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Stable cohesion between sister chromatids before anaphase and their timely separation during anaphase are critical for chromosome inheritance. Additionally we are shipping ESPL1 Antibodies (204) and and many more products for this protein.
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Proximity mapping of human separase has been presented.
The assay was used to quantify Separase proteolytic activity in leukemic cell lines and peripheral blood samples from leukemia patients.
Recruitment and activation of separase at centrosomes are two distinct steps that do not require microtubules.
Separase protein levels decrease and Separase proteolytic activity increases exclusively in b3a2 p210BCR-ABL (show ABL1 ELISA Kits)-positive cell lines under Imatinib treatment.
Separase is an oncogene (show RAB1A ELISA Kits) whose overexpression induces tumorigenesis, and indicate that Separase overexpression and aberrant nuclear localization are common in many tumor types and may predict outcome in some human malignancies.
High ESPL1 mRNA expression was associated with luminal B breast cancers.
Data indicate that separase is subject to native-state cis (show CISH ELISA Kits)/trans isomerization by peptidyl-prolyl-isomerase (show PPI ELISA Kits) Pin1 (show PIN1 ELISA Kits).
Mutation of the homologous position in PTTG1 (show PTTG1 ELISA Kits) (H(134)) switched PTTG1 (show PTTG1 ELISA Kits) from an inhibitor into an activator of ESP1 (show AES ELISA Kits).
By consecutively acting as a protease and a cdk1 (show CDK1 ELISA Kits) inhibitor, separase coordinates two key processes to achieve simultaneous and abrupt separation of sister chromatids.
Kendrin (show PCNT ELISA Kits) is a novel and crucial substrate for separase (ESPL1) at the centrosome, protecting the engaged centrioles from premature disengagement and thereby blocking reduplication until the cell passes through mitosis.
Degradation of the Separase-cleaved Rec8, a Meiotic Cohesin Subunit, by the N-end Rule Pathway.
Separase-overexpressing mammary cells are not only susceptible to chromosomal missegregation-induced aneuploidy but also other genetic instabilities
With the continual loss of cohesins from chromosomes that occurs throughout the natural reproductive lifespan, tight regulation of separase in oocytes may be particularly important to maintain cohesion and prevent aneuploidy.
Separase act synergistically with loss of p53 (show TP53 ELISA Kits) in the initiation and progression of B- and T- cell lymphomas
Separase phospho-regulation is critical for genome stability in oogenesis.
Separase phosphorylation act redundantly to prevent sister chromatid separation.
In embryonic fibroblasts, Separase depletion blocks sister chromatid separation but does not prevent other aspects of mitosis, cytokinesis, or chromosome replication.
Proteolytic activity of separase is therefore essential for Rec8 (show REC8 ELISA Kits)'s removal from chromosome arms and for chiasma resolution but not for PBE (show EHHADH ELISA Kits).
inhibitory phosphorylation of separase plays a critical role in the maintenance of sister chromatid cohesion and genome stability in proliferating postmigratory primordial germ cells
These results collectively suggest that Separase is an oncogene (show RAB1A ELISA Kits), whose overexpression alone in mammary epithelial cells is sufficient to induce aneuploidy and tumorigenesis in a p53 (show TP53 ELISA Kits) mutant background.
Stable cohesion between sister chromatids before anaphase and their timely separation during anaphase are critical for chromosome inheritance. In vertebrates, sister chromatid cohesion is released in 2 steps via distinct mechanisms. The first step involves phosphorylation of STAG1 (MIM 604358) or STAG2 (MIM 300826) in the cohesin complex. The second step involves cleavage of the cohesin subunit SCC1 (RAD21\; MIM 606462) by ESPL1, or separase, which initiates the final separation of sister chromatids (Sun et al., 2009
extra spindle poles like 1
, caspase-like protein ESPL1
, extra spindle poles-like 1 protein
, separin, cysteine protease
, Cut1/ESP1 related protein