Cooperation between the Cdk inhibitors p27(KIP1) and p57(KIP2) in the control of tissue growth and development

Article Abstract:

Cell cycle exit is necessary for terminal differentiation of numerous cell types. Rb, a retinoblastoma protein, seems to have a role in differentiation and cell cycle exit in several tissues. Rb is regulated negatively by cyclin-dependent kinases (Cdks). The most important effectors for down-regulation of Cdk activity for activation of Rb in lens or other tissues are not known Using multiple mutant mice, it has been shown that the Cdk inhibitors p57(KIP2) and p27(KIP1) work in a redundant way to control cell cycle exit as well as differentiation of placental trophoblasts and lens fiber cells. Thus p57(KIP2) and p27(KIP1) are key end effectors of signal transduction paths that control cell differentiation.

Genetic aspects, Observations, Genetic regulation, Genetic transcription, Transcription (Genetics), Cell differentiation, Protein kinases, Cornea, Trophoblast, Trophoblasts

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Fibroblast growth factor receptor 3 is a negative regulator of bone growth

Article Abstract:

The process of endochondral ossification is an important bone formation mechanism. It happens as chondrocytes proliferate, undergo hypertrophy, experience cell death and undertake osteoblastic replacement. In this ossification process, fibroblast growth factor receptor 3 (FGFR-3) acts as a tyrosine kinase that serves as a high affinity receptor for several fibroblast growth factor receptors. FGFR-3 appears to act through a largely negative mechanism, serving to limit osteogenesis rather than promote it, with prolonged endochondral growth leading to progressive bone dysplasia.

Bones, Growth, Protein tyrosine kinase, Protein-tyrosine kinase, Fibroblast growth factors, Bone development, Cartilage cells, Ossification

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Mice lacking p21(superCIP1/WAF1) undergo normal development, but are defective in G1 checkpoint control

Article Abstract:

The role in p21(superCIP1/WAF)1 in the G1 checkpoint is revealed by the fact that mice lacking p21(superCIP1/WAF1) develop normally but are defective in G1 checkpoint control. p21(superCIP1/WAF1) cells also display a significant growth alteration in vitro, achieving a saturation density as that expressed by the tumor suppressor p53. Nevertheless, p21(superCIP1/WAF)1 embryonic fibroblasts are largely deficient in their ability to arrest in G1 in response to DNA damage and nucleotide pool perturbation.

Analysis, Mice, Mice (Rodents), Developmental biology, Biological research, Genetic research

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