Obesity

Sh2b1 obesity facts: Associated Content

Considering the pivotal role of the sympathetic nervous system SNS in BAT activation, we assessed the impact of Sh2b1 deficiency on the ability of leptin to stimulate sympathetic nerve transmissions in BAT. Source data are provided as a Source Data file.

J Sg2b1 Biochem. All growth parameters including height, weight, and BMI were at or above the 95th percentile in three of these four patients, whereas weight and BMI were above the 95th percentile and height was above the 90th percentile in the fourth. Background A large-scale genome-wide association study GWAS meta-analysis including a total ofindividuals of European ancestry confirmed 14 known obesity-susceptibility loci and newly identified 18 genetic loci associated with body mass index BMI. Download PDF. Send Reset Link.

  • Some features of the site may not work correctly. Cheetham and I.

  • We next aimed to further map Sh2b1 target neurons.

  • The kb 16p Acknowledgements We thank all the probands and their families for their participation.

Background

In addition, with STAT3 mediated leptin signalling, we only tested one of the many potential interaction partners of SH2B1 in regulation of energy homeostasis. Has PDF. The kb 16p Research Feed.

Haploinsufficiency HI Score Details. Fqcts mark sh2b1 obesity facts position of exchange g. Skip to search form Skip to main content You are currently offline. TS Evidence Strength:. Table 1 Phenotypic description of analyzed study groups Full size table. The rating of a single gene within the CNV should not necessarily be the only criteria by which one defines a clinical interpretation.

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We demonstrated that LepR neuron-specific deletion of Factsor adult-onset deletion of Sh2b1 in the hypothalamus containing LepR neuronsresulted in severe obesity, insulin resistance, and liver steatosis. Rupp, A. Guo, A. For healthcare professionals, visit www. Authorship note: Michael E.

AH conceived of the study, its design and coordination and writing of the manuscript. TS Obfsity Strength:. Identification of SH2-B as a sh2b1 obesity facts regulator of leptin sensitivity, energy balance, and body weight in mice. Written informed consent was given by all participants and in case of minors by their parents. Remember Me. Leptin receptor-expressing neuron Sh2b1 supports sympathetic nervous system and protects against obesity and metabolic disease.

Deletion of the distal 16p According to the authors, "four of the six patients had a BMI at or above the 95th percentile. Sh2b1 obesity facts Metab Lond. In addition, with STAT3 mediated leptin signalling, we only tested one of the many potential interaction partners of SH2B1 in regulation of energy homeostasis. We calculated that the control group would need to include more thanindividuals to reveal a p-value below 0. Additional evidence for an involvement of Sh2b1 in the regulation of energy homeostasis is derived from expression analyses in mice and rats. Save to Library Save.

Publication types

Region Facts Region Name 16p Electronic supplementary material. Little Evidence for Triplosensitivity 1 Read full report The 16p Winfried Rief declares that he received financial support for presentations and for scientific advice from Astra Zeneca, Heel, and Berlin Chemie; he also declares that this did not influence the content of this manuscript.

In addition, with STAT3 mediated leptin signalling, we only tested one of the many potential interaction partners of Sh2b1 obesity facts in regulation of energy homeostasis. Figure 2. However, for a polygenic variant a large functional effect is rather unlikely. Nutr Metab Lond. The other five individuals are heterozygous carriers of a deletion at chr16p Correspondence to Anke Hinney.

Abstract Src homology 2 B adapter protein 1 SH2B1 modulates signaling by a variety of ligands that bind to receptor tyrosine kinases or JAK-associated cytokine receptors, including leptin, insulin, growth hormone GHand sh2b1 obesity facts su2b1 factor NGF. Body temperature was maintained within a normal range during the entire procedures using a thermal pad. Leptin receptor signaling and action in the central nervous system. All studies were approved by the Anglia and Oxford multiregional ethics committee. Large, rare chromosomal deletions associated with severe early-onset obesity. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.

Introduction

The rating of a single gene within the CNV should not necessarily be the only criteria by which one defines a clinical interpretation. View author publications. Additional references: Barge-Schaapveld et al.

Body composition and liver TAG levels Mice were euthanized and organs were harvested and weighted. Journal ID doi : Collective and individual functions of leptin receptor modulated neurons controlling metabolism and ingestion. Coppack, S.

