| First Author | Marschall AL | Year | 2014 |
| Journal | MAbs | Volume | 6 |
| Issue | 6 | Pages | 1394-401 |
| PubMed ID | 25484057 | Mgi Jnum | J:330458 |
| Mgi Id | MGI:6882616 | Doi | 10.4161/mabs.34377 |
| Citation | Marschall AL, et al. (2014) Functional knock down of VCAM1 in mice mediated by endoplasmatic reticulum retained intrabodies. MAbs 6(6):1394-401 |
| abstractText | Functional knockdowns mediated by endoplasmatic reticulum-retained antibodies (ER intrabodies) are a promising tool for research because they allow functional interference on the protein level. We demonstrate for the first time that ER intrabodies can induce a knock-down phenotype in mice. Surface VCAM1 was suppressed in bone marrow of heterozygous and homozygous ER intrabody mice (iER-VCAM1 mice). iER-VCAM1 mice did not have a lethal phenotype, in contrast to the constitutive knockout of VCAM1, but adult mice exhibited physiological effects in the form of aberrant distribution of immature B-cells in blood and bone marrow. The capability to regulate knock-down strength may spark a new approach for the functional study of membrane and plasma proteins, which may especially be valuable for generating mouse models that more closely resemble disease states than classic knockouts do. |
