3.4.22.53 malfunction calpain 2 depletion impairs mitosis and induces apoptosis, low Capn2 levels induce chromosome alignment defects, the loss of histone H3 threonine 3 phosphorylation at centromeres, and premature sister chromatid separation 708140 3.4.22.53 malfunction calpain 2 knockdown in breast cancer cells correlates with reduced in vitro proliferation, migration, and in vivo tumorigenicity as well as reduced Akt activation, increased nuclear FoxO localization, and increased p27Kip1 expression 732050 3.4.22.53 malfunction calpain inhibition blocks the increased colonic epithelial cell invasion caused by NM IIA knockdown 707044 3.4.22.53 malfunction calpain inhibition favors differentiation of neuronal stem cells. Calpain 2 silencing elicits decreased levels of glial fibrillary acidic protein 732688 3.4.22.53 malfunction in vivo knockdown of calpain2 disrupts metastasis among apoptosis-resistant tumors 707980 3.4.22.53 malfunction inhibition of calpain activity limits cell migration and in vitro wound healing of IEC-6 cells 717669 3.4.22.53 malfunction inhibition of m-calpain induces expression of the adult alpha- and beta-globin genes 709031 3.4.22.53 malfunction knockdown of calpain 2 expression or chemical inhibition of calpain activity reduces glioblastoma cell invasion by 90%. Decreased expression of calpain 2 does not influence morphology or migration 718169 3.4.22.53 malfunction knockdown of calpain 2 inhibits T cell migration at both the level of single cell tracking and general cell speed 718262 3.4.22.53 malfunction knockdown of calpain 2 results in a 2.9fold decrease in the invasion of human glioblastoma cells in zebrafish brain. Calpain 2 knockdown cells demonstrate a 2.3fold lower area of dispersal compared with control cells 732365 3.4.22.53 malfunction short interfering RNA-induced silencing of m-calpain results in increased RhoA activity and hyperpermeability in the aortic arch, which is accompanied by ROCK inhibitor-sensitive phosphorylation of downstream effecter LIM kinase 2, stress fibre accumulation in endothelium and enhanced interendothelial gaps 708018 3.4.22.53 malfunction the blockage of calpain 2 suppresses p38 MAPK phosphorylation 709241 3.4.22.53 malfunction the knockdown of calpain 2 significantly reduces cord formation, adhesion, and migration of human lymphatic microvascular dermal-derived endothelial cells on Matrigel compared to the control 731892 3.4.22.53 metabolism calpain 2 regulates endothelial nitric oxide synthase phosphorylation during cord formation by lymphatic endothelial cells on Matrigel 731892 3.4.22.53 metabolism isoform-specific hyperactivation of calpain-2, but not calpain-1 occurs at the synapse early in the pathogenesis of Alzheimer's disease potentially contributing to the deregulation of synaptic signaling in Alzheimer's disease 755493 3.4.22.53 metabolism MARCKS protein i.e. myristoylated alanine-rich C kinase substrate is a substrate of calpain-2 in the presence of Ca2+. Calpain-2 proteolysis of MARCKS promotes its interaction with lipids and ENaC at the plasma membrane to allow for the phosphatidylinositol 4,5-bisphosphate (PIP2)-dependent regulation of epithelial sodium channel (ENaC) activity in the kidney 752437 3.4.22.53 metabolism nuclear translocation of calpain-2 mediates apoptosis of hypertrophied cardiomyocytes in transverse aortic constriction rat. Angiotensin II enhances the interaction between activated calpain-2 and Ca2+/calmodulin-dependent protein kinase II deltaB (CaMKIIdB), and promotes the degradation of CaMKIIdB by calpain-2 in the nuclei of hypertrophied cardiomyocytes. The depressed CaMKIIdeltaB downregulates the expression of antiapoptotic Bcl-2 leading to mitochondrial depolarization and release of cytochrome c which leads to apoptosis of hypertrophied cardiomyocytes 754244 3.4.22.53 physiological function an endoplasmic reticulum stress-related calpain-down-regulated PPAR-gamma/HO-1 pathway