This review refers deletions and duplications involving recurrent breakpoint BP regions BP2 and BP3, located in the distal region of 16p Correspondence to Anke Hinney. Download PDF. JH participated in the design of the study and writing of the manuscript.

The selection of individuals for the mutation screen was based on genotypes at SNP rs proxy of rs in the vicinity of SH2B1. Back To Top. Volckmar, AL. The 16p For example, the melanocortin 4 receptor gene MC4Ra well known obesity gene, harbors two polymorphisms ValIle and IleLeu that are negatively associated with obesity [ 4445 ].

More Filters. Pearce and J. Am J Hum Genet. To enhance the sensitivity of detection of homozygous mutation carriers, DNA of an individual with wild type genotype re-sequenced was added to each sample prior to PCR amplification.

Shen, and M. Abstract Src homology 2 B adapter protein 1 SH2B1 modulates signaling by a variety of ligands that bind to receptor tyrosine kinases or JAK-associated cytokine receptors, including leptin, insulin, growth hormone GHand nerve growth factor NGF. Zheng, Z. Diabetes 49—

Blood samples were collected from tail veins. Howard, J. A P value less than 0. Sh2b1 -null mice develop severe leptin resistance, obesity, and type 2 diabetes 23 Immunoprecipitated proteins and proteins in cell lysates were immunoblotted using anti-Flag and anti-GFP antibodies.

Association to obesity of detected variants was analyzed in three steps Figure 1 : i. PLoS Genet. A mutation in the human leptin receptor gene causes obesity and pituitary dysfunction. Publication Type.

However, these individuals did not facys to further behavioral testing, so the precise nature and severity of these phenotypes could not be determined. Nat Commun 11, In agreement with the previous reports 43central injection of leptin progressively and markedly increased SNA in wild type i. Our studies imply an unexpected role for SH2B1 in human behavior. Find articles by Henning, E. We next aimed to further map Sh2b1 target neurons.

Protein tyrosine phosphatase sh2b1 obesity facts affects body weight by downregulating leptin signaling in a phosphorylation-dependent manner. Cao, L. See Supplemental Methods for details. Together, these data suggest that POMC neuron-specific ablation of Sh2b1 is insufficient to induce obesity and metabolic disease. Reprints and Permissions. Functional characterization of SH2B1 mutations.

Neuron 21— Figure 2 Functional characterization of SH2B1 mutations. Positional cloning of the mouse obese gene and its human homologue.

For the non-synonymous SNP facrs ThrAspin silico analyzes predict sh2b1 obesity facts neutral outcome for the altered amino acid Additional file 1 : Table S1. In addition, with STAT3 mediated leptin signalling, we only tested one of the many potential interaction partners of SH2B1 in regulation of energy homeostasis. The rating of a single gene within the CNV should not necessarily be the only criteria by which one defines a clinical interpretation. Haploinsufficiency HI Score Details. View on PubMed.

The dose response curves depict leptin receptor activity after sh2b1 obesity facts with leptin favts values for each data point see Additional file 1 : Table S2. PUBMED: Bachmann-Gagescu et al reported clinical phenotypes and provided a population-level prevalence comparison for 16p Nat Methods. Carter-Su and I. Evidence in humans and from animal models suggests that SH2B1 is a likely obesity gene. Some features of the site may not work correctly.

The organic phase was dried via evaporation and dissolved in isopropanol. Figure 2 Functional characterization of SH2B1 mutations. Reporting Summary. Abstract Src homology 2 B adapter protein 1 SH2B1 modulates signaling by a variety of ligands that bind to receptor tyrosine kinases or JAK-associated cytokine receptors, including leptin, insulin, growth hormone GHand nerve growth factor NGF.

Download america statistics childhood obesity. Written informed consent was given by all participants and in case of minors by their parents. Leptin receptor activity measured by STAT3 mediated luciferase response. The Genetics of Obesity. It was additionally detected in two of 11, extremely obese or overweight children, adolescents and adults, but not in 4, population-based normal-weight or lean controls. Skip to main content. These extremely obese patients offspring from the family-based GWAS sample were homozygous for the risk allele T of rs and had at least one heterozygous parent, thus substantially contributing to the observed over-transmission of the rs T-allele.

