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High LIN9 expression is associated with Triple-negative breast cancers.
The MuvB multiprotein complex, together with B-MYB (Montrer MYBL2 Anticorps) and FOXM1 (Montrer FOXM1 Anticorps) (MMB-FOXM1 (Montrer FOXM1 Anticorps)) 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 (Montrer MYBL2 Anticorps), FoxM1 (Montrer FOXM1 Anticorps) 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 (Montrer HIF1A Anticorps)-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 (Montrer RB1 Anticorps).
Mutation of BARA/LIN-9 restores the expression of E2F (Montrer E2F1 Anticorps) target genes.
Mip (Montrer TNPO1 Anticorps)/LIN-9 is required for the expression of B-Myb (Montrer MYBL2 Anticorps), and both proteins collaborate in the control of the cell cycle progression via the regulation of S phase and cyclin A (Montrer CCNA2 Anticorps), cyclin B, and CDK1 (Montrer CDK1 Anticorps)
human LIN-9, together with B-MYB (Montrer MYBL2 Anticorps), 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 (Montrer NR2E3 Anticorps) 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 (Montrer E2F1 Anticorps) target genes in CDK4 (Montrer CDK4 Anticorps) 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 (Montrer MIP Anticorps)/LIN-9 is required for the expression of B-Myb (Montrer MYBL2 Anticorps), and both proteins collaborate in the control of the cell cycle progression via the regulation of S phase and cyclin A (Montrer CCNA2 Anticorps), cyclin B, and CDK1 (Montrer CDK1 Anticorps)
The repressor complex that Mip (Montrer MIP Anticorps)/LIN-9 forms with p107 (Montrer RBL1 Anticorps) takes functional precedence over the transcriptional activation linked to the Mip (Montrer MIP Anticorps)/LIN-9 and B-Myb (Montrer MYBL2 Anticorps) interaction.
Lin-9 and B-Myb (Montrer MYBL2 Anticorps) were both required for transcription of G(2)/M genes such as Cyclin B1 (Montrer CCNB1 Anticorps) and Survivin (Montrer BIRC5 Anticorps).
Mip130/LIN-9 contributes to the repression of these E2F (Montrer E2F1 Anticorps)-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