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Book ; Online: Computational Approach Revealed Potential Affinity of Antiasthmatics Against Receptor Binding Domain of 2019n-Cov Spike Glycoprotein

LAMIAE ELKHATTABI / Hicham Charoute / Rachid Saile / Abdelhamid Barakat

2020

Abstract: The novel COVID-19 pandemic is now a health threat, with a deep-felt impact worldwide. The new coronavirus 2019 (2019 n-Cov) binds to host human receptors through Receptor Binding Domain RBD of Spike glycoprotein (S), making it a prominent drug target. ... ...

Abstract	The novel COVID-19 pandemic is now a health threat, with a deep-felt impact worldwide. The new coronavirus 2019 (2019 n-Cov) binds to host human receptors through Receptor Binding Domain RBD of Spike glycoprotein (S), making it a prominent drug target. The present study aims to identify new potential hits that can inhibit the S protein using in silico approaches. Several natural and synthetics compounds (antiasthmatics, Antiviral, Antimalarial, Antibacterial, Anti-Inflammatory, cyclic peptide, and cyclic bis) were screened by molecular docking using AutoDock Vina. Additionally, we tested calcitriol and three known drugs (Azithromycin, HydroxyChloroquine, and Chloroquine ) against the spike protein to found if they have any direct interaction. Our finding consists of 4 potential synthetic compounds from PubChem database, known for their antiasthmatic effects, that show highly binding energies each (-8.6 kcal/mol, 7.7kcal/mol, -7.2 kcal/mol and -7.0 kcal/mol). Another 5 natural compounds from the South African natural sources database (SANCDB) that bind to RBD of Spike with significant energy each: (Marchantin C with -7.3 kcal/mol, Riccardin C with -7.0 kcal/mol, Digitoxigenin-glucoside with -6.9 kcal/mol, D-Friedoolean-14-en-oic acid with -6.8 kcal/mol and, Spongotine A with -6.7 kcal/mol). The FaF-Drugs server was used to evaluate the drug-like properties of the identified compounds. Additionally, Calcitriol, Azithromycin, and HydroxyChloroquine have an appreciable binding affinity to 2019-nCoV S, suggesting a possible mechanism of action. Using in silico approaches like molecular docking and pharmacokinetic properties, we showed new potential inhibitors. Our findings need further analysis, and chemical design for more effective derivatives of these compounds speculated to disrupt the viral recognition of host receptors.
Keywords	Bioinformatics and Computational Biology ; Covid-19 Spike ; antiasthmatics ; natural compounds ; Molecular Docking ; prediction ; treatment ; covid19
Subject code	540
Publishing date	2020-04-13T11:45:12Z
Document type	Book ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Clinical and genetic spectrums of 413 North African families with inherited retinal dystrophies and optic neuropathies

Aymane Bouzidi / Hicham Charoute / Majida Charif / Ghita Amalou / Mostafa Kandil / Abdelhamid Barakat / Guy Lenaers

Orphanet Journal of Rare Diseases, Vol 17, Iss 1, Pp 1-

2022 Volume 21

Abstract: Abstract Background Inherited retinal dystrophies (IRD) and optic neuropathies (ION) are the two major causes world-wide of early visual impairment, frequently leading to legal blindness. These two groups of pathologies are highly heterogeneous and ... ...