Chen, Z. Receptor-mediated ssh2b1 sympathetic nerve activation by sh2b1 obesity facts. Leptin and insulin act on POMC neurons to promote the browning of white fat. Identification of SH2-B as a key regulator of leptin sensitivity, energy balance, and body weight in mice. The publisher and the editor s disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements. Considering the pivotal role of the sympathetic nervous system SNS in BAT activation, we assessed the impact of Sh2b1 deficiency on the ability of leptin to stimulate sympathetic nerve transmissions in BAT.

Six new loci associated with body mass index highlight a neuronal influence on body weight regulation. Human SH2B1 missense mutations are facts with the obesity and metabolic disease traits 3334353637 Brain sections were prepared from wild type factss global Sh2b1 knockout negative control mice and stained with anti-Sh2b1 antibody. Nasdaq: RYTMa biopharmaceutical company aimed at developing and commercializing therapies for the treatment of rare genetic diseases of obesity, today announced positive proof-of-concept data from multiple cohorts in its Phase 2 Basket Study evaluating setmelanotide in patients with severe obesity due to genetic variants in the melanocortin-4 receptor MC4R pathway, and provided an update on its genetic sequencing efforts. Arrows red signal intensity peak indicate position of the plasma membrane on the linescan. Rectal temperature was measured upon cold exposure.

Cheng, A. Six new loci associated with body mass index highlight a neuronal influence on body weight regulation. Advanced search. Download citation. Ren, D.

Address correspondence to: I. Since SeptemberRhythm has increased its internal database of sequencing samples from 13, facts approximately 37, SH2B1 has been implicated in GH regulation of the actin cytoskeleton Large, rare chromosomal deletions associated with severe early-onset obesity. Peer review information Nature Communications thanks Qingchun Tong and the other anonymous reviewer s for their contribution to the peer review of this work. European Journal of Nutrition

We demonstrated that LepR neuron-specific deletion of Sh2b1or adult-onset deletion of Sh2b1 in the eh2b1 childhood obesity LepR neuronsresulted in severe obesity, insulin resistance, and liver steatosis. This article has been updated. Nature— Clinical studies were conducted in accordance with the principles of the Declaration of Helsinki. Forward-Looking Statements This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of Furthermore, hypothalamic Sh2b1 may increase body temperature by a SNS-independent mechanism, perhaps by enhancing the ability of hypothalamic—pituitary—thyroid axis to increase thermogenesis and body temperature. SH2B1 regulation of energy balance, body weight, and glucose metabolism.

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  • Moreover, the positive interim data in these new patient cohorts, while representing diseases which are individually rare, expand our sh2bb1 of the potential of setmelanotide to serve a far larger cumulative patient population than has been examined to date. Aside from JAK2, Sh2b1 also binds to receptor tyrosine kinases, including insulin receptors, platelet-derived growth factor receptors, nerve growth factor receptor TrkA, and brain-derived neurotrophic factor BDNF receptor TrkB 161718192021 ,

  • Article Google Scholar 7. To enhance the sensitivity of detection of homozygous mutation carriers, DNA of an individual with wild type genotype re-sequenced was added to each sample prior to PCR amplification.

  • You can also search for this author in PubMed Google Scholar. A founder effect of this mutation is likely.

  • Little Evidence for Triplosensitivity 1 Read full report

We detected two additional obese cases with this obseity and no mutation carrier among the controls. Acknowledgements We thank all the probands and their families for their participation. Facts of SH2-B as a key regulator of leptin sensitivity, energy balance, and body weight in mice. TS Evidence Strength:. Our findings suggest that this new rare mutation predisposes to increased BMI, possibly related to decreased leptin signalling. Mol Endocrinol. Available rs-numbers, if applicable amino acid exchanges and minor allele frequencies in obese cases MAF according to Table 1 are given for each variant.

Has PDF. In addition, with STAT3 mediated leptin signalling, we only tested one of the many potential interaction partners of SH2B1 in regulation of energy homeostasis. News Article. Further studies are warranted to investigate the functional impact of the mutation for both affected splice variants on the interaction of SH2B1 effector systems e. Available rs-numbers, if applicable amino acid exchanges and minor allele frequencies in obese cases MAF according to Table 1 are given for each variant.

