Search

Your search keyword '"Talib, S. Zakiah A."' showing total 12 results
Start Over Author "Talib, S. Zakiah A."
12 results on '"Talib, S. Zakiah A."'

1. Metabolic Remodeling during Liver Regeneration

Author

Caldez, Matias J., Van Hul, Noémi, Koh, Hiromi W.L., Teo, Xing Qi, Fan, Jun Jun, Tan, Peck Yean, Dewhurst, Matthew R., Too, Peh Gek, Talib, S. Zakiah A., Chiang, Beatrice E., Stünkel, Walter, Yu, Hanry, Lee, Philip, Fuhrer, Tobias, Choi, Hyungwon, Björklund, Mikael, and Kaldis, Philipp

Published
2018
Full Text
View/download PDF

2. CDK10 Mutations in Humans and Mice Cause Severe Growth Retardation, Spine Malformations, and Developmental Delays

Author

Windpassinger, Christian, Piard, Juliette, Bonnard, Carine, Alfadhel, Majid, Lim, Shuhui, Bisteau, Xavier, Blouin, Stéphane, Ali, Nur’Ain B., Ng, Alvin Yu Jin, Lu, Hao, Tohari, Sumanty, Talib, S. Zakiah A., van Hul, Noémi, Caldez, Matias J., Van Maldergem, Lionel, Yigit, Gökhan, Kayserili, Hülya, Youssef, Sameh A., Coppola, Vincenzo, de Bruin, Alain, Tessarollo, Lino, Choi, Hyungwon, Rupp, Verena, Roetzer, Katharina, Roschger, Paul, Klaushofer, Klaus, Altmüller, Janine, Roy, Sudipto, Venkatesh, Byrappa, Ganger, Rudolf, Grill, Franz, Ben Chehida, Farid, Wollnik, Bernd, Altunoglu, Umut, Al Kaissi, Ali, Reversade, Bruno, and Kaldis, Philipp

Published
2017
Full Text
View/download PDF

3. Discovery of a chemical probe for PRDM9

Author

Allali-Hassani, Abdellah, Szewczyk, Magdalena M., Ivanochko, Danton, Organ, Shawna L., Bok, Jabez, Ho, Jessica Sook Yuin, Gay, Florence P. H., Li, Fengling, Blazer, Levi, Eram, Mohammad S., Halabelian, Levon, Dilworth, David, Luciani, Genna M., Lima-Fernandes, Evelyne, Wu, Qin, Loppnau, Peter, Palmer, Nathan, Talib, S. Zakiah A., Brown, Peter J., Schapira, Matthieu, Kaldis, Philipp, O’Hagan, Ronan C., Guccione, Ernesto, Barsyte-Lovejoy, Dalia, Arrowsmith, Cheryl H., Sanders, John M., Kattar, Solomon D., Bennett, D. Jonathan, Nicholson, Benjamin, and Vedadi, Masoud

Published
2019
Full Text
View/download PDF

7. CDK2 regulates the NRF1/Ehmt1 axis during meiotic prophase I

Author

Palmer, Nathan, primary, Talib, S. Zakiah A., additional, Ratnacaram, Chandrahas Koumar, additional, Low, Diana, additional, Bisteau, Xavier, additional, Lee, Joanna Hui Si, additional, Pfeiffenberger, Elisabeth, additional, Wollmann, Heike, additional, Tan, Joel Heng Loong, additional, Wee, Sheena, additional, Sobota, Radoslaw, additional, Gunaratne, Jayantha, additional, Messerschmidt, Daniel M., additional, Guccione, Ernesto, additional, and Kaldis, Philipp, additional

