MalaCards based summary : Maturity-Onset Diabetes of the Young, Type 10, also known as mody10, is related to maturity-onset diabetes of the young, and has symptoms including maturity-onset diabetes of the young An important gene associated with Maturity-Onset Diabetes of the Young, Type 10 is INS (Insulin). The drugs Moxonidine and Pitavastatin have been mentioned in the context of this disorder. Affiliated tissues include liver, testes and breast ...
Maturity-onset diabetes of the young (MODY) is a monogenic form of diabetes responsible for approximately 1-2% of all cases of diabetes. The disease is clinically defined by: 1) autosomal dominant inheritance (diabetes for at least two consecutive generations), 2) non-insulin dependent diabetes at onset (or measurable serum C-peptide three years after onset), and 3) diagnosis in a young age (at least one family member with onset before the age of 25 years). Clinically, MODY-patients resemble patients with type 2 diabetes (T2DM) more than patients with type 1 diabetes mellitus (T1DM). MODY is genetically heterogeneous, with known mutations in eight different genes and mutations in either of these genes leads to specific forms of MODY. Based on a national epidemiological survey, we know that in Denmark, approximately 50% of patients who are diagnosed with MODY have mutations in the hepatocyte nuclear factor (HNF) 4 alpha (HNF4A) (MODY1), glucokinase (GCK) (MODY2), or HNF1A (MODY3) genes.. MODY3 is ...
What is Maturity Onset Diabetes of the Young (MODY)? - Find more information and articles related to Maturity Onset Diabetes of the Young (MODY) at onlymyhealth.com
Maturity onset diabetes of the young" (MODY) refers to any of several hereditary forms of diabetes mellitus caused by mutations in an autosomal dominant gene disrupting insulin production. MODY is often referred to as "monogenic diabetes" to distinguish it from the more common types of diabetes (especially type 1 and type 2), which involve more complex combinations of causes involving multiple genes and environmental factors. MODY 2 and MODY 3 are the most common forms. MODY should not be confused with latent autoimmune diabetes of adults (LADA) - a form of type 1 DM, with slower progression to insulin dependence than child-onset type 1 DM, and which occurs later in life. The term MODY dates back to 1964, when diabetes mellitus was considered to have two main forms: juvenile-onset and maturity-onset, which roughly corresponded to what we now call type 1 and type 2. MODY was originally applied to any child or young adult who had persistent, asymptomatic hyperglycemia without progression to ...
It is important to identify patients with Maturity-onset diabetes of the young (MODY) as a molecular diagnosis determines both treatment and prognosis. Genetic testing is currently expensive and many patients are therefore not assessed and are misclassified as having either type 1 or type 2 diabetes. Biomarkers could facilitate the prioritisation of patients for genetic testing. We hypothesised that patients with different underlying genetic aetiologies for their diabetes could have distinct metabolic profiles which may uncover novel biomarkers. The aim of this study was to perform metabolic profiling in urine from patients with MODY due to mutations in the genes encoding glucokinase (GCK) or hepatocyte nuclear factor 1 alpha (HNF1A), type 2 diabetes (T2D) and normoglycaemic control subjects. Urinary metabolic profiling by Nuclear Magnetic Resonance (NMR) and ultra performance liquid chromatography hyphenated to Q-TOF mass spectrometry (UPLC-MS) was performed in a Discovery set of subjects with HNF1A
The most common types of diabetes are type 1 and type 2 diabetes. Along with gestational and LADA, these forms of diabetes are polygenic diseases that require the involvement of many genes and a wide variety of environmental factors to cause each disease. There are some rare forms of diabetes, Maturity Onset Diabetes of the Young (MODY) and Neonatal Diabetes Mellitus (NDM) that are monogenic where only one gene is responsible for the disease. Of the 30,000 genes in the human body, about 20 genes have been linked to monogenic diabetes so far.
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Maturity-Onset Diabetes of the Young (MODY) is an autosomal dominant form of diabetes typically occurring before age 25 and caused by a primary insulin secretion defect. MODY is not a single entity but represents nine classifications with genetic, metabolic, and clinical heterogeneity. MODY is estimated to affect approximately 1-2% of people with diabetes, although this may be an underestimate since the genetic etiology of this type of diabetes often goes undiagnosed ...
