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High LIN9 expression is associated with Triple-negative breast cancers.
The MuvB multiprotein complex, together with B-MYB (show MYBL2 ELISA Kits) and FOXM1 (show FOXM1 ELISA Kits) (MMB-FOXM1 (show FOXM1 ELISA Kits)) 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 ELISA Kits), FoxM1 (show FOXM1 ELISA Kits) 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 ELISA Kits)-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 ELISA Kits).
Mutation of BARA/LIN-9 restores the expression of E2F (show E2F1 ELISA Kits) target genes.
Mip (show TNPO1 ELISA Kits)/LIN-9 is required for the expression of B-Myb (show MYBL2 ELISA Kits), and both proteins collaborate in the control of the cell cycle progression via the regulation of S phase and cyclin A (show CCNA2 ELISA Kits), cyclin B, and CDK1 (show CDK1 ELISA Kits)
human LIN-9, together with B-MYB (show MYBL2 ELISA Kits), 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 ELISA Kits) 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 ELISA Kits) target genes in CDK4 (show CDK4 ELISA Kits) 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 (show MIP ELISA Kits)/LIN-9 is required for the expression of B-Myb (show MYBL2 ELISA Kits), and both proteins collaborate in the control of the cell cycle progression via the regulation of S phase and cyclin A (show CCNA2 ELISA Kits), cyclin B, and CDK1 (show CDK1 ELISA Kits)
The repressor complex that Mip (show MIP ELISA Kits)/LIN-9 forms with p107 (show RBL1 ELISA Kits) takes functional precedence over the transcriptional activation linked to the Mip (show MIP ELISA Kits)/LIN-9 and B-Myb (show MYBL2 ELISA Kits) interaction.
Lin-9 and B-Myb (show MYBL2 ELISA Kits) were both required for transcription of G(2)/M genes such as Cyclin B1 (show CCNB1 ELISA Kits) and Survivin (show BIRC5 ELISA Kits).
Mip130/LIN-9 contributes to the repression of these E2F (show E2F1 ELISA Kits)-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