Published
2019
Full Text
View/download PDF

8. CDK10 Mutations in Humans and Mice Cause Severe Growth Retardation, Spine Malformations, and Developmental Delays

Author

Regenerative Medicine, Stem Cells & Cancer, Windpassinger, Christian, Piard, Juliette, Bonnard, Carine, Alfadhel, Majid, Lim, Shuhui, Bisteau, Xavier, Blouin, Stéphane, Ali, Nur'Ain B, Ng, Alvin Yu Jin, Lu, Hao, Tohari, Sumanty, Talib, S Zakiah A, van Hul, Noémi, Caldez, Matias J, Van Maldergem, Lionel, Yigit, Gökhan, Kayserili, Hülya, Youssef, Sameh A, Coppola, Vincenzo, de Bruin, Alain, Tessarollo, Lino, Choi, Hyungwon, Rupp, Verena, Roetzer, Katharina, Roschger, Paul, Klaushofer, Klaus, Altmüller, Janine, Roy, Sudipto, Venkatesh, Byrappa, Ganger, Rudolf, Grill, Franz, Ben Chehida, Farid, Wollnik, Bernd, Altunoglu, Umut, Al Kaissi, Ali, Reversade, Bruno, Kaldis, Philipp, Regenerative Medicine, Stem Cells & Cancer, Windpassinger, Christian, Piard, Juliette, Bonnard, Carine, Alfadhel, Majid, Lim, Shuhui, Bisteau, Xavier, Blouin, Stéphane, Ali, Nur'Ain B, Ng, Alvin Yu Jin, Lu, Hao, Tohari, Sumanty, Talib, S Zakiah A, van Hul, Noémi, Caldez, Matias J, Van Maldergem, Lionel, Yigit, Gökhan, Kayserili, Hülya, Youssef, Sameh A, Coppola, Vincenzo, de Bruin, Alain, Tessarollo, Lino, Choi, Hyungwon, Rupp, Verena, Roetzer, Katharina, Roschger, Paul, Klaushofer, Klaus, Altmüller, Janine, Roy, Sudipto, Venkatesh, Byrappa, Ganger, Rudolf, Grill, Franz, Ben Chehida, Farid, Wollnik, Bernd, Altunoglu, Umut, Al Kaissi, Ali, Reversade, Bruno, and Kaldis, Philipp

Published
2017

9. CDK10 mutations in humans and mice cause severe growth retardation, spine malformations, and developmental delays

Author

Karabey, Hülya Kayserili; Wollnik, Bernd; Kaldis, Philipp, Windpassinger, Christian; Piard, Juliette; Bonnard, Carine; Alfadhel, Majid; Lim, Shuhui; Bisteau, Xavier; Blouin, Stéphane; Ali, Nur'Ain B.; Ng, Alvin Yu Jin; Lu, Hao; Tohari, Sumanty; Talib, S. Zakiah A.; van Hul, Noémi; Caldez, Matias J.; Van Maldergem, Lionel; Yiğit, Gökhan; Youssef, Sameh A.; Coppola, Vincenzo; de Bruin, Alain; Tessarollo, Lino; Choi, Hyungwon; Rupp, Verena; Roetzer, Katharina; Roschger, Paul; Klaushofer, Klaus; Altmüller, Janine; Roy, Sudipto; Venkatesh, Byrappa; Ganger, Rudolf; Grill, Franz; Ben Chehida, Farid; Altunoglu, Umut; Al Kaissi, Ali; Reversade, Bruno, School of Medicine, Department of Medical Genetics, Karabey, Hülya Kayserili; Wollnik, Bernd; Kaldis, Philipp, Windpassinger, Christian; Piard, Juliette; Bonnard, Carine; Alfadhel, Majid; Lim, Shuhui; Bisteau, Xavier; Blouin, Stéphane; Ali, Nur'Ain B.; Ng, Alvin Yu Jin; Lu, Hao; Tohari, Sumanty; Talib, S. Zakiah A.; van Hul, Noémi; Caldez, Matias J.; Van Maldergem, Lionel; Yiğit, Gökhan; Youssef, Sameh A.; Coppola, Vincenzo; de Bruin, Alain; Tessarollo, Lino; Choi, Hyungwon; Rupp, Verena; Roetzer, Katharina; Roschger, Paul; Klaushofer, Klaus; Altmüller, Janine; Roy, Sudipto; Venkatesh, Byrappa; Ganger, Rudolf; Grill, Franz; Ben Chehida, Farid; Altunoglu, Umut; Al Kaissi, Ali; Reversade, Bruno, School of Medicine, and Department of Medical Genetics

