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High LIN9 expression is associated with Triple-negative breast cancers.
The MuvB multiprotein complex, together with B-MYB (show MYBL2 Proteins) and FOXM1 (show FOXM1 Proteins) (MMB-FOXM1 (show FOXM1 Proteins)) regulate the expression of mitotic kinesins in breast cancer cells.
LIN-9 phosphorylation on threonine-96 is required for transcriptional activation of LIN-9 target genes and promotes cell cycle progression.
Results show that E7 interacts with the B-Myb (show MYBL2 Proteins), FoxM1 (show FOXM1 Proteins) and LIN9 components of this activator complex, leading to cooperative transcriptional activation of mitotic genes in primary cells and E7 recruitment to the corresponding promoters.
Study links hTRM9L and tRNA modifications to inhibition of tumour growth via LIN9 and HIF1-alpha (show HIF1A Proteins)-dependent mechanisms.
inactivation of LIN9, a subunit of DREAM, results in premature senescence, which can be overcome by the SV40 large T (LT) antigen
Human Lin-9 has tumor-suppressing activities and the ability of hLin-9 to inhibit transformation is mediated through its association with pRB (show RB1 Proteins).
Mutation of BARA/LIN-9 restores the expression of E2F (show E2F1 Proteins) target genes.
Mip (show TNPO1 Proteins)/LIN-9 is required for the expression of B-Myb (show MYBL2 Proteins), and both proteins collaborate in the control of the cell cycle progression via the regulation of S phase and cyclin A (show CCNA2 Proteins), cyclin B, and CDK1 (show CDK1 Proteins)
human LIN-9, together with B-MYB (show MYBL2 Proteins), has a critical role in the activation of genes that are essential for progression into mitosis
LIN9 is essential for proliferation and genome stability of ESCs (show NR2E3 Proteins) by activating genes with important functions in mitosis and cytokinesis
These experiments provide the first direct genetic evidence for the role of LIN9 in development and mitotic gene regulation and they suggest that it may function as a haploinsufficient tumor suppressor.
there is a feedback mechanism between ARF and Mip130/LIN-9 in which either the increase of ARF or the decrease in Mip130/LIN-9
Mutation of BARA/LIN-9 restores the expression of E2F (show E2F1 Proteins) target genes in CDK4 (show CDK4 Proteins) null Mouse Embryo Fibroblasts, indicating that the wild-type protein plays a role in the expression of genes required for the G1/S transition.
Mip/LIN-9 is required for the expression of B-Myb (show MYBL2 Proteins), and both proteins collaborate in the control of the cell cycle progression via the regulation of S phase and cyclin A (show CCNA2 Proteins), cyclin B, and CDK1 (show CDK1 Proteins)
The repressor complex that Mip/LIN-9 forms with p107 (show RBL1 Proteins) takes functional precedence over the transcriptional activation linked to the Mip/LIN-9 and B-Myb (show MYBL2 Proteins) interaction.
Lin-9 and B-Myb (show MYBL2 Proteins) were both required for transcription of G(2)/M genes such as Cyclin B1 (show CCNB1 Proteins) and Survivin (show BIRC5 Proteins).
Mip130/LIN-9 contributes to the repression of these E2F (show E2F1 Proteins)-regulated genes in G0/G1 in mice.
This gene encodes a tumor suppressor protein that inhibits DNA synthesis and oncogenic transformation through association with the retinoblastoma 1 protein. The encoded protein also interacts with a complex of other cell cycle regulators to repress cell cycle-dependent gene expression in non-dividing cells. Alternatively spliced transcript variants encoding multiple isoforms have been observed for this gene.
TUDOR gene similar protein
, beta subunit-associated regulator of apoptosis
, pRB-associated protein
, protein lin-9 homolog
, rb related pathway actor
, type I interferon receptor beta chain-associated protein
, TUDOR gene similar 1 protein