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Neuronal SH2B1 is essential for controlling energy and glucose homeostasis. By clicking accept or america statistics childhood obesity wh2b1 use the site, you agree to the terms outlined in our Privacy PolicyTerms of Serviceand Dataset License. While the three tyrosine motifs in the N-terminal part of SH2B1, which regulate interaction with the insulin receptor [ 42 ], are not directly affected by this exchange, it is possible that altered protein folding due to an non-conservative amino acid exchange in a highly conserved position prevents their phosphorylation.

MBH-specific ablation of Sh2b1 substantially childhood obesity body weight and fat content Fig. Jiang, L. Thank you for visiting nature. Furthermore, hypothalamic Sh2b1 may increase body temperature by a SNS-independent mechanism, perhaps by enhancing the ability of hypothalamic—pituitary—thyroid axis to increase thermogenesis and body temperature.

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Hs2b1 A recent mutation screen in children from the GOOS cohort which display insulin resistance in addition to obesity revealed three variants and one SNP that showed an effect on cell differentiation and migration, but with the exception of the frameshift variant Phefs no other functional deficiencies [ 47 ]. Triplosensitivity TS Score Details. Nat Genet. J Clin Invest. Volckmar, AL.

J Cell Biochem. Winfried Rief sh2b1 obesity facts that he received financial support for presentations and for scientific advice from Astra Zeneca, Heel, and Berlin Chemie; he also declares that this did not influence the content of this manuscript. Bochukava et al. Send Feedback.

Sufficient Evidence for Haploinsufficiency 3 Read full report This sh2b1 obesity facts deletion For the non-synonymous SNP rs ThrAspin silico analyzes predict a neutral outcome for the altered amino acid Additional file 1 : Table S1. This non-coding variant was detected twice within the screening sample, and once in an obese case in the association testing step Figure 1. Available rs-numbers, if applicable amino acid exchanges and minor allele frequencies in obese cases MAF according to Table 1 are given for each variant.

You ffacts also search for this author in PubMed Google Scholar. Additional sh2b1 obesity facts Competing interests Winfried Rief declares that he received financial support for presentations and for scientific advice from Astra Zeneca, Heel, and Berlin Chemie; he also declares that this did not influence the content of this manuscript. Doche and E. All samples with deviant dHPLC patters were re-sequenced. A potential additive effect of small functional changes in leptinergic and insulinergic signalling could result in stronger impact on body weight maintenance.

Blood samples were collected from tail veins. About Rhythm Sh2b1 obesity facts Rhythm is a commercial-stage biopharmaceutical company committed to transforming the treatment ogesity for people living with rare genetic diseases of obesity. Deletion of Sh2b results in fat accumulation in Drosophila To examine Sh2b1 function in vivo, we generate and characterize global Sh2b1 knockout mice. Nature— Skip to main navigation.

Hypothalamic mTORC1 signaling controls sympathetic nerve activity and arterial pressure and mediates leptin effects. Amendment history: Corrigendum January The subcutaneous lipolytic response to regional neural stimulation is reduced in obese women. A P value less than 0. Find articles by Barroso, I.

However, in view of ongoing research, changes in sh2b1 obesity facts regulations, and the constant flow of obesihy relating to drug therapy and drug reactions, the reader is obesitt to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This analysis did not include 15 patients who withdrew early due to COVID-related issues, adverse events or were lost to follow-up. Shen, and M. SH2B1 enhances insulin sensitivity by both stimulating the insulin receptor and inhibiting tyrosine dephosphorylation of insulin receptor substrate proteins. Feldmann, H. MBH-specific ablation of Sh2b1 substantially increased body weight and fat content Fig. Except as required by law, we undertake no obligations to make any revisions to the forward-looking statements contained in this release or to update them to reflect events or circumstances occurring after the date of this release, whether as a result of new information, future developments or otherwise.

In addition, with STAT3 mediated leptin signalling, we only tested one of the many potential interaction partners of SH2B1 in regulation of energy homeostasis. Download references. View on PubMed. All samples with deviant dHPLC patters were re-sequenced.

All authors read and approved the final version of the manuscript. Sh2b1 obesity facts and discussion We performed a mutation screen of the coding region of SH2B1 in 95 extremely obese children and adolescents. Forgot password? Article Google Scholar 7.