Abstract

In five separate families, we identified nine individuals affected by a previously unidentified syndrome characterized by growth retardation, spine malformation, facial dysmorphisms, and developmental delays. Using homozygosity mapping, array CGH, and exome sequencing, we uncovered bi-allelic loss-of-function CDK10 mutations segregating with this disease. CDK10 is a protein kinase that partners with cyclin M to phosphorylate substrates such as ETS2 and PKN2 in order to modulate cellular growth. To validate and model the pathogenicity of these CDK10 germline mutations, we generated conditional-knockout mice. Homozygous Cdk10-knockout mice died postnatally with severe growth retardation, skeletal defects, and kidney and lung abnormalities, symptoms that partly resemble the disease's effect in humans. Fibroblasts derived from affected individuals and Cdk10-knockout mouse embryonic fibroblasts (MEFs) proliferated normally; however, Cdk10-knockout MEFs developed longer cilia. Comparative transcriptomic analysis of mutant and wild-type mouse organs revealed lipid metabolic changes consistent with growth impairment and altered ciliogenesis in the absence of CDK10. Our results document the CDK10 loss-of-function phenotype and point to a function for CDK10 in transducing signals received at the primary cilia to sustain embryonic and postnatal development., NIH, the National Cancer Institute; Center for Cancer Research; Strategic Positioning Fund for the Genetic Orphan Diseases program; Industry Alignment Fund for the Singapore Childhood Undiagnosed Diseases program from the A*STAR (Agency for Science, Technology, and Research) Biomedical Research Council; A*STAR Biomedical Research Council

Published
2017

11. CDK10 Mutations in Humans and Mice Cause Severe Growth Retardation, Spine Malformations, and Developmental Delays

Author

Sudipto Roy, Noémi van Hul, Janine Altmüller, Hyungwon Choi, Nur'Ain Binte Ali, Xavier Bisteau, Shuhui Lim, Christian Windpassinger, Stéphane Blouin, Verena Rupp, Carine Bonnard, Franz Grill, Byrappa Venkatesh, Bruno Reversade, Rudolf Ganger, Vincenzo Coppola, S. Zakiah A. Talib, Klaus Klaushofer, Majid Alfadhel, Gökhan Yigit, Farid Ben Chehida, Paul Roschger, Ali Al Kaissi, Matias J. Caldez, Umut Altunoglu, Bernd Wollnik, Hülya Kayserili, Lionel Van Maldergem, Alvin Yu Jin Ng, Sameh A. Youssef, Lino Tessarollo, Katharina M. Roetzer, Hao Lu, Philipp Kaldis, Juliette Piard, Alain de Bruin, Sumanty Tohari, Karabey, Hülya Kayserili, Wollnik, Bernd, Kaldis, Philipp, Windpassinger, Christian, Piard, Juliette, Bonnard, Carine, Alfadhel, Majid, Lim, Shuhui, Bisteau, Xavier, Blouin, Stéphane, Ali, Nur'Ain B., Ng, Alvin Yu Jin, Lu, Hao, Tohari, Sumanty, Talib, S. Zakiah A., van Hul, Noémi, Caldez, Matias J., Van Maldergem, Lionel, Yiğit, Gökhan, Youssef, Sameh A., Coppola, Vincenzo, de Bruin, Alain, Tessarollo, Lino, Choi, Hyungwon, Rupp, Verena, Roetzer, Katharina, Roschger, Paul, Klaushofer, Klaus, Altmüller, Janine, Roy, Sudipto, Venkatesh, Byrappa, Ganger, Rudolf, Grill, Franz, Ben Chehida, Farid, Altunoglu, Umut, Al Kaissi, Ali, Reversade, Bruno, School of Medicine, Department of Medical Genetics, Regenerative Medicine, Stem Cells & Cancer, Amsterdam Cardiovascular Sciences, Amsterdam Reproduction & Development (AR&D), Center for Reproductive Medicine, ACS - Heart failure & arrhythmias, and ACS - Diabetes & metabolism

