Disease relevance of Casp14

• METHODS: Mice were subjected to 75 or 120 minutes of 70% hepatic ischemia and 3 hours of reperfusion [1].
• METHODS AND RESULTS: Mice were assigned to receive regular chow or chow containing NCX 4016 or aspirin (both at 300 mumol/kg body weight, daily) throughout the 3-week experimental period [2].
• Increased Myeloid Cell Responses to M-CSF and RANKL Cause Bone Loss and Inflammation in SH3BP2 "Cherubism" Mice [3].
• Hapten-specific responses to the phenyltrimethylamino hapten. III. Mice whose delayed-type hypersensitivity responses cannot be abrogated by the presence of anti-idiotypic suppressor T cells lack a critical modulatory T cell function [4].
• Mammary tumors, hepatocellular carcinomas, and pancreatic islet changes in C3H-Avy Mice [5].

Psychiatry related information on Casp14

• Long-Term Memory Deficits in Pavlovian Fear Conditioning in Ca2+/Calmodulin Kinase Kinase {alpha}-Deficient Mice [6].
• METHODS: Mice treated with either methionine (MET) (5.2 mmol/kg/SC/twice daily) or valproate (1.5 mmol/kg/SC/twice daily) or MET+ valproate combination were tested for prepulse inhibition of startle (PPI) and social interaction (SI) [7].
• 1. Mice were subjected to gastrectomy (GX) or food deprivation (24 h) [8].
• MEASUREMENTS AND RESULTS: Mice homozygous for the BMAL1/Mop3 deletion showed an attenuated rhythm of sleep and wakefulness distribution across the 24-hr period [9].
• METHODS: Mice were tested using locomotor activity as well as a functional observational battery (FOB) both before and after a regimen of daily exposures to various concentrations of TCE [10].

High impact information on Casp14

• SUMMARY: Mice lacking p27(Kip1) have been created by gene targeting in embryonic stem cells [11].
• Developmental biology. Mice with half a mind [12].
• Perspectives: microbiology. Mice are not furry petri dishes [13].
• Toll-like Receptor 7-Dependent Loss of B Cell Tolerance in Pathogenic Autoantibody Knockin Mice [14].
• Cellular Mechanisms of Fatal Early-Onset Autoimmunity in Mice with the T Cell-Specific Targeting of Transforming Growth Factor-beta Receptor [15].

Chemical compound and disease context of Casp14

• RESULTS: Mice infected with Helicobacter bilis or coinfected with Helicobacter hepaticus and Helicobacter rodentium and fed a lithogenic diet developed cholesterol gallstones at 80% prevalence by 8 weeks compared with approximately 10% in uninfected controls [16].
• METHODS: Mice with trinitrobenzene sulfonic acid (TNBS)-induced colitis were treated with 0.5%, 2.0%, or 5.0% curcumin in the diet, and changes in body weight together with histologic scores were evaluated [17].
• METHODS: Mice were gavaged with Lactobacillus paracasei, Lactobacillus johnsonii, Bifidobacterium longum, or Bifidobacterium lactis in spent culture medium from days 10 to 21 after infection [18].
• Transgenic Mice Expressing the p75 CCAAT-Displacement Protein/Cut Homeobox Isoform Develop a Myeloproliferative Disease-Like Myeloid Leukemia [19].
• Recombinant Soluble Forms of Extracellular TLR4 Domain and MD-2 Inhibit Lipopolysaccharide Binding on Cell Surface and Dampen Lipopolysaccharide-Induced Pulmonary Inflammation in Mice [20].

Biological context of Casp14

• In particular, caspase-3 has been implicated in the differentiation of embryonic KC as well as in programmed cell death of KC, and caspase-14 has been suggested to function in the formation or homeostasis of the stratum corneum (SC) [21].
• The caspase-14 pro-enzyme was processed into its catalytic subunits, a step required for enzyme activity, on day E17.5, coinciding with SC formation [21].
• Tolerance of Mice to Lipopolysaccharide is Correlated with Inhibition of Caspase-3-mediated Apoptosis in Mouse Liver Cells [22].
• Like other caspases, caspase-14 has a conserved active site, pentapeptide QACRG [23].
• Human caspase-14 is assigned to chromosome 19p13 [24].