Abstract	Abstract Background Inherited retinal dystrophies (IRD) and optic neuropathies (ION) are the two major causes world-wide of early visual impairment, frequently leading to legal blindness. These two groups of pathologies are highly heterogeneous and require combined clinical and molecular diagnoses to be securely identified. Exact epidemiological studies are lacking in North Africa, and genetic studies of IRD and ION individuals are often limited to case reports or to some families that migrated to the rest of the world. In order to improve the knowledge of their clinical and genetic spectrums in North Africa, we reviewed published data, to illustrate the most prevalent pathologies, genes and mutations encountered in this geographical region, extending from Morocco to Egypt, comprising 200 million inhabitants. Main body We compiled data from 413 families with IRD or ION together with their available molecular diagnosis. The proportion of IRD represents 82.8% of index cases, while ION accounted for 17.8%. Non-syndromic IRD were more frequent than syndromic ones, with photoreceptor alterations being the main cause of non-syndromic IRD, represented by retinitis pigmentosa, Leber congenital amaurosis, and cone-rod dystrophies, while ciliopathies constitute the major part of syndromic-IRD, in which the Usher and Bardet Biedl syndromes occupy 41.2% and 31.1%, respectively. We identified 71 ION families, 84.5% with a syndromic presentation, while surprisingly, non-syndromic ION are scarcely reported, with only 11 families with autosomal recessive optic atrophies related to OPA7 and OPA10 variants, or with the mitochondrial related Leber ION. Overall, consanguinity is a major cause of these diseases within North African countries, as 76.1% of IRD and 78.8% of ION investigated families were consanguineous, explaining the high rate of autosomal recessive inheritance pattern compared to the dominant one. In addition, we identified many founder mutations in small endogamous communities. Short conclusion As both IRD and ION ...
Keywords	Inherited retinal dystrophies ; Inherited optic neuropathies ; Molecular diagnosis ; North Africa ; Consanguinity ; Phenotypic spectrum ; Medicine ; R
Subject code	610
Language	English
Publishing date	2022-05-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Computational Analysis of the Potential Impact of MTC Complex Missenses SNPs Associated with Male Infertility

Houda Harmak / Hicham Charoute / Salaheddine Redouane / Ouafaa Aniq Filali / Abdelhamid Barakat / Hassan Rouba

BioMed Research International, Vol

2022 Volume 2022

Abstract: Meiotic chromosomes endure rapid prophase movements that ease the formation of interhomologue recombination intermediates that drive synapsis, crossing over, and segregation process. To generate these fast moves, the meiotic telomere complex (MTC) ... ...

Abstract	Meiotic chromosomes endure rapid prophase movements that ease the formation of interhomologue recombination intermediates that drive synapsis, crossing over, and segregation process. To generate these fast moves, the meiotic telomere complex (MTC) enables telomere-inner nuclear membrane attachment during meiotic prophase I and transfers cytoskeletal signals via another complex: the LINC complex. Furthermore, disruption or mutations of any of the MTC genes (TERB1, TERB2, and MAJIN) alters telomere association with the nuclear envelope leading to impairment of homologous pairing and synapsis, a meiotic arrest, and consequently to male infertility. To decipher the effect of TERB1, TERB2, and MAJIN missense mutations on protein structure, stability, and function, different bioinformatic tools were used in this study including VEP, Mutabind2, Haddock, Prodigy, Ligplot, ConSurf, DUET and MusiteDeep. In total, thirty mutations were predicted to be deleterious using VEP web server: seventeen for TERB1, eleven for TERB2, and two for MAJIN. All these single nucleotide polymorphisms were further analyzed and only 11 SNPs (W8R, G25R, P649A, I624T, C618R, F607V, S604G, C592Y, C592R, G187W, and R53C) were found to be the most damaging by at least six software tools and exert deleterious effect on the TERB1, TERB2, and MAJIN protein structures and likely functions. They revealed high conservation, less stability, and having a role in posttranslational modifications. This in silico approach provides information to gain further insights about variants that might affect stability, change binding affinity, and edit protein-protein interactions to facilitate their identification and functional characterization associated with male infertility.
Keywords	Medicine ; R
Subject code	572
Language	English
Publishing date	2022-01-01T00:00:00Z
Publisher	Hindawi Limited
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: An Unusual Case of Gullo’s Syndrome Concomitant with Serious Endometriosis Disease in a Postmenopausal Woman

Abdelhakim Ainahi / Abdellaziz Ziane / Lahcen Wakrim / Naima Elmdaghri / Abdelhamid Barakat

Case Reports in Medicine, Vol

2018 Volume 2018

Abstract: Gullo’s syndrome is a singular physiological phenomenon defined by an abnormal increase in serum pancreatic enzyme levels that may occur in healthy subjects in the absence of pancreatic disorders. During routine health examination in a 54-year-old ... ...

