FAK deficiency in cells contributing to the basal lamina results in cortical abnormalities resembling congenital muscular dystrophies. [electronic resource]
Producer: 20040105Description: 501-14 p. digitalISSN:- 0896-6273
- Animals
- Astrocytes -- metabolism
- Bacterial Proteins -- metabolism
- Basement Membrane -- metabolism
- Blotting, Western
- Calbindin 2
- Calbindins
- Carrier Proteins -- metabolism
- Cell Adhesion Molecules, Neuronal -- metabolism
- Cells, Cultured
- Cerebral Cortex -- abnormalities
- Cytoskeletal Proteins -- metabolism
- DNA-Binding Proteins -- metabolism
- Disease Models, Animal
- Dura Mater
- Dystroglycans
- Embryo, Mammalian
- Extracellular Matrix Proteins -- metabolism
- Fibroblasts -- metabolism
- Focal Adhesion Kinase 1
- Focal Adhesion Protein-Tyrosine Kinases
- Glial Fibrillary Acidic Protein -- metabolism
- Heterozygote
- Homeodomain Proteins -- metabolism
- Immunohistochemistry
- Infections
- Intracellular Signaling Peptides and Proteins
- Lamins -- metabolism
- Membrane Glycoproteins -- metabolism
- Mice
- Mice, Knockout
- Microscopy, Electron
- Microtubule-Associated Proteins -- metabolism
- Muscular Dystrophies -- congenital
- Mutation
- Nerve Tissue Proteins
- Neurons -- metabolism
- Otx Transcription Factors
- Phosphopyruvate Hydratase -- metabolism
- Phosphotyrosine -- metabolism
- Precipitin Tests
- Protein-Tyrosine Kinases -- deficiency
- Reelin Protein
- S100 Calcium Binding Protein G -- metabolism
- Serine Endopeptidases
- Silver Staining
- Staining and Labeling
- Transcription Factors -- metabolism
- src-Family Kinases -- metabolism
No physical items for this record
Publication Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
There are no comments on this title.
Log in to your account to post a comment.