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Human Monoclonal GMNN Primary Antibody pour ELISA, WB - ABIN532939
Tsunematsu, Takihara, Ishimaru, Pagano, Takata, Kudo: Aurora-A controls pre-replicative complex assembly and DNA replication by stabilizing geminin in mitosis. dans Nature communications 2013
Show all 4 Pubmed References
Human Polyclonal GMNN Primary Antibody pour FACS, ELISA - ABIN1574066
Wang, Kirschner: Emi1 preferentially inhibits ubiquitin chain elongation by the anaphase-promoting complex. dans Nature cell biology 2013
Human Polyclonal GMNN Primary Antibody pour ICC, IF - ABIN251510
Yim, Erikson: Polo-like kinase 1 depletion induces DNA damage in early S prior to caspase activation. dans Molecular and cellular biology 2009
Human Polyclonal GMNN Primary Antibody pour IP, WB - ABIN2668583
Wohlschlegel, Dwyer, Dhar, Cvetic, Walter, Dutta: Inhibition of eukaryotic DNA replication by geminin binding to Cdt1. dans Science (New York, N.Y.) 2000
In the absence of geminin, limited pre-replicative complex assembly was restricted to the heterochromatin by elevated cyclin A-CDK activity.
Gem and Brm act antagonistically to modulate the EGFR-Ras-MAPK signaling pathway, by affecting Mek levels during Drosophila development
In cycling cells, Dup destruction is coupled to DNA replication and that increased levels of Gem balance elevated Dup levels to prevent pre-replicative complex reformation when Dup degradation fails.
Down-regulation of APC/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
GemC1 and Geminin can tune the proportion of neural stem cells and ependymal cells. Findings reveal the controlled dynamic of the neurogenic niche ontogeny and identify the Geminin family members as key regulators of the initial pool of adult neural stem cells.
Geminin acts as a tumor suppressor by safeguarding genome stability, whereas its overexpression is associated with genomic instability and enhanced tumorigenicity.
Geminin plays important roles in pre-meiotic DNA replication and subsequent spermatogenesis.
Geminin and Zic1 could cooperatively activate the expression of several shared targets encoding transcription factors that control neurogenesis, neural plate patterning, and neuronal differentiation.
Lack of Geminin promotes adult neural stem cell commitment toward the oligodendrocytic lineage at the expense of the neuronal differentiation without altering their ability to self-renew.
These results provide proof-of-principle that preventing geminin function could prevent malignancy in tumors derived from pluripotent cells by selectively eliminating the progenitor cells with little harm to normal cells.
cell penetrating (CP) Geminin is imported into the nucleus after incorporation and also the incorporated CP-Geminin directly interacted with Cdt1 or Brahma/Brg1 as the same manner as Geminin
Study shows that ablation of Geminin induces massive rereplication as a result of unrestrained Cdt1 activity in embryonic stem cells, whereas it has no such effect in embryonic fibroblasts in which alternative regulation of Cdt1 activity is intact.
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 expression, and thus for the maintenance of totipotency, pluripotency and the early neural lineage.
geminin acts both like a component of the FGF4 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. Geminin knockdown inhibited the epithelial to mesenchymal transition via its ability to affect Wnt signaling and E-cadherin expression.
Geminin promotes the neuronal precursor cell state by modulating both the epigenetic status and expression of genes encoding neurogenesis-promoting factors.
Geminin is absolutely required for mitotic proliferation of spermatogonia but does not regulate their differentiation.
Geminin family members are master regulators of centriole amplification and multiciliogenesis. (Review)
High Geminin expression is associated with triple negative breast cancers.
these data identify DUB3 and USP7 as factors that regulate DNA replication by controlling Geminin protein stability, and suggest that USP7 may be involved in Geminin dysregulation during breast cancer progression.
geminin selectively couples the transcription factor forkhead box O3 (FoxO3) to HDAC3, thereby specifically facilitating FoxO3 deacetylation.
summarize current information on the molecular functions of Geminin and the regulatory system for Geminin protein expression, and argue for the molecular role of Geminin in cell fate determination of hematopoietic stem cells [review]
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 and geminin expression distinguish a fraction of metastatic breast carcinoma with worse prognosis.
These findings suggest that E2F-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 are tightly regulated through the cell cycle, and the Cdt1-Geminin complex likely acts as a molecular switch that can enable or disable the firing of each origin of replication.
The Aurora-A-geminin-Cdt1 axis represents a critical regulator of proper DNA replication.
The properties of the Idas-Geminin complex suggest it as the functional form of Idas and provide a possible mechanism to modulate Geminin activity
Human geminin, when expressed in human cells in culture under a constitutive promoter, is excluded from the nucleus during part of the G1 phase and at the transition from G0 to G1.
MCM 7, geminin and topo IIalpha can be reliable tools for the differential diagnosis of reactive mesothelial cells and malignant mesothelioma cells.
Data indicate that retroviral transduction-mediated overexpression or siRNA-mediated knock-down of Hoxa9 respectively down-regulated or up-regulated Geminin in hematopoietic cells.
Coincidently amplified CDK13, GMNN, and CENPF genes can play a role as common cancer-driver genes in human cancers.
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