Identification of SH2-B as a key regulator of leptin sensitivity, energy balance, and body weight in mice. Conclusion A recent mutation screen in children from the GOOS cohort which display insulin resistance in addition to obesity revealed three variants and one SNP that showed an effect on cell differentiation and migration, but with the exception of the frameshift variant Phefs no other functional deficiencies [ 47 ]. Send Feedback. TS Evidence Comments:.

Publication date Print : December BMC Med. To quantify SNA, the number of sh2b1 obesity facts potentials crossing a pre-set threshold was determined per second. We previously validated that anti-TH antibody specifically recognizes TH in immunostaining Find articles by Cheetham, T. Cell 2—

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Diabetes 63— In sh2b1 obesity facts with the previous reports 43central injection of leptin progressively and markedly increased SNA in wild type i. Shen, H. Authorship note: Michael E. Abstract Leptin stimulates the sympathetic nervous system SNSenergy expenditure, and weight loss; however, the underlying molecular mechanism remains elusive. Advanced search.

Conclusion : With the current study we were able to replicate and confirm that the SH2B1 gene locus is significantly associated with complex obesity in a Caucasian population. Below, green and red signal intensity along the yellow arrows was determined using MetaVue Linescan. Genome-wide association yields new sequence variants at seven loci that associate with measures of obesity. Mice were fed an HFD to induce obesity.

Full size image. The kb 16p Supplementary material: Sh2b1 obesity facts silico analysis tool description. Alternatively, genetic variation outside of the SH2B1 coding region with a regulatory effect on this gene explains the association in functional terms. ISCA View legacy report

Src homology 2 Fadts adapter protein 1 SH2B1 modulates signaling by a variety of ligands that bind to receptor tyrosine kinases or JAK-associated cytokine receptors, including leptin, insulin, growth hormone GHand nerve growth factor NGF. Version 1 - Current Version 1 Version 1. Ucp1 mediates adaptive thermogenesis and energy expenditure Diet-induced obesity in rodents, and common forms of obesity in humans, are characterized by resistance to endogenous and exogenous leptin 4.

Sign up for Nature Briefing. Central neural control of thermoregulation and brown adipose tissue. Neuron 42— Skip to main content Thank you for visiting nature. Advanced search. Mori, H.

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Across five cohorts, 65 patients with severe obesity were eligible for analysis as of a cutoff date of Dec. Abstract Leptin stimulates the sympathetic nervous system SNSenergy expenditure, and weight loss; however, the underlying molecular facys remains elusive. Willer, C. In agreement with the previous reports 43central injection of leptin progressively and markedly increased SNA in wild type i. You are using a browser version with limited support for CSS. However, we note that these phenotypes were not seen in association with the other genetic obesity syndromes we have characterized to date 1112although the socioeconomic status of mutation carriers was comparable. This effect is reversible upon discontinuation of the drug.

In total, we analyzed 95 individuals, 90 of whom were likely enriched fact the presence of mutations in SH2B1. Cell Metab. We thank all the probands and their families for their participation. The domain structure Quian and Ginty with dimerization, Pleckstrin homology and SH2 domain is shown as underlying grey boxes.

Sh2b1 was detected in hypothalamic cells in wild-type mice Supplementary Fig. Ucp1 mediates adaptive thermogenesis and energy expenditure Journal: Obesity Facts. We have demonstrated that loss-of-function mutations in SH2B1 were associated with severe early-onset obesity, insulin resistance, and reduced final height. In contrast, the FLfsX20 mutant exhibited significantly reduced expression and was unable to activate JAK2 Figure 2 D and data not shownpresumably due to the fact that it lacks the SH2 domain previously shown to be required for JAK2 activation

The Rosenfeld dataset represents an increase in the number of cases reported sh2b1 obesity facts the Cooper dataset. Genomic View. Am J Hum Genet. If not stated otherwise, all p-values are asymptotic, two-sided and not corrected for multiple testing. A new mutation at position g. J Clin Invest.

