Ortiz, M.M and Garay-Sevilla, M.E and Tejero, M.E and Perez-Luque, E.L
British Journal of Nutrition, ISSN 0007-1145, 09/2016, Volume 116, Issue 6, pp. 969 - 978
The transcription factor 7-like 2 (TCF7L2) genetic variants have shown differential effect on low-fat and high-fat diet in obese subjects. Nopal is a Mexican... 
Type 2 diabetes | Wholegrain fibre | Transcription factor 7-like 2 polymorphism | Nopal fibre | TCF7L2 POLYMORPHISMS | PREVENTION | RISK | OBESITY | NUTRITION & DIETETICS | DIET | GRAIN | GLUCOSE | EXPRESSION | CONSUMPTION | PROGRESSION | Genetic Variation | Dietary Fiber - pharmacology | Food Analysis | Transcription Factor 7-Like 2 Protein - genetics | Diet | Diabetes Mellitus, Type 2 - genetics | Humans | Gene Expression Regulation - physiology | Diabetes Mellitus, Type 2 - metabolism | Triticum - chemistry | Cactaceae - chemistry | Transcription Factor 7-Like 2 Protein - metabolism | Transcription factors | Genetic diversity | Diabetes | Dietary fiber | Metabolism | Hypoglycemia
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11. Full Text Pancreatic pericytes support β-cell function in a Tcf7l2-dependent manner
by Sakhneny, Lina and Rachi, Eleonor and Epshtein, Alona and Guez, Helen C and Wald-Altman, Shane and Lisnyansky, Michal and Khalifa-Malka, Laura and Hazan, Adina and Baer, Daria and Priel, Avi and Weil, Miguel and Landsman, Limor
Diabetes, ISSN 0012-1797, 03/2018, Volume 67, Issue 3, pp. 437 - 447
Polymorphism in TCF7L2, a component of the canonical Wnt signaling pathway, has a strong association with beta-cell dysfunction and type 2 diabetes through a... 
VARIANTS | GLUCOSE-METABOLISM | CLONING | TRANSCRIPTION-FACTOR-7-LIKE-2 TCF7L2 GENE | INSULIN-SECRETION | MOUSE | ENDOCRINOLOGY & METABOLISM | RISK | EXPRESSION | BETA-CATENIN/TCF-4 | DELETION | Glucose Intolerance - metabolism | Recombinant Proteins - therapeutic use | Bone Morphogenetic Protein 4 - genetics | Bacterial Proteins - chemistry | Male | Glucose Intolerance - pathology | Bone Morphogenetic Protein 4 - metabolism | Recombinant Fusion Proteins - metabolism | Transcription Factor 7-Like 2 Protein - metabolism | Glucose Intolerance - drug therapy | Transcription Factor 7-Like 2 Protein - chemistry | Insulin-Secreting Cells - metabolism | Pericytes - pathology | Luminescent Proteins - chemistry | Cell Differentiation | Insulin Secretion | Glucose Intolerance - physiopathology | Recombinant Proteins - metabolism | Bone Morphogenetic Protein 4 - therapeutic use | Transcription Factor 7-Like 2 Protein - genetics | Tissue Culture Techniques | Pericytes - metabolism | Bacterial Proteins - genetics | Gene Expression Regulation | Cell Communication | Cellular Microenvironment | Mice, Transgenic | Recombinant Fusion Proteins - chemistry | Insulin - metabolism | Animals | Glucose - metabolism | Bacterial Proteins - metabolism | Ligands | Luminescent Proteins - genetics | Insulin-Secreting Cells - pathology | Mutation | Luminescent Proteins - metabolism | Usage | Genetic aspects | Research | B cells | Diabetes | Diagnosis | Glucose tolerance tests | Genetic polymorphisms
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12. Full Text Diabetes Risk Gene and Wnt Effector Tcf7l2/TCF4 Controls Hepatic Response to Perinatal and Adult Metabolic Demand
by Boj, Sylvia F and van Es, Johan H and Huch, Meritxell and Li, Vivian S.W and José, Anabel and Hatzis, Pantelis and Mokry, Michal and Haegebarth, Andrea and van den Born, Maaike and Chambon, Pierre and Voshol, Peter and Dor, Yuval and Cuppen, Edwin and Fillat, Cristina and Clevers, Hans
Cell, ISSN 0092-8674, 12/2012, Volume 151, Issue 7, pp. 1595 - 1607
Most studies on SNP variants in the pathogenesis of type 2 diabetes (T2D) focus on a role of the encoded transcription factor TCF4 in β cells. Here, a mouse... 
