Induction of terminal differentiation by constitutive activation of p38 MAP kinase in human rhabdomyosarcoma cells

Article Abstract:

Terminal differentiation by constitutive activation of p38 mitogen-activated protein (MAP) kinase in rhabdomyosarcoma (RMS) cells and its induction are discussed. RMS comes from muscle precursors. The block in RMS of the differentiation program is a paradox. The deregulated proliferation exists despite MyoD expression. MyoD inhibits proliferation of cells and promotes muscle differentiation. A lack of a factor needed for MyoD activity in RMS has been implicated before, and it has now been shown that p38 MAPK activaction, necessary for muscle differentiation is lacking in RMS cells.

Italy, United States, Physiological aspects, Cytochemistry, Cell differentiation, Protein kinases, Mitogens, Rhabdomyosarcoma

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Inhibition of DNA synthesis by RB: effects on G1/S transition and S-phase progression

Article Abstract:

The retinoblastoma tumor suppressor protein (RB) negatively regulates cell proliferation. RB has a novel role in inhibition of S-phase progression. The role is separate from the inhibition of the G1/S transition. It seems that continued phosphorylation of RB after G1/S is necessary for DNA replication to reach completion.

DNA, Cell cycle, Cell division, Tumor suppressor genes, Retinoblastoma, Antigens

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JNKK1 organizes a MAP kinase model through specific and sequential interactions with upstream and downstream components mediated by its amino-terminal extension

Article Abstract:

JNK and MEKK1 are probably activated through sequential interactions such as MEKK1:JNKK1 and JNKK1:JNK. Most MAP kinase cascades are specifically activated, and research has shown JNKK1 mutants can disrupt JNK activation by tumor necrosis factor or MEKK1 only when they contain intact amnio-terminal extensions. These findings suggest the importance of amnio-terminal extensions for MAPKKs in determining response specificity.

Analysis, Cell research, Cytological research, Genetic research

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