A team from the NYSCF has generated patient-specific beta cells, or insulin-producing cells, that accurately reflect the features of maturity-onset diabetes of the young (MODY).
Plasmid HNF4A_P2-135 from Dr. Gerhart Ryffels lab contains the insert HNF4A P2 promoter and is published in Hum Mol Genet. 2001 Sep 15. 10(19):2089-97. This plasmid is available through Addgene.
برينستون ــ لم يكن لهذه المهمة أن تصبح سهلة أبدا: فرض خسائر تبلغ 5,8 مليار يورو (7,5 مليار دولار أميركي) على المقرضين للحكومة القبرصية والمودعين لدى البنوك في البلاد. والآن دفع هذا الجهد بأوروبا إلى أحدث مآزقها.. ففي مفاوضات ماراثونية، وافقت الحكومة القبرصية تحت إشراف الترويكا (المفوضية الأوروبية، والبنك المركزي الأوروبي، وصندوق النقد الدولي) على فرض ضريبة لمرة واحدة على الودائع المصرفية. ولكن على الرغم من التعديل الوارد لإعفاء الحسابات التي لا تحتوي على أكثر من عشرين ألف يورو، فإن البرلمان القبرصي رفض الخطة بأغلبية ساحقة، الأمر الذي أدى إلى انزلاق ...
A family of transcription factors (hepatocyte nuclear factors) enriched in liver. HNF1 is predominantly expressed in liver and kidney and selectively interacts with the control regions of several liver-specific genes. Heterozygous mutations in hepatocyte nuclear factor (HNF)-1α and HNF-1β result in maturity-onset diabetes of the young. ...
One form of maturity-onset diabetes of the young, MODY3, is characterized by a severe insulin secretory defect, compared with MODY2, a glucokinase-deflcient diabetes. It has recently been shown that mutations of the gene encoding the transcription factor hepatocyte nuclear factor (HNF)-1α cause MODY3. Because of the rapid progress to overt diabetes and the high prevalence of required insulin treatment in patients with MODY3, we screened the HNF-1α gene for mutations in Japanese subjects with IDDM. Ten exons and flanking introns of the HNF-1α gene in these subjects were amplified by polymerase chain reaction and direct sequencing of the products. Mutations were identified in three (5.5%) of the 55 unrelated subjects with IDDM. A missense mutation of R272H (replacement of Arg by His in codon 272) in the DNA binding domain of HNF-1α was found in a subject who developed IDDM 1 year after diagnosis of NIDDM at 8 years of age. A frameshift mutation of P291fsinsC (insertion of a C in a polyC tract ...
Use of statin and/or aspirin therapy had negligible effects on the comparisons with the HNF1A-MODY group (Table 1). In the type 2 diabetic group, the hs-CRP level was the same for the statin/aspirin users as for the nonusers (P = 0.27), whereas in the type 1 diabetic group those taking statins and/or aspirin had a higher hs-CRP than nonusers (P = 0.004). Thus, it seems unlikely that use of these drugs would lower hs-CRP toward the range seen in the HNF1A-MODY group. In contrast, adjustment for BMI had a large impact on the estimated means (Table 1) and, given the correlation between BMI and CRP (r2 = 0.28, P , 10−6 for control subjects), abolished much of the difference observed between the type 2 diabetic and other groups. However, the differ- ences in hs-CRP levels between the HNF1A-MODY and other groups were preserved (P ≤ 0.01). Estimated mean adjusted hs-CRP (95% CI) levels for the HNF1A-MODY group compared with the other diabetic groups combined were 0.28 (0.16-0.49) vs. 0.82 ...
Hepatocyte nuclear factor 4alpha (HNF4alpha) is a regulator of hepatocyte and pancreatic transcription. Hnf4alpha deletion in the mouse is embryonically lethal with severe defects in visceral endoderm formation. It has been concluded in the past that the role of Hnf4alpha in the developing colon was …
The transcription factor hepatocyte nuclear factor 4-alpha (HNF4-alpha) plays a key role in colon cancer and colitis. HNF4-alpha comes in two major isoforms, P1 and P2, but how these are distributed in the gut is not understood. Now UC Riverside researchers have determined the distribution of the P1 and P2 isoforms in the colon. They report that maintaining a balance of P1 and P2 is crucial for reducing risk of contracting colon cancer and colitis.
