Literature DB >> 8081888

Developmental expression of nicein adhesion protein (laminin-5) subunits suggests multiple morphogenic roles.

D Aberdam1, A Aguzzi, C Baudoin, M F Galliano, J P Ortonne, G Meneguzzi.   

Abstract

Nicein/kalinin (laminin-5) is a heterotrimeric laminin-like adhesion protein, which is secreted at the basement membrane of subsets of epithelia and is involved in the etiology of junctional epidermolysis bullosa, a severe human blistering disease characterized by disadhesion of epidermis from dermis. cDNA clones encoding the three chains of mouse nicein and antibodies specific to each polypeptide were used to examine the expression of the protein in the developing mouse embryo from 10.5 day post coitum to 7 days after birth. At various stages of development, co-expression of the three chains of nicein was observed in amnion, skin, and in epithelia of respiratory, urinary and digestive systems. High level expression of nicein was seen in enamel-secreting ameloblasts in developing teeth. Cell-specific distribution of nicein was also detected in other specialized tissues representative of the three primary embryonic germ layers with prominent secretory or protective functions. Differential and focal expression of nicein subunits was observed in the choroid plexus and the floor plate of the neural tube. Messenger for the heavy chain of nicein was detected in the floor plate, where mouse s-laminin messengers were also found. This suggests that nicein genes may play a role in the migration and polarization of motor neurons in the developing spinal cord.

Entities:  

Mesh:

Substances:

Year:  1994        PMID: 8081888     DOI: 10.3109/15419069409004431

Source DB:  PubMed          Journal:  Cell Adhes Commun        ISSN: 1023-7046


  23 in total

1.  Digenic junctional epidermolysis bullosa: mutations in COL17A1 and LAMB3 genes.

Authors:  M Floeth; L Bruckner-Tuderman
Journal:  Am J Hum Genet       Date:  1999-12       Impact factor: 11.025

2.  DNA conformation driven by AP-1 triggers cell-specific expression via a strong epithelial enhancer.

Authors:  T Virolle; Z Djabari; J P Ortonne; D Aberdam
Journal:  EMBO Rep       Date:  2000-10       Impact factor: 8.807

Review 3.  Laminin isoforms in development and disease.

Authors:  Susanne Schéele; Alexander Nyström; Madeleine Durbeej; Jan F Talts; Marja Ekblom; Peter Ekblom
Journal:  J Mol Med (Berl)       Date:  2007-04-11       Impact factor: 4.599

4.  Differential expression of mRNAs encoding laminin chain variants during in vitro development of mouse blastocysts.

Authors:  M Azimi; T Niimi; N Yoshida; Y Kitagawa
Journal:  Cytotechnology       Date:  1999-09       Impact factor: 2.058

5.  Location of the 9257 and ataxia mutations on mouse chromosome 18.

Authors:  A J Griffith; G L Radice; D L Burgess; D C Kohrman; G M Hansen; M J Justice; K R Johnson; M T Davisson; M H Meisler
Journal:  Mamm Genome       Date:  1996-06       Impact factor: 2.957

6.  High-resolution mapping of the spm (Niemann-Pick Type C) locus on mouse chromosome 18.

Authors:  R P Erickson; R A Aviles; J Zhang; M A Kozloski; W S Garver; R A Heidenreich
Journal:  Mamm Genome       Date:  1997-05       Impact factor: 2.957

Review 7.  The molecular basis of hereditary enamel defects in humans.

Authors:  J T Wright; I A Carrion; C Morris
Journal:  J Dent Res       Date:  2014-11-11       Impact factor: 6.116

8.  Laminin-5 induces osteogenic gene expression in human mesenchymal stem cells through an ERK-dependent pathway.

Authors:  Robert F Klees; Roman M Salasznyk; Karl Kingsley; William A Williams; Adele Boskey; George E Plopper
Journal:  Mol Biol Cell       Date:  2004-12-01       Impact factor: 4.138

Review 9.  Oral manifestations in the epidermolysis bullosa spectrum.

Authors:  J Timothy Wright
Journal:  Dermatol Clin       Date:  2010-01       Impact factor: 3.478

Review 10.  Molecular genetics of ameloblast cell lineage.

Authors:  Marianna Bei
Journal:  J Exp Zool B Mol Dev Evol       Date:  2009-07-15       Impact factor: 2.656

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.