IndraLab
Statements
reach
"To find out the potential therapeutic strategies, we screened the combination of inhibitors against the FGF/FGFR signaling pathway and the CCND1/CDK4 complex and revealed that gefitinib combined with LY2874455 and abemaciclib exhibited the most effective inhibition of resistance in vitro and in vivo ."
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"We further revealed the molecular mechanism by which nuclear-localized GHR regulates MSCs proliferation, and found that nuclear-targeted GHR enhanced the phosphorylation of STAT5, and the activated STAT5 initiates the transcription of CyclinD1, after which, the complex of CyclinD1 and CDK4 further phosphorylates Rb, and the activated Rb releases E2F1, the released E2F1 ultimately realizes the biological function of GH promoting cell proliferation."
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"The activation of cyclin D1, which subsequently interacts with CDK4 or CDK6, leads to the inactivation of the restrictive G1 checkpoint, suppressing cell cycle arrest. xref In our study, DCZ0858 induced cell cycle arrest in the G0/G1 phase and inhibited cell transition into the S phase."
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"In the presence of mitogenic stimuli and abundant nutrients, cyclin D1 is synthesized; to perform its functions, cyclin D1 assembles with CDK4 or CDK6 to form a kinase complex; conversely, growth factor withdrawal or nutrient depletion compromises the formation of new cyclin D1-CDK4/6 complexes, leading to an immediate degradation of cyclin D1 in order to facilitate cell cycle exit [ xref ]."
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"In human cells, cyclin D1 interacts with CDK4 and CDK6 to form holoenzymes and then phosphorylates the tumor-suppressor protein Rb in G1 phase, which is important for cell cycle progression. xref The E2F transcription factor binds to Rb and is released when Rb is phosphorylated, inducing the expression levels of a series of genes, such as cyclin E, cyclin A, PCNA and MCM7, which are involved in entry into S phase of the cell division cycle. xref Our study showed that SH treatment downregulated the expression levels of the cell cycle-positive regulators, including CDK4, cyclin D1, cyclin E, phospho-Rb, PCNA and MCM7."
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"To investigate the requirement for p53 and Rb activity in senescence-associated OPN regulation, we ectopically expressed a well-characterized dominant negative p53 cDNA (p53-DD) ( xref ) or a cDNA expressing a fusion protein consisting of a mutant form of cyclin dependent kinase 4 R24C (Cdk4) and cyclin D1 (DK) that inhibits Rb ( xref ) ( xref )."
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"In fact, the proline-rich N-terminal portion of INSM1 has recently been shown to specifically bind cyclin D1, a key cell cycle regulator, and that through this interaction, INSM1 interrupts the interaction between cyclin D1 and cyclin-dependent kinase 4 (CDK4), which subsequently inhibits Rb phosphorylation [ xref ]."
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"The proliferation-promoting action of isoprenaline was abolished by a β1-selective antagonist and was more effectively abolished by a β2-selective antagonist; the mechanism for the action of the antagonists was a G0/G1 phase cell cycle arrest which was associated with decreased cyclin D1, CDK-4, CDK-6 and phospho-Rb expression."
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"The remaining patients that have neither gene mutation typically have de-regulated kinases including amplification and overexpression of PAK1 [ xref , xref ], inactivation of the NF-1 tumor suppressor [ xref ], loss of NF-1 associated with RAS activation [ xref , xref ] and cell cycle aberrations such as CCND1 and CDK4 amplification [ xref ]."
CCND1 binds CDK4, CDK8, and NCIT:C95407. 1 / 1
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"From the analysis, NSC765600 and NSC765691- CCND1 , CDK4 , PLK1 , and CD44 complexes displayed the highest binding energies of −9.3, −8.3, −7.4 and −7.0 kcal/mol and (−9.6, −8.0, −7.7 and −7.3 kcal/mol, respectively ( xref and xref and accompanying tables), as compared to the standard inhibitors’ results, which were −7.5, −7.6 and −7.9 kcal/mol for fascaplysin, ribociclib, and volasertib- CCND1 , CDK4 , and PLK1, respectively ( xref , accompanying table)."
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"Further, GSEA revealed that KIAA1429, METTL3, and IGF2BP1 were significantly related to multiple biological behaviors, including proliferation, apoptosis, metastasis, energy metabolism, drug resistance, and recurrence, and that KIAA1429 and IGF2BP1 had potential target genes, including E2F3, WTAP, CCND1, CDK4, EGR2, YBX1, and TLX, which were associated with cancers."
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"From the analysis, NSC765600 and NSC765691- CCND1 , CDK4 , PLK1 , and CD44 complexes displayed the highest binding energies of −9.3, −8.3, −7.4 and −7.0 kcal/mol and (−9.6, −8.0, −7.7 and −7.3 kcal/mol, respectively ( xref and xref and accompanying tables), as compared to the standard inhibitors’ results, which were −7.5, −7.6 and −7.9 kcal/mol for fascaplysin, ribociclib, and volasertib- CCND1 , CDK4 , and PLK1, respectively ( xref , accompanying table)."