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anti-Rat (Rattus) FZR1 Antikörper:
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Cow (Bovine) Polyclonal FZR1 Primary Antibody für WB - ABIN2784494
Hu, Li, Li, Tan, Wan, Zhu, Zhang, Zhang, Yao: Downregulation of Cdh1 signalling in spinal dorsal horn contributes to the maintenance of mechanical allodynia after nerve injury in rats. in Molecular pain 2016
Human Polyclonal FZR1 Primary Antibody für ICC, IF - ABIN4312932
Giráldez, Galindo-Moreno, Limón-Mortés, Rivas, Herrero-Ruiz, Mora-Santos, Sáez, Japón, Tortolero, Romero: G1/S phase progression is regulated by PLK1 degradation through the CDK1/βTrCP axis. in FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2017
Human Polyclonal FZR1 Primary Antibody für ICC, IF - ABIN4312933
Fuchsberger, Martínez-Bellver, Giraldo, Teruel-Martí, Lloret, Viña: Aβ Induces Excitotoxicity Mediated by APC/C-Cdh1 Depletion That Can Be Prevented by Glutaminase Inhibition Promoting Neuronal Survival. in Scientific reports 2016
Human Monoclonal FZR1 Primary Antibody für ELISA, WB - ABIN4273099
Yamamoto, Takano, Ishiwata, Ohmura, Nagahata, Matsuura, Kamata, Sakamoto, Nakanishi, Kubo, Hishiki, Suematsu: Reduced methylation of PFKFB3 in cancer cells shunts glucose towards the pentose phosphate pathway. in Nature communications 2014
porcine FZR1 and CDC20 work on the maintenance of meiotic arrest at the first meiotic prophase and on the exit from M1
demonstration using human cell models that cell-cycle commitment is mediated by an EMI1-APC/C(CDH1) dual-negative feedback switch, in which EMI1 is both a substrate and an inhibitor of APC/C(CDH1)
Cdh1-dependent degradation of FoxM1 is required to shut down transcriptional activation of mitotic regulators during exit from mitosis.
Cdh1 reciprocally regulates the Rb pathway through competing with E2F1 to bind the hypophosphorylated form of Rb.
these findings suggest that Cdh1 controls TACC3 protein stability during mitotic exit.
Data report that a nuclear-localized portion of the stress-activated kinase JNK is degraded by the APC/C(Cdh1) during exit from mitosis and the G1 phase of the cell cycle.
We identified the known APC/C regulator Cdh1 and the F-box protein Fbxl15 as specific modulators of N-cyclin B1-luciferase steady-state levels and turnover. Collectively, our studies suggest that analyzing the steady-state levels of luciferase fusion proteins in parallel facilitates identification of specific regulators of protein turnover.
Findings document the differential expression, subcellular localization and cell-cycle-regulatory activity of alternatively spliced human CDH1 isoforms.
upon infection of quiescent cells human cytomegalovirus not only activates the E2F-dependent G(1)/S transcription program but also facilitates protein accumulation of APC/C substrates by rapid Cdh1 dissociation
Cell cycle regulation of Six1 occurs both transcriptionally and post-translationally via phosphorylation
Cdh1 may act as an important component in tumor suppression and could be considered as a novel biomarker in breast cancer.
Reduced Cdh1 levels have no effect on destruction of many APC/C substrates during mitotic exit but strongly and specifically stabilize Aurora kinases.
Low Cdh1 expression is associated with breast cancer.
Glycolysis-promoting enzyme 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase, isoform 3 (PFKFB3), is degraded by the E3 ubiquitin ligase APC/C-Cdh1.
DDB1 modulates the function of APC/C(Cdh1) in a manner independent of the Cul4-DDB1 complex
Proteolysis of Rad17 by Cdh1/APC regulates checkpoint termination and recovery from genotoxic stress
Inactivation and disassembly of the anaphase-promoting complex during human cytomegalovirus infection is associated with degradation of the APC5 and APC4 subunits and does not require UL97-mediated phosphorylation of Cdh1.
Substrates are recruited to the Anaphase-promoting complex by binding to a bipartite substrate receptor composed of Cdh1 and Doc1.
APC/CCdh1 is a master G0/G1 regulator and involved in differentiation and development processes. (Review)
The deubiquitinase USP37 binds CDH1 and removes degradative polyubiquitin from cyclin A. USP37 was induced by E2F factors in G1, peaked at G1/S, and was degraded in late mitosis. Phosphorylation of USP37 by CDK2 stimulated its full activity.
Ect2 is subject to proteasomal degradation after mitosis, following ubiquitination by the APC/C complex and its co-activator Cdh1
Key regulator of ligase activity of the anaphase promoting complex/cyclosome (APC/C), which confers substrate specificity upon the complex. Associates with the APC/C in late mitosis, in replacement of CDC20, and activates the APC/C during anaphase and telophase. The APC/C remains active in degrading substrates to ensure that positive regulators of the cell cycle do not accumulate prematurely. At the G1/S transition FZR1 is phosphorylated, leading to its dissociation from the APC/C. Following DNA damage, it is required for the G2 DNA damage leads to the ubiquitination of PLK1, preventing entry into mitosis (By similarity).
fizzy-related protein homolog
, fizzy/cell division cycle 20 related 1 (Drosophila)
, fizzy-related protein FZR
, Fizzy-related protein-like protein
, fizzy/cell division cycle 20 related 1
, CDC20-like 1b
, CDC20-like protein 1
, cdh1/Hct1 homolog
, cell division cycle 20 related 1