Human connective tissue growth factor is expressed in advanced atherosclerotic lesions. These results indicate that KLF2 is an important regulator of late-stage lung development. Biochem J. Communication between myocytes and fibroblasts in cardiac remodeling in angiotensin chimeric mice.
These results suggest that KLF12 has an important role in the progression of gastric cancer. A search of gene expression databases showed that KLF4 mRNA levels are lower in breast tumor tissues, compared with normal tissues, in 9 of 11 data sets and that the levels are inversely correlated with tumor grade 5.
You can reuse this answer Creative Commons License. KLFs regulate erythropoiesis, lymphopoiesis, and formation and functions of monocytes and macrophages. Multiple sequence alignment and phylogenetic analysis were performed using the ClustalW tool, Version 2.
Post-translational Modifications Co-regulatory proteins modify KLF family members via acetylation, phosphorylation, ubiquitination, and sumoylation to refine their transcriptional activity.
The role of epithelial-mesenchymal transition in cancer pathology. Many KLFs are also involved in tumor biology, in reprogramming somatic cells into inducible pluripotent stem iPS cells, and maintaining the pluripotent state of embryonic stem ES cells, Conditional expression of KLF4 in basal keratinocytes of transgenic mice blocks the proliferation-differentiation switch between the basal and parabasal epithelial cells and leads to hyperplasia, dysplasia, and squamous cell carcinoma in situ
Cell stiffening in response to external stress is correlated to actin recruitment. Mechanical Changes as a Function of Age Changes in the mechanical properties of cells are hallmarks of the aging process Hypoxia and the extracellular matrix: drivers of tumour metastasis.
Neurodegenerative Diseases Neurodegenerative diseases encompass a group of disorders that are characterized by the progressive loss of the function or structure of neurons and the central nervous system. This increased level of ROS facilitates the perpetual cell-associated damage 43 and fuels bidirectional ECM dysfunction through enhanced collagen fragmentation and activation of MMPs 22 , as well as by altering the architecture and activity of actomyosin cytoskeletal contractility Figure 4.
Many key cellular components and their mutual interactions orchestrate the complex response of cells to changes in their mechanical properties, which undergo dysfunctional changes with age and age-associated pathogenesis.