Table 2.
Intestinal phenotypes of murine keratin mutants (n.d. = no phenotype detected).
| Transgenesis | Intestinal Phenotype | Reference |
|---|---|---|
| KRT8−/− | colorectal hyperplasia | [20] |
| scattered γ-tubulin, disorganized microtubules, reduced apical syntaxin, aberrant intracellular localization of CFTR, sucrase isomaltase, alkaline phosphatase | [21] | |
| diarrhea, reduced apical F-actin, partial loss of H+, K+-ATPase and basolateral redistribution of the anion exchanger AE1/2 and the Na-transporter EnaC-γ | [49] | |
| spontaneous chronic T helper type 2 colitis | [50] | |
| microflora-dependent resistance to apoptosis | [51] | |
| KRT8+/− | increased crypt length, increased sensitivity to experimental colitis | [22] |
| KRT7−/− | n.d. | [52] |
| KRT18−/− | n.d. | [46] |
| KRT19−/− | n.d. | [45] |
| keratin type I−/− (except KRT18) | n.d. | [44] |
| hK18 R89C | partial disruption of keratin filament network | [48] |
| aggregate formation | [47] | |
| hK20 R80H | partial disruption of keratin filament network | [15] |