In the article entitled “The Endothelin-Converting Enzyme-1/Endothelin-1 Pathway Plays a Critical Role in Inflammation-Associated Premature Delivery in a Mouse Model” (Volume 173, pages 1077–1084 of the October 2008 issue of The American Journal of Pathology), the second author’s name was spelled incorrectly. The correct spelling is Haoting Yen.
In the article entitled “The Krebs Cycle and Mitochondrial Mass Are Early Victims of Endothelial Dysfunction: Proteomic Approach” (Volume 174, pages 34–43 of the January 2009 issue), two authors’ names were spelled incorrectly. The correct spellings are Anna Csiszar and Boris Krasnikov.
In the article entitled, “Muscleblind-Like Proteins: Similarities and Differences in Normal and Myotonic Dystrophy Muscle” (Volume 174, pages 216–227 of the January 2009 issue), the production quality of Figure 4, page 222, and Figure 6, page 223, was impaired. The corrected figures and legends should have appeared as shown:
In the article entitled, “The Chemokine Receptor CXCR4 and the Metalloproteinase MT1-MMP Are Mutually Required during Melanoma Metastasis to Lungs” (Volume 174, pages 602–612 of the February 2009 issue), the production quality of Figure 5 panel D, page 608, was impaired. The corrected figure and legend should have appeared as shown:
Figure 4.
Changes in subcellular distribution of MBNL1 and MBNL2 during myoblast culture. Normal human myoblasts were grown on coverslips for various times before fixation with formalin, permeabilization with Triton X-100, and development with MB1a or MB2a mAbs, as described in the Materials and Methods. At day 1, the growth medium was changed to differentiation medium.
Figure 6.
Higher levels of MBNL2 in regenerating muscle fibers in a skeletal muscle biopsy from a Duchenne muscular dystrophy patient. Five regenerating fibers were identified by immunostaining with MHCn mAb (Novocastra, Newcastle, UK; 1:20) against neonatal myosin (A–C). In a serial section (D–F), nuclei in the regenerating fibers were more strongly stained for MBNL2 than nuclei in mature fibers (MB2a mAb; 1:4). The center panels show ethidium bromide staining of nuclei and the right panels are merged images. In (F), MBNL2 staining is indicated by horizontal white arrows in the nuclei of regenerating fibers and by vertical white arrows in the nuclei of mature fibers.
Figure 5.
Rac-Erk1/2 signaling controls up-regulation by CXCL12 of MT1-MMP expression. A: Cells were incubated for 24 hours with CXCL12 in the absence (control) or presence of LY (20 μmol/L) or UO126 (5 μmol/L), and tested with Western blot analyses for MT1-MMP expression. BLM melanoma cells were transfected with control or Rac1 siRNA (B), or with GFP-fused wild-type (wt) or constitutively activated (CA) forms of Rac (C). Transfectants were subsequently incubated for 24 hours with CXCL12 and subjected to Western blotting for expression of MT1-MMP, phospho-Erk1/2, total Erk1/2, and Rac1. D: Transfectants expressing Rac wt or Rac CA were subjected to Matrigel invasion assays toward CXCL12, in the absence or presence of UO126 and control or anti-MT1-MMP mAb (left). Supernatants from these invasions were tested by gelatinolytic zymography for MMP-2 activity (right).