Maturity-onset diabetes of the young (MODY) is a genetically and clinically heterogeneous subtype of familial diabetes mellitus characterized by autosomal dominant inheritance, early onset before 25 years of age and primary insulin secretion defects. Mutations in six genes, encoding the glucose sensor enzyme glucokinase and five transcription factors that participate in a regulatory network essential for adult beta cell function, cause most of the MODY cases ...
J:62595 Jacquemin P, Durviaux SM, Jensen J, Godfraind C, Gradwohl G, Guillemot F, Madsen OD, Carmeliet P, Dewerchin M, Collen D, Rousseau GG, Lemaigre FP, Transcription factor hepatocyte nuclear factor 6 regulates pancreatic endocrine cell differentiation and controls expression of the proendocrine gene ngn3. Mol Cell Biol. 2000 Jun;20(12):4445-54 ...
Zhang, Z., Chu, M., Hu, J., Yi, W., Wang, B., & Ma, X. (2017). P1-Hepatocyte Nuclear Factor 4α Expression Significantly Correlates with the Severity of Chronic Gastritis. International Journal of Clinical and Experimental Pathology, 10 (6). http://dx.doi.org/no doi ...
MODY2 (mature onset diabetes of the young, type2) is associated with mutations in the GCK gene that result in impaired glucokinase activity. Although more than 200 inactivating GCK mutations have been reported, only less than 20% of these mutations have been functionally characterized. In this work we describe the biochemical characterization of six missense glucokinase mutations associated to MODY2 from Spanish patients, namely Y61S, V182L, C233R, E265K, A379V and K420E. All these mutations produced enzymes that presented reduced enzymatic activity in various degrees, from a mild affectation (K420E) to a more severe effect (C233R). The severity of the mutation correlated with the importance of the structural changes introduced by the mutations. For example, the C233R affected a critical residue of the active centre of the enzyme and rendered a protein with undetectable enzymatic activity. These data add new information on the structure-function relationship of human glucokinase ...
Describes rare forms of diabetes that result from mutations in a single gene. Discusses diagnosis, genetic testing, and counseling.
Diabetes mellitus is a chronic disease characterized by high blood glucose levels that requires long-term medical attention both to limit the development of its devastating complications and to manage them when they do occur. The pancreatic Beta-cell and its secretory [...]
p>The checksum is a form of redundancy check that is calculated from the sequence. It is useful for tracking sequence updates.,/p> ,p>It should be noted that while, in theory, two different sequences could have the same checksum value, the likelihood that this would happen is extremely low.,/p> ,p>However UniProtKB may contain entries with identical sequences in case of multiple genes (paralogs).,/p> ,p>The checksum is computed as the sequence 64-bit Cyclic Redundancy Check value (CRC64) using the generator polynomial: x,sup>64,/sup> + x,sup>4,/sup> + x,sup>3,/sup> + x + 1. The algorithm is described in the ISO 3309 standard. ,/p> ,p class="publication">Press W.H., Flannery B.P., Teukolsky S.A. and Vetterling W.T.,br /> ,strong>Cyclic redundancy and other checksums,/strong>,br /> ,a href="http://www.nrbook.com/b/bookcpdf.php">Numerical recipes in C 2nd ed., pp896-902, Cambridge University Press (1993),/a>),/p> Checksum:i ...
Cited for: VARIANTS MODY2 GLU-16; ASN-19; PRO-20; TRP-36; SER-43; SER-44; 61-TYR--GLN-465 DEL; SER-61; LYS-70; ARG-72; PRO-77; GLU-78; ASP-80; ILE-82; HIS-108; PRO-116; LEU-182; 186-ARG--GLN-465 DEL; TYR-187; TRP-191; LEU-200; THR-202; MET-206; MET-209; SER-223; ARG-224; SER-227; MET-228; ARG-233; 234-TYR--GLN-465 DEL; GLY-252; ALA-255; LYS-256; ARG-261; LYS-265; LYS-298; TRP-308; HIS-377; VAL-379; LEU-383; 399-GLU--GLN-465 DEL; PHE-411; PRO-416; GLU-420 AND TRP-441; Biochemical characterization of novel glucokinase mutations isolated from Spanish maturity-onset diabetes of the young (MODY2) patients. ...