Abstract	Gullo’s syndrome is a singular physiological phenomenon defined by an abnormal increase in serum pancreatic enzyme levels that may occur in healthy subjects in the absence of pancreatic disorders. During routine health examination in a 54-year-old postmenopausal woman with severe endometriosis, elevated values of serum amylase and lipase were fortuitously observed (198 and 1461 U/L, resp.). Over five years of regular pancreas surveillance, all clinical, biological, and imaging investigations were normal. However, the pancreatic enzyme levels have shown considerable fluctuations including some episodic transient normalization. The description of this benign pancreatic hyperenzymemia case incidentally associated with endometriosis disease is a very rare clinical situation. More in-depth documentation of this phenomenon may help clinicians to avoid unnecessary diagnostic management approaches and reassure the concerned patients that this affection would not be so worrying.
Keywords	Medicine ; R
Subject code	610
Language	English
Publishing date	2018-01-01T00:00:00Z
Publisher	Hindawi Limited
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Novel ITGB2 Mutation Is Responsible for a Severe Form of Leucocyte Adhesion Deficiency Type 1

Ahmed Bouhouche / Yasmin Tabache / Omar Askander / Hicham Charoute / Nada Mesnaoui / Lamiae Belayachi / Naima El Hafidi / Houyam Hardizi / Elmostafa El Fahime / Naima Erreimi / Abdelhamid Barakat / Mohammed Khattab / Fouad Seghrouchni / Amine El Hassani

BioMed Research International, Vol

2022 Volume 2022

Abstract: Leukocyte adhesion deficiency type 1 (LAD1) is a rare autosomal recessive hereditary disorder characterized by recurrent infections, impaired pus formation, delayed wound healing, omphalitis, and delayed separation of the umbilical cord as hallmark ... ...

Abstract	Leukocyte adhesion deficiency type 1 (LAD1) is a rare autosomal recessive hereditary disorder characterized by recurrent infections, impaired pus formation, delayed wound healing, omphalitis, and delayed separation of the umbilical cord as hallmark features of the disease. It results from mutations in the integrin β2 subunit gene ITGB2, which encodes the integrin beta chain-2 protein CD18. In this study, we aimed to investigate the case of a five-month-old boy who presented with a clinical phenotype and flow cytometry results suggesting LAD1 disease. Sanger sequencing of all exons and intron boundaries of ITGB2 identified a novel in-frame deletion in exon 7 (ITGB2 c.844_846delAAC, p.Asn282del) in the patient. The p.Asn282del mutation was heterozygous in the child’s parents, whereas it was absent in the 96 control individuals from North Africa. This variant was evaluated by two in silico mutation analysis tools, PROVEAN and MutationTaster, which predicted that the mutation was likely to be pathogenic. In addition, molecular modeling with the YASARA View software suggested that this novel mutation may affect the structure of integrin beta-2 and, subsequently, its interaction with integrin alpha-X. In summary, we report a novel pathogenic mutation p.Asn282del associated with LAD1 that expands the mutation diversity of ITGB2 and suggest the combination of flow cytometry and ITGB2 sequencing as a first-line diagnostic approach for LAD disease.
Keywords	Medicine ; R
Subject code	610
Language	English
Publishing date	2022-01-01T00:00:00Z
Publisher	Hindawi Limited
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Prediction and Structural Comparison of Deleterious Coding Nonsynonymous Single Nucleotide Polymorphisms (nsSNPs) in Human LEP Gene Associated with Obesity

Hind Bouafi / Sara Bencheikh / AL Mehdi Krami / Imane Morjane / Hicham Charoute / Hassan Rouba / Rachid Saile / Fouad Benhnini / Abdelhamid Barakat

BioMed Research International, Vol

2019 Volume 2019

Abstract: Leptin is a peptide hormone that regulates fat stores in the body and appetite by controlling the feeling of satiety. This hormone is secreted by the white adipose tissue and plays a role in the storage and mobilization of fatty acids. Mutations of the ... ...