POLYMORPHISMS | GLUCOSE | BIOCHEMISTRY & MOLECULAR BIOLOGY | LIVER | RECEPTOR | BETA-CATENIN | EXPRESSION | CORRELATE | CELL BIOLOGY | Animals, Newborn | Transcription Factor 7-Like 2 Protein - genetics | Diabetes Mellitus - genetics | Liver - metabolism | Transcriptional Activation | Diabetes Mellitus - metabolism | Transcription Factor 7-Like 2 Protein - metabolism | Mice, Knockout | Animals | Metabolic Networks and Pathways | Islets of Langerhans - metabolism | Diet, High-Fat | Glucose - metabolism | Mice | Fasting - metabolism | Animal genetics | Type 2 diabetes | Chromatin | Genes | Physiological aspects | Genetic aspects | Glucose | Gene expression | Risk factors | Dextrose | Diabetes therapy
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13. Full Text Wnt/β-catenin signaling enhances hypoxia-induced epithelial-mesenchymal transition in hepatocellular carcinoma via crosstalk with hif-1α signaling
by Zhang, Qi and Bai, Xueli and Chen, Wei and Ma, Tao and Hu, Qida and Liang, Chao and Xie, Shangzhi and Chen, Conglin and Hu, Liqiang and Xu, Shiguo and Liang, Tingbo
Carcinogenesis, ISSN 0143-3334, 05/2013, Volume 34, Issue 5, pp. 962 - 973
Epithelialmesenchymal transition (EMT) is a critical process for tumor invasion and metastasis. Hypoxia may induce EMT, and upregulated -catenin expression has... 
PATHWAYS | TARGETING HYPOXIA | STEM-CELLS | ACTIVATION | ONCOLOGY | MECHANISMS | BETA-CATENIN | CANCER | EMT | CONTRIBUTES | PROGRESSION | Wnt3A Protein - metabolism | RNA, Small Interfering - genetics | Cell Hypoxia - physiology | Cell Proliferation | Cadherins - metabolism | Vimentin - metabolism | Humans | Cell Survival - genetics | Epithelial-Mesenchymal Transition - genetics | Transcription Factor 7-Like 2 Protein - metabolism | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Vimentin - genetics | Carcinoma, Hepatocellular - genetics | Cell Cycle Checkpoints - genetics | Liver Neoplasms - pathology | Cadherins - genetics | Transcription Factor 7-Like 2 Protein - genetics | Wnt3A Protein - genetics | Liver Neoplasms - genetics | Signal Transduction | Hypoxia-Inducible Factor 1, alpha Subunit - genetics | beta Catenin - metabolism | beta Catenin - genetics | Hep G2 Cells | Carcinoma, Hepatocellular - pathology | Liver Neoplasms - metabolism | Cell Line, Tumor | Transcription, Genetic - genetics | Cell Hypoxia - genetics | Carcinoma, Hepatocellular - metabolism
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14. Full Text TCF7L2 is a master regulator of insulin production and processing
by Zhou, Yuedan and Park, Soo-Young and Su, Jing and Bailey, Kathleen and Ottosson-Laakso, Emilia and Shcherbina, Liliya and Oskolkov, Nikolay and Zhang, Enming and Thevenin, Thomas and Fadista, João and Bennet, Hedvig and Vikman, Petter and Wierup, Nils and Fex, Malin and Rung, Johan and Wollheim, Claes and Nobrega, Marcelo and Renström, Erik and Groop, Leif and Hansson, Ola and Medicinska fakulteten and Medicinska och farmaceutiska vetenskapsområdet and Institutionen för immunologi, genetik och patologi and Uppsala universitet
Human molecular genetics, ISSN 0964-6906, 12/2014, Volume 23, Issue 24, pp. 6419 - 6431
Genome-wide association studies have revealed > 60 loci associated with type 2 diabetes ( T2D), but the underlying causal variants and functional mechanisms... 
PROVIDES INSIGHTS | COMMON VARIANTS | RISK LOCI | BIOCHEMISTRY & MOLECULAR BIOLOGY | SUSCEPTIBILITY | GENETICS & HEREDITY | GENE-EXPRESSION | PANCREATIC BETA-CELLS | TYPE-2 DIABETES-MELLITUS | PROINSULIN LEVELS | GENOME-WIDE ASSOCIATION | ADIPOSE-TISSUE | LIM-Homeodomain Proteins - metabolism | Proinsulin - metabolism | Diabetes Mellitus, Type 2 - genetics | Homeodomain Proteins - metabolism | Humans | Diabetes Mellitus, Type 2 - metabolism | Genetic Loci | Transcription Factor 7-Like 2 Protein - metabolism | Maf Transcription Factors, Large - metabolism | Basic Helix-Loop-Helix Transcription Factors - metabolism | Maf Transcription Factors, Large - genetics | Islets of Langerhans - metabolism | Trans-Activators - genetics | Transcription, Genetic | Insulin - genetics | Genetic Predisposition to Disease | Genome-Wide Association Study | Basic Helix-Loop-Helix Transcription Factors - genetics | Transcription Factor 7-Like 2 Protein - genetics | Islets of Langerhans - pathology | Signal Transduction | Gene Expression Regulation | Mice, Transgenic | Proinsulin - genetics | Transcription Factors - genetics | Homeodomain Proteins - genetics | Transcription Factors - metabolism | Insulin - metabolism | LIM-Homeodomain Proteins - genetics | Animals | Alleles | Trans-Activators - metabolism | High-Throughput Nucleotide Sequencing | Mice | Polymorphism, Single Nucleotide | Diabetes Mellitus, Type 2 - pathology | Biological Sciences | Biochemistry and Molecular Biology | Naturvetenskap | Natural Sciences | Biokemi och molekylärbiologi | Biologiska vetenskaper
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