Recombinant protein of human hepatocyte nuclear factor 4, alpha (HNF4A), transcript variant 5, 20 ug available for purchase from OriGene - Your Gene Company.
Recombinant protein of human hepatocyte nuclear factor 4, alpha (HNF4A), transcript variant 3, 20 ug available for purchase from OriGene - Your Gene Company.
HNF4 gamma antibody (hepatocyte nuclear factor 4, gamma) for IHC-P. Anti-HNF4 gamma pAb (GTX70879) is tested in Human samples. 100% Ab-Assurance.
This gene encodes a member of the forkhead class of DNA-binding proteins. These hepatocyte nuclear factors are transcriptional activators for liver-specific transcripts such as albumin and transthyretin, and they also interact with chromatin. Similar family members in mice have roles in the regulation of metabolism and in the differentiation of the pancreas and liver. The crystal structure of a similar protein in rat has been resolved. [provided by RefSeq, Jul 2008] ...
Hepatocyte nuclear factors (HNFs) are a group of phylogenetically unrelated transcription factors that regulate the transcription of a diverse group of genes into proteins. These proteins include blood clotting factors and in addition, enzymes and transporters involved with glucose, cholesterol, and fatty acid transport and metabolism. As the name suggests, hepatocyte nuclear factors are expressed predominately in the liver. However HNFs are also expressed and play important roles in a number of other tissues so that the name hepatocyte nuclear factor is somewhat misleading. Nevertheless, the liver is the only tissue in which a significant number of different HNFs are expressed at the same time. In addition, there are a number of genes which contain multiple promoter and enhancer regions each regulated by a different HNF. Furthermore, efficient expression of these genes require synergistic activation by multiple HNFs. Hence hepatocyte nuclear factors function to ensure liver specific expression ...
Pcbd1 (GFP-tagged) - Mouse pterin 4 alpha carbinolamine dehydratase/dimerization cofactor of hepatocyte nuclear factor 1 alpha (TCF1) 1 (Pcbd1),, 10 µg.
TY - JOUR. T1 - Retinoic acid mediates down-regulation of the α-fetoprotein gene through decreased expression of hepatocyte nuclear factors. AU - Magee, Thomas R.. AU - Cai, Yan. AU - El-Houseini, Motawa E.. AU - Locker, Joseph. AU - Wan, Yu-Jui Yvonne. PY - 1998/11/6. Y1 - 1998/11/6. N2 - α-Fetoprotein (AFP), a protein highly induced during fetal liver development, is down-regulated by retinoids in the human hepatoma cell line Hep3B, in contrast to up-regulation observed in other cell types. Previously, we have documented that such up-regulation involves direct effects through cis-retinoid X receptor-binding sites in the AFP enhancer. In this report, we show a distinctive effect of all-trans-retinoic acid (RA) in Hep3B cells. RA caused a marked decrease in AFP transcripts. Deletion analysis of the upstream regulatory region of the AFP gene revealed that cis-acting sites required for down-regulation resided near the promoter. Gel mobility shift assays for factors binding to key elements in the ...
This gene encodes pterin-4 alpha-carbinolamine dehydratase, an enzyme involved in phenylalanine hydroxylation. A deficiency of this enzyme leads to hyperphenylalaninemia. The enzyme regulates the homodimerization of the transcription factor hepatocyte nuclear factor 1 (HNF1 ...
Maturity-onset diabetes of the young type 3 (MODY3) is a non-ketotic form of diabetes associated with poor insulin secretion. Over the past years, several studies have reported the association of missense mutations in the Hepatocyte Nuclear Factor 1 Alpha (HNF1A) with MODY3. Missense mutations in the POU homeodomain (POUH) of HNF1A hinder binding to the DNA, thereby leading to a dysfunctional protein. Missense mutations of the HNF1A were retrieved from public databases and subjected to a three-step computational mutational analysis to identify the underlying mechanism. First, the pathogenicity and stability of the mutations were analyzed to determine whether they alter protein structure and function. Second, the sequence conservation and DNA-binding sites of the mutant positions were assessed; as HNF1A protein is a transcription factor. Finally, the biochemical properties of the biological system were validated using molecular dynamic simulations in Gromacs 4.6.3 package. Two arginine residues ...