Abstract	Leptin is a peptide hormone that regulates fat stores in the body and appetite by controlling the feeling of satiety. This hormone is secreted by the white adipose tissue and plays a role in the storage and mobilization of fatty acids. Mutations of the LEP gene have been associated with obesity in different populations; it is a multifactorial disease that constitutes a major public health problem. In this study, we evaluated the impact of missense SNPs in the LEP gene extracted from dbSNP using 8 computational prediction tools. Out of the total of 4337 SNPs, 93 were nsSNPs (nonsynonymous single nucleotide polymorphisms). Among 93 nsSNPs, 12 (S46L, G59S, D61N, D100N, N103K, C117S, D76V, S88C, P90R, I95N, L161R, and R105W) variants were predicted to be the most deleterious by prediction software. On these 12 deleterious SNPs, 8 variants (S46L, G59S, D61N, D100N, N103K, C117S, L161R, and R105W) were located in the conserved positions and showed a decrease in structure stability which was evaluated by I-Mutant and Mupro. Then, by analyzing the different interactions between different amino acids in wild and mutated proteins, we assessed the structural impact of the deleterious modifications using the YASARA software. Among 8 deleterious nsSNPs, we revealed structure changes in the 6 variants S46L, G59S, D100N, L103K, R105W, L161R, two of which R105W, N103K were previously reported as associated with obesity. Our study suggests 6 deleterious mutations could play an important role in contributing to human obesity and worth to be included in association and functional studies, then may be a drug target.
Keywords	Medicine ; R
Subject code	616
Language	English
Publishing date	2019-01-01T00:00:00Z
Publisher	Hindawi Limited
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: La part de l’hérédité dans les déficits auditifs ou surdités

Abdelhamid BARAKAT / Omar ABIDI

Technologies de Laboratoire, Vol 3, Iss 12, Pp 11-

2008 Volume 16

Abstract: La surdité est le déficit neurosensoriel le plus fréquent. Elle touche environ 1/1000 enfants à la naissance. Elle peut être soit acquise ou d’origine génétique. Les surdités héréditaires, environ 60%, sont divisées en non-syndromique (isolées) et ... ...

Abstract	La surdité est le déficit neurosensoriel le plus fréquent. Elle touche environ 1/1000 enfants à la naissance. Elle peut être soit acquise ou d’origine génétique. Les surdités héréditaires, environ 60%, sont divisées en non-syndromique (isolées) et syndromiques. A ce jour, plus de 100 gènes, dont l’atteinte peut être à l’origine d’une surdité, ont été identifiés. Par ailleurs, l’atteinte d’un gène particulier, nommé GJB2, codant la connexine-26 est responsable à elle seule entre 30% à 50 % des cas de surdités isolées autour du bassin méditerranéen. Parmi 90 mutations décrites au niveau de ce gène comme responsables de la surdité, la mutation 35delG est majoritaire chez ces populations. Chez les sourds marocains, trois mutations GJB2, 35delG, V37I et E47X, ont été détectées. La mutation 35delG reste la cause héréditaire de la surdité la plus fréquente avec 37% des cas. Cette mutation est présente à l’état hétérozygote chez 2.65% des individus normo-entendants de la population marocaine. Ces données ont rendu le test moléculaire des surdités héréditaires disponible au Maroc, ce qui a permis d’améliorer considérablement un conseil génétique adapté aux familles ayant des individus sourds.
Keywords	Déficits auditifs ; Hérédité ; 35delG ; Diagnostic moléculaire ; Conseil génétique ; Biology (General) ; QH301-705.5 ; Science ; Q ; DOAJ:Biology ; DOAJ:Biology and Life Sciences
Language	French
Publishing date	2008-12-01T00:00:00Z
Publisher	TECHNOP
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Prediction of the Impact of Deleterious Nonsynonymous Single Nucleotide Polymorphisms on the Human RRM2B Gene

Chaimaa Ait El Cadi / Al Mehdi Krami / Hicham Charoute / Zouhair Elkarhat / Najat Sifeddine / Hamid Lakhiari / Hassan Rouba / Abdelhamid Barakat / Halima Nahili

BioMed Research International, Vol

A Molecular Modeling Study

2020 Volume 2020

Abstract: RRM2B gene encodes ribonucleoside-diphosphate reductase subunit M2 B, the p53-inducible small subunit (p53R2) of ribonucleotide reductase (RNR), an enzyme catalyzing dNTP synthesis for mitochondrial DNA. Defects in this gene may cause severe ... ...

