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High LIN9 expression is associated with Triple-negative breast cancers.
The MuvB multiprotein complex, together with B-MYB (zeige MYBL2 Proteine) and FOXM1 (zeige FOXM1 Proteine) (MMB-FOXM1 (zeige FOXM1 Proteine)) 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 (zeige MYBL2 Proteine), FoxM1 (zeige FOXM1 Proteine) 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 (zeige HIF1A Proteine)-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 (zeige RB1 Proteine).
Mutation of BARA/LIN-9 restores the expression of E2F (zeige E2F1 Proteine) target genes.
Mip (zeige TNPO1 Proteine)/LIN-9 is required for the expression of B-Myb (zeige MYBL2 Proteine), and both proteins collaborate in the control of the cell cycle progression via the regulation of S phase and cyclin A (zeige CCNA2 Proteine), cyclin B, and CDK1 (zeige CDK1 Proteine)
human LIN-9, together with B-MYB (zeige MYBL2 Proteine), 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 (zeige NR2E3 Proteine) 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 (zeige E2F1 Proteine) target genes in CDK4 (zeige CDK4 Proteine) 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 (zeige MYBL2 Proteine), and both proteins collaborate in the control of the cell cycle progression via the regulation of S phase and cyclin A (zeige CCNA2 Proteine), cyclin B, and CDK1 (zeige CDK1 Proteine)
The repressor complex that Mip/LIN-9 forms with p107 (zeige RBL1 Proteine) takes functional precedence over the transcriptional activation linked to the Mip/LIN-9 and B-Myb (zeige MYBL2 Proteine) interaction.
Lin-9 and B-Myb were both required for transcription of G(2)/M genes such as Cyclin B1 and Survivin.
Mip130/LIN-9 contributes to the repression of these E2F (zeige E2F1 Proteine)-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