We examined the relationship of maturity-onset clinical diabetes mellitus with the subsequent incidence of coronary heart disease, stroke, total cardiovascular
Hepatic nuclear factor 4α (HNF4A) is a nuclear transcription factor that regulates the expression of many genes involved in drug disposition. To identify additional molecular mechanisms that regulate HNF4A, we identified microRNAs (miRNAs) that target HNF4A expression. In silico analyses suggested that HNF4A is targeted by many miRNAs. We conducted in vitro studies to validate several of these predictions. With use of an HNF4A 3-untranslated region (UTR) luciferase reporter assay, five of six miRNAs tested significantly down-regulated (∼20-40%) the luciferase activity. In HepG2 cells, miR-34a and miR-449a also down-regulated the expression of both the HNF4A protein and an HNF4A target gene, PXR (∼30-40%). This regulation appeared without reduction in HNF4A mRNA expression, suggesting that they must be blocking HNF4A translation. Using additional bioinformatic algorithms, we identified polymorphisms that are predicted to alter the miRNA targeting of HNF4A. Luciferase assays indicated that miR-34a
Mutations in the genes encoding hepatocyte nuclear factor 4α (HNF-4α) and HNF-1α impair insulin secretion and cause maturity onset diabetes of the young (MODY). HNF-4α is known to be an essential positive regulator of HNF-1α. More recent data demonstrates that HNF-4α expression is dependent on HNF-1α in mouse pancreatic islets and exocrine cells. This effect is mediated by binding of HNF-1α to a tissue-specific promoter (P2) located 45.6 kb upstream from the previously characterized Hnf4α promoter (P1). Here we report that the expression of HNF-4α in human islets and exocrine cells is primarily mediated by the P2 promoter. Furthermore, we describe a G → A mutation in a conserved nucleotide position of the HNF-1α binding site of the P2 promoter, which cosegregates with MODY. The mutation results in decreased affinity for HNF-1α, and consequently in reduced HNF-1α-dependent activation. These findings provide genetic evidence that HNF-1α serves as an upstream regulator of HNF-4α ...
Rat hepatoma-human fibroblast hybrids of two independent lineages containing only 8-11 human chromosomes show pleiotropic extinction of thirteen out of fifteen hepatic functions examined. Reexpression of the entire group of functions most often occurs in a block, and except for one discordant subclone, correlates with loss of human chromosome 2. The extinguished cells and their reexpressing derivatives have been examined for the expression of seven liver-enriched transcription factors. C/EBP, LAP, DBP, HNF3, and vHNF1 expression are not systematically extinguished in parallel with the hepatic functions. However, HNF1 and HNF4 show a perfect correlation with phenotype: these factors are expressed only in the cells showing pleiotropic reexpression. Since recent evidence indicates that HNF4 controls HNF1 expression, it can be proposed that the HNF4 gene is the primary target of the pleiotropic extinguisher. ...
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
Purpose Type 2 diabetes mellitus (type 2 DM) and maturity-onset diabetes of the young present some similar clinical and biochemical characteristics that make them difficult to differentiate. Currently, the polymorphism T130I (rs1800961) in the HNF4A (hepatocyte nuclear factor 4A) gene has been described as a risk factor to type 2 DM and shows an autosomal dominant inheritance pattern associated to β-cell function decrease. The aim of the present work was to characterize the phenotypic profile of the T130I carrier and noncarrier relatives included in 3 unrelated families. ...
Animals. Ppargfl/fl, Akt2fl/fl, Ptenfl/fl, and Hnf1a-/- mouse lines have been previously described (12, 30, 59, 60). SR2595 was synthesized and purified as previously described (35). Animals were maintained in grouped cages in a temperature-controlled pathogen-free facility on a 12-hour/12-hour (8 am-8 pm) light/dark cycle and had free access to water and standard chow (Teklad global protein diet; 20% protein, 75% carbohydrate, 5% fat). Animals were sacrificed between 2 and 4 pm. For the in vivo pharmacological treatments with pioglitazone incorporated in chow food (200 mg/kg), mice had free access to food and were treated for 3 months, from the ages of 5 months to 8 months. For the in vivo pharmacological treatments, SR2595 was administered daily by oral gavage (20 mg/kg). In the pretumoral group, mice were treated daily by oral gavage for 1 month from the ages of 5 to 6 months. For the tumoral group, treatment was initiated at 11 months of age for 1 month. For 5-bromo-2′-deoxyuridine (BrdU) ...
