Do dDR1-deficient mice show localized subepithelial GBM thickening with focal loss of slit diaphragms and proteinuria?
The loss of cell-matrix communication in DDR1-deficient podocytes appears to result in excess synthesis of basement membrane proteins leading to disturbed anchorage of foot processes and disruption of the slit diaphragm. Our data suggest that the interaction between type IV collagen and DDR1 plays an important role in maintaining the structural integrity of the GBM.
Cytotoxic T cells can be effectively redirected against primary human pancreatic cancer cells by T-cell-engaging BiTE antibody MT110 including a subpopulation of highly tumorigenic CSCs.