In addition, based on the evidence for involvement of SH2B1 in energy homeostasis, rare coding variants in the gene could potentially result in monogenic obesity. J Obezity Chem. In total, we analyzed 95 individuals, 90 of whom were likely enriched for the presence of mutations in SH2B1. Highly Influenced. In humans, the SH2B1 protein increase serum leptin levels and whole body fat mass in females [ 11 ]. In DIO diet-induced obese rats, fed a high fat diet, the expression of Sh2b1 in hypothalamus was decreased [ 17 ], while in mice on a high fat and high carbohydrate diet, Sh2b1 expression increased in the same tissue [ 18 ]. This interaction enhances insulin signalling and insulin receptor auto-phosphorylation, leading in turn to activation of downstream pathways [ 41 ].

  • Article Google Scholar 7. This non-coding variant was detected twice within the screening sample, and once in an obese case in the association testing step Figure 1.

  • We report that neuron-specific restoration of Sh2b1 expression reverses the obesity phenotypes of Sh2b1 -null mice 39indicating that neurons mediate Sh2b1 actions on body weight and metabolism.

  • TS Published Evidence:. Allele and genotype distributions of all detected variants did not deviate from Hardy-Weinberg equilibrium.

  • This non-coding variant was detected twice within the screening sample, and once in an obese case in the association testing step Figure 1.

We sh2b11 that the control group would need to include more thanindividuals to reveal a p-value below 0. A cross-sectional study in school children focusing on age and bodyweight at the onset of menarche. Contact us Submission enquiries: bmcmedicalgenomics biomedcentral. Research Feed. We detected two additional obese cases with this mutation and no mutation carrier among the controls. The other five individuals are heterozygous carriers of a deletion at chr16p Full size image.

The loss of function sh2b1 obesity facts should be used to evaluate deletions, and the triplosensitivity score should be used to evaluated duplications. A mutation in the human leptin receptor gene causes obesity and pituitary dysfunction. J Clin Invest. Table 3 In silico prediction of splice sites, transcription factor binding sites and o-glycosylation sites of detected variants in SH2B1 Full size table.

Article Google Scholar 7. A new mutation at position g. J Biol Chem. Detailed clinical information was available for six patients, who all had developmental delays of varying severity.

AAV vectors 0. PTP1B regulates leptin signal sh2b1 obesity facts in vivo. Therefore, we set out to replicate the reported association with rs in our Belgian study population and to extend our study with an additional tagSNP for the SH2B1 gene region. Immunoaffinity enrichment and mass spectrometry analysis of protein methylation.

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Shen, H. Sympathetic neuro-adipose connections mediate leptin-driven lipolysis. Copyright: All rights reserved. Thus, SH2B1 is emerging as a critical regulator of body weight and metabolism in both animals and humans; however, SH2B1 target cell types remain poorly understood. All studies were approved by the Anglia and Oxford multiregional ethics committee. Human SH2B1 mutations are associated with maladaptive behaviors and obesity.

Citation Type. Nat Genet. Eur J Endocrinol. Conclusion A recent mutation screen in children from the Sh2b1 obesity facts cohort which display insulin resistance in addition to obesity revealed three variants and one SNP that showed an effect on cell differentiation and migration, but with the exception of the frameshift variant Phefs no other functional deficiencies [ 47 ].

Sufficient America statistics childhood obesity for Haploinsufficiency Disclaimer. Citation Obesiyt. We screened the coding region of SH2B1 for infrequent mutations in 95 extremely obese children and adolescents. Identification of SH2-B as a key regulator of leptin sensitivity, energy balance, and body weight in mice. Our results could, of course, indicate that the two variants are not functionally relevant.

Note that genes used as landmarks are not necessarily causative of the complete sh2b1 obesity facts s associated with the region. More Filters. The non-coding mutation g. The dose response curves depict leptin receptor activity after stimulation with leptin exact values for each data point see Additional file 1 : Table S2. All growth parameters including height, weight, and BMI were at or above the 95th percentile in three of these four patients, whereas weight and BMI were above the 95th percentile and height was above the 90th percentile in the fourth. ISCA View legacy report Figure 1.

Detailed description of used tools can be found in the Additional file 1 : Supplementary materials. Electronic supplementary material. Article Google Scholar. Data on weight, height, body mass index BMI and head circumference HC were available for 39 unrelated carriers. Supplementary material: In silico analysis tool description.

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