Subjects
0301 basic medicine, Male, Developmental Disabilities, medicine.disease_cause, Mice, 0302 clinical medicine, Phosphorylation, Child, Genetics (clinical), Exome sequencing, Cells, Cultured, Growth Disorders, Mice, Knockout, Mutation, Cultured, Cilium, Cell Cycle, Disease gene identification, Phenotype, Cyclin-Dependent Kinases, Pedigree, Embryo, 030220 oncology & carcinogenesis, Child, Preschool, Female, Signal Transduction, medicine.medical_specialty, Cells, Knockout, Biology, Article, 03 medical and health sciences, Germline mutation, Internal medicine, Ciliogenesis, Journal Article, Genetics, medicine, Animals, Humans, Star syndrome, Genome browser, Protein-kinase, Cdk10/Cyclin M, Family, Gene, Pisslre, DNA, Melanoma, Member, Cilia, Preschool, Cell Proliferation, Medicine, Genetics and heredity, Mammalian, Infant, Fibroblasts, medicine.disease, Embryo, Mammalian, Spine, 030104 developmental biology, Endocrinology, Congenital disorder, Al Kaissi syndrome knockout mice, CDK10, ETS2, cilia, congenital disorder, growth retardation, metabolism, spine malformation
Abstract

In five separate families, we identified nine individuals affected by a previously unidentified syndrome characterized by growth retardation, spine malformation, facial dysmorphisms, and developmental delays. Using homozygosity mapping, array CGH, and exome sequencing, we uncovered bi-allelic loss-of-function CDK10 mutations segregating with this disease. CDK10 is a protein kinase that partners with cyclin M to phosphorylate substrates such as ETS2 and PKN2 in order to modulate cellular growth. To validate and model the pathogenicity of these CDK10 germline mutations, we generated conditional-knockout mice. Homozygous Cdk10-knockout mice died postnatally with severe growth retardation, skeletal defects, and kidney and lung abnormalities, symptoms that partly resemble the disease's effect in humans. Fibroblasts derived from affected individuals and Cdk10-knockout mouse embryonic fibroblasts (MEFs) proliferated normally; however, Cdk10-knockout MEFs developed longer cilia. Comparative transcriptomic analysis of mutant and wild-type mouse organs revealed lipid metabolic changes consistent with growth impairment and altered ciliogenesis in the absence of CDK10. Our results document the CDK10 loss-of-function phenotype and point to a function for CDK10 in transducing signals received at the primary cilia to sustain embryonic and postnatal development., NIH, the National Cancer Institute; Center for Cancer Research; Strategic Positioning Fund for the Genetic Orphan Diseases program; Industry Alignment Fund for the Singapore Childhood Undiagnosed Diseases program from the A*STAR (Agency for Science, Technology, and Research) Biomedical Research Council; A*STAR Biomedical Research Council

Published
2017
Full Text
View/download PDF

12. CDK2 regulates the NRF1/ Ehmt1 axis during meiotic prophase I.

Author

Palmer N, Talib SZA, Ratnacaram CK, Low D, Bisteau X, Lee JHS, Pfeiffenberger E, Wollmann H, Tan JHL, Wee S, Sobota R, Gunaratne J, Messerschmidt DM, Guccione E, and Kaldis P

Subjects
Animals, Cyclin-Dependent Kinase 2 genetics, Gene Deletion, Histone-Lysine N-Methyltransferase genetics, Male, Mice, Mice, Knockout, Nuclear Respiratory Factor 1 genetics, Spermatocytes cytology, Cyclin-Dependent Kinase 2 metabolism, Gene Expression Regulation, Enzymologic, Histone-Lysine N-Methyltransferase biosynthesis, Meiotic Prophase I physiology, Nuclear Respiratory Factor 1 metabolism, Spermatocytes metabolism
Abstract

Meiosis generates four genetically distinct haploid gametes over the course of two reductional cell divisions. Meiotic divisions are characterized by the coordinated deposition and removal of various epigenetic marks. Here we propose that nuclear respiratory factor 1 (NRF1) regulates transcription of euchromatic histone methyltransferase 1 (EHMT1) to ensure normal patterns of H3K9 methylation during meiotic prophase I. We demonstrate that cyclin-dependent kinase (CDK2) can bind to the promoters of a number of genes in male germ cells including that of Ehmt1 through interaction with the NRF1 transcription factor. Our data indicate that CDK2-mediated phosphorylation of NRF1 can occur at two distinct serine residues and negatively regulates NRF1 DNA binding activity in vitro. Furthermore, induced deletion of Cdk2 in spermatocytes results in increased expression of many NRF1 target genes including Ehmt1 We hypothesize that the regulation of NRF1 transcriptional activity by CDK2 may allow the modulation of Ehmt1 expression, therefore controlling the dynamic methylation of H3K9 during meiotic prophase., (© 2019 Palmer et al.)

Published
2019
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results