Zobrazeno 1 - 10
of 12
pro vyhledávání: '"Helen M. Bellchambers"'
Autor:
Helen M. Bellchambers, Amruta R. Phatak, Mardi J. Nenni, Maria B. Padua, Hongyu Gao, Yunlong Liu, Stephanie M. Ware
Publikováno v:
Scientific Reports, Vol 13, Iss 1, Pp 1-12 (2023)
Abstract The establishment of left–right patterning in mice occurs at a transient structure called the embryonic node or left–right organizer (LRO). Previous analysis of the LRO has proven challenging due to the small cell number and transient na
Externí odkaz:
https://doaj.org/article/00a210c9f6484fb2bb079dad96489a29
Publikováno v:
International Journal of Molecular Sciences, Vol 22, Iss 19, p 10437 (2021)
The mechanisms of neural crest cell induction and specification are highly conserved among vertebrate model organisms, but how similar these mechanisms are in mammalian neural crest cell formation remains open to question. The zinc finger of the cere
Externí odkaz:
https://doaj.org/article/6c1cc9d533ce47beaa40749f91e60003
Autor:
Jehangir N. Ahmed, Radiya G. Ali, Nicholas Warr, Heather M. Wilson, Helen M. Bellchambers, Kristen S. Barratt, Amelia J. Thompson, Ruth M. Arkell
Publikováno v:
Disease Models & Mechanisms, Vol 6, Iss 3, Pp 755-767 (2013)
SUMMARY The ZIC transcription factors are key mediators of embryonic development and ZIC3 is the gene most commonly associated with situs defects (heterotaxy) in humans. Half of patient ZIC3 mutations introduce a premature termination codon (PTC). In
Externí odkaz:
https://doaj.org/article/6d3b4c00b6344c7a9e083b9e338dc3e4
Autor:
Maria B Padua, Benjamin M Helm, John R Wells, Amanda M Smith, Helen M Bellchambers, Arthi Sridhar, Stephanie M Ware
Publikováno v:
Human Molecular Genetics.
FOXJ1 is expressed in ciliated cells of the airways, testis, oviduct, central nervous system and the embryonic left–right organizer. Ablation or targeted mutation of Foxj1 in mice, zebrafish and frogs results in loss of ciliary motility and/or redu
Publikováno v:
Hum Mol Genet
Loss of function of ZIC3 causes heterotaxy (OMIM #306955), a disorder characterized by organ laterality defects including complex heart defects. Studies using Zic3 mutant mice have demonstrated that loss of Zic3 causes heterotaxy due to defects in es
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::9db51459f6dabd76f2c352e0262813d8
https://europepmc.org/articles/PMC8643499/
https://europepmc.org/articles/PMC8643499/
Autor:
Nicholas Warr, Helen M. Bellchambers, Ruth M. Arkell, Jehangir N. Ahmed, Kristen S. Barratt, Radiya G. Ali, Koula E. M. Diamand, Kieran Neill
Publikováno v:
Journal of Cell Science. 134
Zinc finger of the cerebellum (Zic) proteins act as classic transcription factors to promote transcription of the Foxd3 gene during neural crest cell specification. Additionally, they can act as co-factors that bind proteins from the T-cell factor/ly
Autor:
Kristen S. Barratt, Helen M. Bellchambers, Ruth M. Arkell, Diamand Kem, Neill K, Warr N, Jehangir N. Ahmed, Radiya G. Ali
Zinc finger of the cerebellum (Zic) proteins act as classical transcription factors to promote transcription of the Foxd3 gene during neural crest cell specification. Additionally, they can act as co-factors that bind TCF molecules to repress WNT/β-
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::a95d1efb04950f6652ba341ab2e8e819
https://doi.org/10.1101/2020.11.04.369124
https://doi.org/10.1101/2020.11.04.369124
Publikováno v:
Scientific Reports
Scientific Reports, Vol 10, Iss 1, Pp 1-14 (2020)
Scientific Reports, Vol 10, Iss 1, Pp 1-14 (2020)
The ZIC proteins are a family of transcription regulators with a well-defined zinc finger DNA-binding domain and there is evidence that they elicit functional DNA binding at a ZIC DNA binding site. Little is known, however, regarding domains within Z
Publikováno v:
Adv Exp Med Biol
Advances in Experimental Medicine and Biology ISBN: 9789811073106
Advances in Experimental Medicine and Biology ISBN: 9789811073106
Mutation of ZIC3 causes X-linked heterotaxy, a syndrome in which the laterality of internal organs is disrupted. Analysis of model organisms and gene expression during early development suggests ZIC3-related heterotaxy occurs due to defects at the ea
Autor:
Helen M. Bellchambers, Kristen S. Barratt, Nicholas Warr, Heather L. Wilson, Amelia J. Thompson, Radiya G. Ali, Jehangir N. Ahmed, Ruth M. Arkell
Publikováno v:
Disease Models & Mechanisms, Vol 6, Iss 3, Pp 755-767 (2013)
Disease Models & Mechanisms
Disease Models & Mechanisms
SummaryThe ZIC transcription factors are key mediators of embryonic development and ZIC3 is the gene most commonly associated with situs defects (heterotaxy) in humans. Half of patient ZIC3 mutations introduce a premature termination codon (PTC). In