Pubfacts - Scientific Publication Data
  • Categories
  • |
  • Journals
  • |
  • Authors
  • Login
  • Categories
  • Journals

Search Our Scientific Publications & Authors

Publications
  • Publications
  • Authors
find publications by category +
Translate page:

Analysis of early human neural crest development.

Authors:
Erin Betters Ying Liu Anders Kjaeldgaard Erik Sundström Martín I García-Castro

Dev Biol 2010 Aug 15;344(2):578-92. Epub 2010 May 15.

Department of Molecular, Cellular and Developmental Biology, Yale University, New Haven, CT 06520-8103, USA.

The outstanding migration and differentiation capacities of neural crest cells (NCCs) have fascinated scientists since Wilhelm His described this cell population in 1868. Today, after intense research using vertebrate model organisms, we have gained considerable knowledge regarding the origin, migration and differentiation of NCCs. However, our understanding of NCC development in human embryos remains largely uncharacterized, despite the role the neural crest plays in several human pathologies. Here, we report for the first time the expression of a battery of molecular markers before, during, or following NCC migration in human embryos from Carnegie Stages (CS) 12 to 18. Our work demonstrates the expression of Sox9, Sox10 and Pax3 transcription factors in premigratory NCCs, while actively migrating NCCs display the additional transcription factors Pax7 and AP-2alpha. Importantly, while HNK-1 labels few migrating NCCs, p75(NTR) labels a large proportion of this population. However, the broad expression of p75(NTR) - and other markers - beyond the neural crest stresses the need for the identification of additional markers to improve our capacity to investigate human NCC development, and to enable the generation of better diagnostic and therapeutic tools.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.ydbio.2010.05.012DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2927129PMC
August 2010

Publication Analysis

Top Keywords

neural crest
16
ncc development
8
migration differentiation
8
transcription factors
8
human embryos
8
migrating nccs
8
human
5
nccs
5
stages work
4
expression sox9
4
sox9 sox10
4
work demonstrates
4
demonstrates expression
4
factors premigratory
4
actively migrating
4
nccs display
4
nccs actively
4
premigratory nccs
4
pax3 transcription
4
sox10 pax3
4

Keyword Occurance

Similar Publications

A de novo mutation of the SOX10 gene associated with inner ear malformation in a Guangxi family with Waardenburg syndrome type II.

Authors:
Zhijie Niu Yongjing Lai Songhua Tan Fen Tang Xianglong Tang Yupei Su Lei Liu Lihong Xie Qin Fang Mao Xie Anzhou Tang

Int J Pediatr Otorhinolaryngol 2021 Apr 14;145:110711. Epub 2021 Apr 14.

Department of Otolaryngology-Head and Neck Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, 530021, China; Regional Key Laboratory of Early Prevention and Treatment of High-Rise Tumors, Nanning, 530021, China. Electronic address:

Objective: Waardenburg syndrome type 2 (WS2) is a rare neural-crest disorder, characterized by heterochromic irides or blue eyes and sensorineural hearing loss. The aim of this study was to analyze the clinical features and investigate the genetic cause of WS2 in a small family from Guangxi Zhuang Autonomous region.

Methods: Whole-exome sequencing and mutational analysis were used to identify disease-causing genes in this family. Read More

View Article and Full-Text PDF
April 2021
Similar Publications

Molecular mechanisms of hearing loss in Nager syndrome.

Authors:
Santosh Kumar Maharana Jean-Pierre Saint-Jeannet

Dev Biol 2021 Apr 14. Epub 2021 Apr 14.

Department of Molecular Pathobiology, New York University, College of Dentistry, New York, USA. Electronic address:

Nager syndrome is a rare human developmental disorder characterized by hypoplastic neural crest-derived craniofacial bones and limb defects. Mutations in SF3B4 gene, which encodes a component of the spliceosome, are a major cause for Nager. A review of the literature indicates that 45% of confirmed cases are also affected by conductive, sensorineural or mixed hearing loss. Read More

View Article and Full-Text PDF
April 2021
Similar Publications

BMP9 Can Induce Schwann Cells Expressing Simian Virus 40 T Antigen to Differentiate into Fat and Bone and .

Authors:
Rui-Fang Li Guo-Xin Nan Dan Wang Chang Gao Juan Yang Zhong-Lin Zhang

Cell Reprogram 2021 Apr;23(2):108-116

Department of Hepatobiliary Surgery, Zhongnan Hospital of Wuhan University, Wuhan, China.

In our previous study, we constructed Schwann cells (SCs) that stably express Simian virus 40 T antigen (SV40T-SCs). SV40T-SCs functions and markers are similar to those of neural crest cells. There we used bone morphogenetic protein 9 (BMP9) to induce SV40T-SCs differentiation and and study possible related mechanism. Read More

View Article and Full-Text PDF
April 2021
Similar Publications

Mesenteric Neural Crest Cells Are the Embryological Basis of Skip Segment Hirschsprung Disease.

Authors:
Robert O Heuckeroth

Cell Mol Gastroenterol Hepatol 2021 Apr 12. Epub 2021 Apr 12.

Professor of Pediatrics, Irma and Norman Braman Endowed Chair for GI Motility, The Children's Hospital of Philadelphia, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania. Electronic address:

View Article and Full-Text PDF
April 2021
Similar Publications

Peptide Derived from AHNAK Inhibits Cell Migration and Proliferation in Hirschsprung's Disease by Targeting the ERK1/2 Pathway.

Authors:
Yuhan Li Xiurui Lv Huan Chen Zhengke Zhi Zhonghong Wei Binyu Wang LingLing Zhou Hongxing Li Weibing Tang

J Proteome Res 2021 Apr 15. Epub 2021 Apr 15.

State Key Laboratory of Reproductive Medicine, Institute of Toxicology, School of Public Health, Nanjing Medical University, Nanjing 211166, China.

Hirschsprung's disease (HSCR) is characterized by the lack of ganglion cells in the distal part of the digestive tract. It occurs due to migration disorders of enteric neural crest cells (ENCCs) from 5 to 12 weeks of embryonic development. More and more studies show that HSCR is a result of the interaction of multiple genes and the microenvironments, but its specific pathogenesis has not been fully elucidated. Read More

View Article and Full-Text PDF
April 2021
Similar Publications
© 2021 PubFacts.
  • About PubFacts
  • Privacy Policy
  • Sitemap