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Altered endochondral bone development in matrix metalloproteinase 13-deficient mice
TLDR
The hypothesis that proper ECM remodeling is the dominant rate-limiting process for programmed cell death, angiogenesis and osteoblast recruitment during normal skeletal morphogenesis is supported. Expand
Kallikrein 6 induces E-cadherin shedding and promotes cell proliferation, migration, and invasion.
TLDR
KlK6 up-regulation in squamous skin tumors of human patients and in tumors of other epithelial tissues is shown and enhanced epidermal keratinocyte proliferation and migration in concert with decreased E-cadherin protein levels are confirmed in an in vivo Klk6 transgenic mouse model. Expand
Th2 cell‐specific cytokine expression and allergen‐induced airway inflammation depend on JunB
TLDR
Novel functions of JunB in the development of Th2 effector cells, for a normal Th2 cytokine expression pattern and for a complete Th2‐dependent immune response in mice are demonstrated. Expand
Epidermal development and wound healing in matrix metalloproteinase 13-deficient mice.
TLDR
Skin homeostasis and also tissue remodelling processes like embryonic skin development and cutaneous wound healing are independent of MMP13 either owing to M MP13 dispensability or owing to functional substitution by other collagenolytic proteinases such as MMP8. Expand
Cell Cycle Promoting Activity of JunB through Cyclin A Activation*
TLDR
Cyclin A is a direct transcriptional target of JunB driving cell proliferation, which is characterized by an increase in the population of S-phase cells, while that of cells in G2/M-phase was diminished. Expand
MMP13 as a stromal mediator in controlling persistent angiogenesis in skin carcinoma.
TLDR
Data suggest a crucial role of MMP13 in promoting angiogenesis via releasing VEGF from the ECM and thus allowing the invasive growth of the SCC cells. Expand
Histone deacetylase 10 promotes autophagy-mediated cell survival
TLDR
It is demonstrated that HDAC10 protects cancer cells from cytotoxic agents by mediating autophagy and identifies this HDAC isozyme as a druggable regulator of advanced-stage tumor cell survival. Expand
Junb regulates arterial contraction capacity, cellular contractility, and motility via its target Myl9 in mice.
TLDR
Conditional ablation of the transcriptional regulator Junb results in impaired arterial contractility in vivo and in vitro and establishes a molecular link between the activator protein-1 transcription factor subunit Junb and actomyosin-based cellular motility as well as cellular and vascular contractility by governing Myl9 transcription. Expand
Cutting Edge: The AP-1 Subunit JunB Determines NK Cell-Mediated Target Cell Killing by Regulation of the NKG2D-Ligand RAE-1ε1
TLDR
Up-regulated RAE-1ε expression due to low levels of JunB could alert immune cells to tumors and stressed cells, and indicate that the transcription factor AP-1, which is involved in tumorigenesis and cellular stress responses, regulates RAE -1ε. Expand
JunB is required for endothelial cell morphogenesis by regulating core-binding factor β
TLDR
It is demonstrated that cell-autonomous endothelial functions of the AP-1 subunit JunB are required for proper endothelial morphogenesis both in vivo in mouse embryos with endothelial-specific ablation of JunB and in in vitro angiogenesis models. Expand
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