Abstract	RRM2B gene encodes ribonucleoside-diphosphate reductase subunit M2 B, the p53-inducible small subunit (p53R2) of ribonucleotide reductase (RNR), an enzyme catalyzing dNTP synthesis for mitochondrial DNA. Defects in this gene may cause severe mitochondrial disease affecting mainly the nervous system. This study is aimed at examining the effect of deleterious nonsynonymous SNP (nsSNP) on the structure of the RRM2B protein, using a variety of prediction tools followed by a molecular modeling analysis. After using 13 algorithms, 19 nsSNPs were predicted deleterious. Among these variants, 18 decreased the protein stability and 16 were localized in very highly conserved regions. Protein 3D structure analysis showed that 18 variants changed amino acid interactions. These results concur with what has been found in experimental trials; 7 deleterious nsSNPs were previously reported in patients suffering from genetic disorders affecting the nervous system. Thus, our study will provide useful information to design more efficient and fast genetic tests to find RRM2B gene mutations.
Keywords	Medicine ; R
Language	English
Publishing date	2020-01-01T00:00:00Z
Publisher	Hindawi Limited
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Novel compound heterozygous MYO7A mutations in Moroccan families with autosomal recessive non-syndromic hearing loss.

Amina Bakhchane / Majida Charif / Amale Bousfiha / Redouane Boulouiz / Halima Nahili / Hassan Rouba / Hicham Charoute / Guy Lenaers / Abdelhamid Barakat

PLoS ONE, Vol 12, Iss 5, p e

2017 Volume 0176516

Abstract: The MYO7A gene encodes a protein belonging to the unconventional myosin super family. Mutations within MYO7A can lead to either non syndromic hearing loss or to the Usher syndrome type 1B (USH1B). Here, we report the results of genetic analyses performed ...

Abstract	The MYO7A gene encodes a protein belonging to the unconventional myosin super family. Mutations within MYO7A can lead to either non syndromic hearing loss or to the Usher syndrome type 1B (USH1B). Here, we report the results of genetic analyses performed on Moroccan families with autosomal recessive non syndromic hearing loss that identified two families with compound heterozygous MYO7A mutations. Five mutations (c.6025delG, c.6229T>A, c.3500T>A, c.5617C>T and c.4487C>A) were identified in these families, the latter presenting two differently affected branches. Multiple bioinformatics programs and molecular modelling predicted the pathogenic effect of these mutations. In conclusion, the absence of vestibular and retinal symptom in the affected patients suggests that these families have the isolated non-syndromic hearing loss DFNB2 (nonsyndromic autosomal recessive hearing loss) presentation, instead of USH1B.
Keywords	Medicine ; R ; Science ; Q
Language	English
Publishing date	2017-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Novel compound heterozygous mutations in the GPR98 (USH2C) gene identified by whole exome sequencing in a Moroccan deaf family

Bousfiha, Amale / Abdelhamid Barakat / Amina Bakhchane / Guy Lenaers / Hassan Rouba / Hicham Charoute / Majida Charif / Mustapha Detsouli

Molecular biology reports. 2017 Oct., v. 44, no. 5

2017

Abstract: In the present work, we identified two novel compound heterozygote mutations in the GPR98 (G protein-coupled receptor 98) gene causing Usher syndrome. Whole-exome sequencing was performed to study the genetic causes of Usher syndrome in a Moroccan family ...

Abstract	In the present work, we identified two novel compound heterozygote mutations in the GPR98 (G protein-coupled receptor 98) gene causing Usher syndrome. Whole-exome sequencing was performed to study the genetic causes of Usher syndrome in a Moroccan family with three affected siblings. We identify two novel compound heterozygote mutations (c.1054Câ>âA, c.16544delT) in the GPR98 gene in the three affected siblings carrying post-linguale bilateral moderate hearing loss with normal vestibular functions and before installing visual disturbances. This is the first time that mutations in the GPR98 gene are described in the Moroccan deaf patients.
Keywords	genes ; G-protein coupled receptors ; hearing disorders ; heterozygosity ; mutation ; patients ; sequence analysis ; siblings
Language	English
Dates of publication	2017-10
Size	p. 429-434.
Publishing place	Springer Netherlands
Document type	Article
ZDB-ID	186544-4
ISSN	1573-4978 ; 0301-4851
ISSN (online)	1573-4978
ISSN	0301-4851
DOI	10.1007/s11033-017-4129-9
Database	NAL-Catalogue (AGRICOLA)

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