Mody, J K., "Tumourigenesis in intact and sub-totally mammectomized c3h(jaz) mice." (1967). Subject Strain Bibliography 1967. 749 ...
Data from the Pharmacogenomics and Risk of Cardiovascular Disease (PARC) study and the Cardiovascular Health Study (CHS) provide independent and confirmatory evidence for association between common polymorphisms of the HNF1A gene encoding hepatocyte nuclear factor-1 alpha and plasma C-reactive prote …
Powerful evidence for a genetic component to T2D (1) has driven extensive efforts to identify genetic variants contributing to risk. Monogenic forms of diabetes such as maturity-onset diabetes of the young (MODY) have proven to be natural models for understanding mechanisms underlying insulin secretion defects; genes discovered through family-based approaches are important regulators of insulin secretion and β-cell development. Findings that neonatal diabetes is most commonly due to activating mutations in genes encoding the ATP-sensitive potassium channel subunits Kir6.2 or SUR1 and can be treated with high-dose sulfonylureas despite being insulin dependent also provide a compelling case for genetic evaluation of monogenic diabetes with therapeutic and prognostic implications (2-6). Exome-wide and whole-genome sequencing approaches will expand current capacity to study these disorders.. Genome-wide association studies (GWAS) using high-density genotyping arrays have transformed understanding ...
Transcriptionally controlled transcription factor. Binds to DNA sites required for the transcription of alpha 1-antitrypsin, apolipoprotein CIII, transthyretin genes and HNF1-alpha. May be essential for development of the liver, kidney and intestine.
Monogenic diabetes is rare but is an important diagnosis in pediatric diabetes clinics. These patients are often not identified as this relies on the recognition of key clinical features by an alert clinician. Biomarkers (islet autoantibodies and C-peptide) can assist in the exclusion of patients with type 1 diabetes and allow systematic testing that does not rely on clinical recognition. Our study aimed to establish the prevalence of monogenic diabetes in U.K. pediatric clinics using a systematic approach of biomarker screening and targeted genetic testing ...
Worldwide epidemics of metabolic diseases, including liver steatosis, are associated with an increased frequency of malignancies, showing the highest positive correlation for liver cancer. The heterogeneity of liver cancer represents a clinical challenge. In liver, the transcription factor PPARγ promotes metabolic adaptations of lipogenesis and aerobic glycolysis under the control of Akt2 activity, but the role of PPARγ in liver tumorigenesis is unknown. Here we have combined preclinical mouse models of liver cancer and genetic studies of a human liver biopsy atlas with the aim of identifying putative therapeutic targets in the context of liver steatosis and cancer. We have revealed a protumoral interaction of Akt2 signaling with hepatocyte nuclear factor 1α (HNF1α) and PPARγ, transcription factors that are master regulators of hepatocyte and adipocyte differentiation, respectively. Akt2 phosphorylates and inhibits HNF1α, thus relieving the suppression of hepatic PPARγ expression and ...
Worldwide epidemics of metabolic diseases, including liver steatosis, are associated with an increased frequency of malignancies, showing the highest positive correlation for liver cancer. The heterogeneity of liver cancer represents a clinical challenge. In liver, the transcription factor PPARγ promotes metabolic adaptations of lipogenesis and aerobic glycolysis under the control of Akt2 activity, but the role of PPARγ in liver tumorigenesis is unknown. Here we have combined preclinical mouse models of liver cancer and genetic studies of a human liver biopsy atlas with the aim of identifying putative therapeutic targets in the context of liver steatosis and cancer. We have revealed a protumoral interaction of Akt2 signaling with hepatocyte nuclear factor 1α (HNF1α) and PPARγ, transcription factors that are master regulators of hepatocyte and adipocyte differentiation, respectively. Akt2 phosphorylates and inhibits HNF1α, thus relieving the suppression of hepatic PPARγ expression and ...
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PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
J:120667 Bouzin C, Clotman F, Renauld JC, Lemaigre FP, Rousseau GG, The onecut transcription factor hepatocyte nuclear factor-6 controls B lymphopoiesis in fetal liver. J Immunol. 2003 Aug 1;171(3):1297-303 ...