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Conservation of the Chk1 checkpoint pathway in mammals: linkage of DNA damage to Cdk regulation through Cdc25.
Results suggest a model whereby in response to DNA damage, Chk1 phosphorylates and inhibits Cdc25C, thus preventing activation of the Cdc2-cyclin B complex and mitotic entry.
Cooperation between the Cdk inhibitors p27(KIP1) and p57(KIP2) in the control of tissue growth and development.
It is demonstrated that the Cdk inhibitors p27(KIP1) and p57 (KIP2) function redundantly to control cell cycle exit and differentiation of lens fiber cells and placental trophoblasts and are critical terminal effectors of signal transduction pathways that control cell differentiation.
Tumor suppressor Smad4 is a transforming growth factor beta-inducible DNA binding protein
- J. Yingling, M. Datto, C. Wong, J. Frederick, N. Liberati, X. F. Wang
- BiologyMolecular and cellular biology
- 1 December 1997
It is shown that in Mv1Lu cells Smad3 and Smad4 form a TGF-beta-induced, phosphorylation-dependent, DNA binding complex that specifically recognizes a bipartite binding site within p3TP-Lux, and it is demonstrated that Smad 4 itself is a DNA binding protein which recognizes the same sequence.
p21(CIP1) and p57(KIP2) control muscle differentiation at the myogenin step.
- P. Zhang, C. Wong, D. Liu, M. Finegold, J. Harper, S. Elledge
- BiologyGenes & development
- 15 January 1999
It is shown that two Cdk inhibitors, p21(CIP1) and p57(KIP2), redundantly control differentiation of skeletal muscle and alveoli in the lungs and indicates a role for cell-cycle exit in myogenin function.
Potent and selective small-molecule MCL-1 inhibitors demonstrate on-target cancer cell killing activity as single agents and in combination with ABT-263 (navitoclax)
This work represents the first description of small-molecule MCL-1 inhibitors with sufficient potency to induce clear on-target cellular activity, and demonstrates the utility of these molecules as chemical tools for dissecting the basic biology of M CL-1.
Smads bind directly to the Jun family of AP-1 transcription factors.
- N. Liberati, M. Datto, X. F. Wang
- BiologyProceedings of the National Academy of Sciences…
- 27 April 1999
It is reported that Smad3 and Smad4 can physically interact with AP-1 family members, and data suggest that TGFbeta-mediated transcriptional activation through AP- 1 sites may involve a regulated interaction between Smads andAP-1 transcription factors.
Smad3-Smad4 and AP-1 Complexes Synergize in Transcriptional Activation of the c-Jun Promoter by Transforming Growth Factor β
A concurrent requirement for two discrete responsive elements in the regulation of the c-Jun promoter, one a binding site for a Smad3-Smad4 complex and the other an AP-1 binding site is described, suggesting that Smad andAP-1 complexes function synergistically to mediate TGF-β-induced transcriptional activation of thec- Jun promoter.
The bromodomain and extra-terminal inhibitor CPI203 enhances the antiproliferative effects of rapamycin on human neuroendocrine tumors
The data suggest that targeting MYC with a BETi may increase the therapeutic benefits of rapalogs in human PanNET patients and provide a novel clinical strategy for PanNETs, and possibly for other tumors as well.
The yeast peptidyl proline isomerases FPR3 and FPR4, in high copy numbers, suppress defects resulting from the absence of the E3 ubiquitin ligase TOM1
Tom1p probably has one or more functions beyond its involvement in gene expression, and the essential sequences include about 170 highly conserved residues at the proteins' N-termini.
Cytotoxic activity of the MK2 inhibitor CMPD1 in glioblastoma cells is independent of MK2
This study demonstrates how functional and mechanistic studies with appropriate selection of test compounds, combining genetic knock-down and pharmacological inhibition, coordinating timing and dose levels enabled to uncover the primary target of an MK2 inhibitor commonly used in the research community.