Anatomical context of Casp14

• Subcutaneous Fat Modulates Insulin Sensitivity in Mice by Regulating TNF-alpha Expression in Visceral Fat [25].
• These observations strongly suggest that caspase-14 is involved in the keratinocyte terminal differentiation program leading to normal skin cornification, while the executioner caspases are not implicated [26].
• MATERIALS AND METHODS: Mice bearing mammary tumors, developed after inoculation of syngeneic BALBIc mice with a mammary carcinoma cell line carrying a p53 mutation, were treated with celecoxib at 0, 7.5 and 15 mg/kg five times a week for seven weeks [27].
• CD8(+)CD28(-) Regulatory T Lymphocytes Prevent Experimental Inflammatory Bowel Disease in Mice [28].
• RESULTS: Mice treated with YF476 or loxtidine alone showed partial suppression of both gastric acid secretion and progression to neoplasia [29].

Associations of Casp14 with chemical compounds

• Calcium Channel Blocker Azelnidipine Reduces Glucose Intolerance in Diabetic Mice via Different Mechanism Than Angiotensin Receptor Blocker Olmesartan [30].
• METHODS: Mice were randomly assigned to receive oxygen or isoflurane for 30 min with 15 min of washout [31].
• METHODS: Mice were treated with cisplatin with or without administration of OTC [32].
• Purification of caspase-14 from native skin with subsequent N-terminal sequencing of the small subunit and tryptic digest analysis of the large subunit revealed an atypical processing site between Ile152 and Lys153, which distinguishes it from other caspases described to date that are processed at aspartate residues [33].
• METHODS: Mice fed a diet containing 10% creatine, came to accumulate phosphocreatine and to enhance hepatic ATP levels and mitochondrial oxidative phosphorylation activities [34].

Regulatory relationships of Casp14

• Caspase-14 is a developmentally regulated and tissue restricted member of the caspase family present in mammals [35].

Other interactions of Casp14

• Herein we report the characterization of a novel caspase, MICE (for mini-ICE), also designated caspase-14, that possesses an unusually short prodomain and is highly expressed in embryonic tissues but absent from all adult tissues examined [36].
• Transient overexpression of murine caspase-14 in mammalian cells did not elicit cell death and did not interfere with caspase-8-induced apoptosis [24].
• These observations suggest that caspase-14 may play a role in death receptor and granzyme B-induced apoptosis [23].
• Demonstration of in vitro cleavage of recombinant mouse caspase-14 by calpain I in the present study lends support to this hypothesis, further implicating cross-talk between different protease families in the pathophysiology of ischemic neural cell death [37].
• On non-denaturing protein gels, native caspase-14 has a relative electrophoretic mobility of approximately 80kDa, which resolves into caspase-14 proform, large and small subunit in SDS-polyacrylamide [33].

Analytical, diagnostic and therapeutic context of Casp14

• 1. Northern blot analysis revealed that mRNA expression of caspase-14 is undetectable in all mouse adult tissues examined except for skin, while it is abundantly expressed in mouse embryos [24].
• METHODS AND RESULTS: Mice were subjected to transverse aortic constriction (TAC) or sham operation [38].
• 2) Mice received an intraperitoneal injection of either saline (control animals) or recombinant human IL-1 receptor antagonist (rHuIL-1Ra) 2 hours before the injection of cancer cells; thereafter, they received an additional injection of saline or rHuIL-1Ra daily for 20 days [39].
• METHODS: Mice fed UDCA (0.5% wt/wt) or a control diet were subjected to common bile duct ligation (CBDL), selective bile duct ligation (SBDL), or sham operation [40].
• METHODS: Mice were treated with parenteral lipopolysaccharide or vehicle and then irradiated (14 Gy total body irradiation in a cesium irradiator) [41].

References