Anti-MAPK4 (aa 42-151) polyclonal antibody

The main purpose of this study was to explore the effect of tea tree oil (TTO) on lipopolysaccharide (LPS)-induced mastitis model using isolated bovine mammary epithelial cells (BMEC). This mastitis model was used to determine cellular responses to TTO and LPS on cellular cytotoxicity, mRNA abundance and cytokine production. High-throughput sequencing was used to select candidate genes, followed by functional evaluation of those genes. In the first experiment, LPS at a concentration of 200 mu g/mL reduced cell proliferation, induced apoptosis and upregulated protein concentrations of tumor necrosis factor-alpha (TNF-alpha), interleukin 6 (IL-6), and signal transducer and activator of transcription 1 (STAT1). Addition of TTO led to reduced cellular apoptosis along with downregulated protein concentrations of nuclear factor kappa B, mitogen-activated protein kinase 4 (MAPK4) and caspase-3. In the second experiment, BMEC challenged with LPS had a total of 1,270 differentially expressed genes of which 787 were upregulated and 483 were downregulated. Differentially expressed genes includedTNF-alpha,IL6, STAT1, andMAPK4. Overall, results showed that TTO (at leastin vitro) has a protective effect against LPS-induced mastitis. Furtherin vivoresearch should be performed to determine strategies for using TTO for prevention and treatment of mastitis and improvement of milk quality.

Erk4 and Erk3 are atypical members of the mitogen-activated protein ( MAP) kinase family. The high sequence identity of Erk4 and Erk3 proteins and the similar organization of their genes imply that the two protein kinases are paralogs. Recently, we have shown that Erk3 function is essential for neonatal survival and critical for the establishment of fetal growth potential and pulmonary function. To investigate the specific functions of Erk4, we have generated mice with a targeted disruption of the Mapk4 gene. We show that Erk4-deficient mice are viable and fertile and exhibit no gross morphological or physiological anomalies. Loss of Erk4 is not compensated by changes in Erk3 expression or activity during embryogenesis or in adult tissues. We further demonstrate that additional loss of Erk4 does not exacerbate the fetal growth restriction and pulmonary immaturity phenotypes of Erk3(-/-) mice and does not compromise the viability of Erk3(+/-) neonates. Interestingly, behavioral phenotyping revealed that Erk4-deficient mice manifest depression-like behavior in the forced-swimming test. Our analysis indicates that the MAP kinase Erk4 is dispensable for mouse embryonic development and reveals that Erk3 and Erk4 have acquired specialized functions through evolutionary diversification.