is involved in the interleukin-13-enhanced activated death of microglia 708062 3.4.22.53 physiological function Ca2+ overload induces apoptosis, which was correlated with calpain-2 activation 708389 3.4.22.53 physiological function calpain 2 activation is an early event in heat stress-induced male germ cell apoptosis 709241 3.4.22.53 physiological function calpain 2 controls turnover of lymphocyte function-associated antigen-1 adhesions on migrating T lymphocytes 718262 3.4.22.53 physiological function calpain 2 is involved in glial differentiation 732688 3.4.22.53 physiological function calpain 2 is required for matrix metalloproteinase-2 activity in glioblastoma cells. Calpain 2 is required for glioblastoma cell invasion, but not migration 718169 3.4.22.53 physiological function calpain 2 is required for sister chromatid cohesion 708140 3.4.22.53 physiological function calpain 2 is required for the invasion of glioblastoma cells in the living zebrafish brain microenvironment 732365 3.4.22.53 physiological function calpain 2 plays a role in the generation of the low molecular weight-androgen receptor in CWR22-R1 cells 709126 3.4.22.53 physiological function calpain 2 promotes proliferation of cancer cells through Akt-FoxO-p27Kip1 signaling 732050 3.4.22.53 physiological function calpain 2 proteolysis of mAbp1 negatively regulates dorsal ruffle formation 709873 3.4.22.53 physiological function calpain 2-mediated proteolysis of focal adhesion kinase regulates adhesion dynamics in motile cells 709087 3.4.22.53 physiological function calpain-1 and calpain-2 play opposite functions in both synaptic plasticity/learning and memory and neuroprotection/neurodegeneration. Calpain-1 activation is necessary for certain forms of synaptic plasticity and learning and memory, while calpain-2 activation during a brief consolidation period limits the extent of plasticity/learning. Calpain-1 is neuroprotective, while calpain-2 is neurodegenerative. Calpain-2 activation, through the selective degradation of phosphatase PTEN, is linked to the regulation of mTOR-mediated local protein synthesis 755619 3.4.22.53 physiological function calpain-1 and calpain-2 play opposite roles in retinal ganglion cell death induced by acute intraocular pressure elevation. Calpain-1 activity supports survival of retinal ganglion cell after intraocular pressure elevation. Calpain-2 activity promotes cell death of retinal ganglion cells after intraocular pressure elevation. Calpain-2 activation cleaves striatal-enriched protein tyrosine phosphatase and activates STEP-mediated pro-death pathway in retinal ganglion cells after intraocular pressure elevation 754896 3.4.22.53 physiological function calpain-2 is a mediator of beta cell dysfunction and apoptosis in type 2 diabetes 717806 3.4.22.53 physiological function calpain-2 is crucial for promotion of migration and metastasis by caspase-8 707980 3.4.22.53 physiological function calpain-2 is involved in cell motility 707365 3.4.22.53 physiological function m-calpain antagonizes RhoA overactivation and endothelial barrier dysfunction under disturbed shear conditions 708018 3.4.22.53 physiological function m-calpain translocates during ischemia and activates at reperfusion in isolated rat hearts 709566 3.4.22.53 physiological function m-calpain up-regulates alpha- and beta-actin in alveolar rhabdomyosarcoma cells 708416 3.4.22.53 physiological function mitochondrial m-calpain is associated with ERp75 and plays an important role in releasing of truncated apoptosis-inducing factor from mitochondria 707281 3.4.22.53 physiological function mitochondrial m-calpain plays a role in the release of truncated apoptosis-inducing factor from the mitochondria by cleaving voltage-dependent anion channel 707559 3.4.22.53 physiological function the Ca2+-dependent release of m-calpain from the mitochondrial outer membrane has important implications in facilitating apoptotic cell death 717157