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In the absence of geminin, limited pre-replicative complex assembly was restricted to the heterochromatin by elevated cyclin A (show CCNA2 ELISA Kits)-CDK (show CDK4 ELISA Kits) activity.
Gem and Brm (show SMARCA2 ELISA Kits) act antagonistically to modulate the EGFR (show EGFR ELISA Kits)-Ras-MAPK (show MAPK1 ELISA Kits) signaling pathway, by affecting Mek (show MAP2K1 ELISA Kits) levels during Drosophila development
In cycling cells, Dup (show CDT1 ELISA Kits) destruction is coupled to DNA replication and that increased levels of Gem balance elevated Dup (show CDT1 ELISA Kits) levels to prevent pre-replicative complex reformation when Dup (show CDT1 ELISA Kits) degradation fails.
Down-regulation of APC (show APC ELISA Kits)/C activity results in stabilization of Geminin protein and blocks endocycle progression.
results demonstrate that geminin is required for proper Kupffer's vesicle formation and ciliogenesis, thus playing an important part in setting up left-right asymmetry.
Results from a dual-luciferase assay in HEK293 cells showed that ZDND increases the translation of geminin
Maternal geminin does not regulate oogenesis and oocyte meiotic maturation, but it does control accurate DNA replication and timely cleavage of fertilized eggs.
Regulation of gene expression by geminin occurs only after pluripotent cells differentiate into cells in which geminin is not essential for viability.
Geminin is an important regulator of self-renewal and survival of enteric nervous system progenitor cells.
geminin is indispensable for fetal hematopoiesis and regulates the generation of a physiological pool of stem and progenitor cells in the fetal hematopoietic system.
these data demonstrate a requirement for Geminin for neural tube patterning and neuronal differentiation during mammalian neurulation in vivo.
geminin is required for Sox2 (show SOX2 ELISA Kits) expression, and thus for the maintenance of totipotency, pluripotency and the early neural lineage.
geminin acts both like a component of the FGF4 (show FGF4 ELISA Kits) signal transduction pathway that governs trophoblast proliferation and differentiation, and geminin is required to maintain endocycles.
Data indicate that geminin supported neural differentiation.
Geminin dysregulation may be restored by derepressed Hoxb4 and Hoxa9 in Scmh1-deficient mice.
Geminin is required during preimplantation development (show MTA2 ELISA Kits). Geminin knockdown inhibited the epithelial to mesenchymal transition via its ability to affect Wnt (show WNT2 ELISA Kits) signaling and E-cadherin (show CDH1 ELISA Kits) expression.
Studies indicate that geminin expression is associated with different types of cancer.
High geminin expression is associated with breast cancer.
De novo GMNN mutations cause autosomal-dominant primordial dwarfism associated with Meier-Gorlin syndrome.
Elevated Ki67 (show MKI67 ELISA Kits) and geminin expression distinguish a fraction of metastatic breast carcinoma with worse prognosis.
These findings suggest that E2F (show E2F1 ELISA Kits)-mediated activation of Geminin transcription is negatively regulated by Geminin through the inhibition of chromatin remodeling.
Bound Geminin prevents transition of the pre-replicative complexes to a state that is competent for initiation of DNA replication.
Selective expression of geminin during the proliferative phase of the cell cycle and its nuclear specificity increase its potential to be used as an alternative marker of proliferation in breast cancer patients.
Protein levels of Geminin and Cdt1 (show CDT1 ELISA Kits) are tightly regulated through the cell cycle, and the Cdt1 (show CDT1 ELISA Kits)-Geminin complex likely acts as a molecular switch that can enable or disable the firing of each origin of replication.
The Aurora-A (show AURKA ELISA Kits)-geminin-Cdt1 (show CDT1 ELISA Kits) axis represents a critical regulator of proper DNA replication.
This gene encodes a protein that plays a critical role in cell cycle regulation. The encoded protein inhibits DNA replication by binding to DNA replication factor Cdt1, preventing the incorporation of minichromosome maintenance proteins into the pre-replication complex. The encoded protein is expressed during the S and G2 phases of the cell cycle and is degraded by the anaphase-promoting complex during the metaphase-anaphase transition. Increased expression of this gene may play a role in several malignancies including colon, rectal and breast cancer. Alternatively spliced transcript variants have been observed for this gene, and two pseudogenes of this gene are located on the short arm of chromosome 16.
, geminin protein
, geminin, DNA replication inhibitor