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1 h a wound-closure assay in the presence of a mitotic inhibitor.
2  B protein levels in response to colcemid, a mitotic inhibitor.
3 otypes suggest a possible role for Skb1 as a mitotic inhibitor.
4 ibed role for PAK-related protein kinases as mitotic inhibitors.
5 in response to treatment with epirubicin and mitotic inhibitors.
6 complex/cyclosome (APC/C), such as the early mitotic inhibitor 1 (Emi1) and spindle checkpoint protei
7 ntion of mitotic entry by depletion of Early mitotic inhibitor 1 (EMI1) augmented the survival of BRC
8 otic checkpoint complex and interphase early mitotic inhibitor 1 (Emi1) ensures the correct order and
9                   In vertebrate cells, early mitotic inhibitor 1 (Emi1) has been proposed as an impor
10                          Disruption of early mitotic inhibitor 1 (Emi1) interferes with normal cell c
11 rowing body of evidence indicates that early mitotic inhibitor 1 (Emi1) is essential for genomic stab
12                      The APC inhibitor early mitotic inhibitor 1 (Emi1) was recently found to be requ
13   We identify the mutation as being in early mitotic inhibitor 1 (emi1), a negative regulator of the
14         In mouse oocytes, we find that early mitotic inhibitor 1 (Emi1), an inhibitor of the anaphase
15 attenuated by high levels of the Emi1 (early mitotic inhibitor-1) protein.
16                 In mouse, we find that early mitotic inhibitor 2 (Emi2), which is an anaphase-promoti
17 t rather the relative abundance of the Swe1p mitotic inhibitor and the mitosis-promoting cyclins.
18 ompounds 8, 9a, 18 and 19a are highly potent mitotic inhibitors and selectively cytotoxic to cancer c
19 ization to other tyrosine kinase inhibitors, mitotic inhibitors, and platinum-based therapy, there is
20 rapeutic drugs, including kinase inhibitors, mitotic inhibitors, and topoisomerase II inhibitors, on
21 AdBDNF, and intraventricular infusion of the mitotic inhibitor Ara-C completely blocked the performan
22 dicate that MCAK affects cell sensitivity to mitotic inhibitors by modulating the frequency of microt
23  can protect normal proliferating cells from mitotic inhibitors by preventing their entry into mitosi
24                                          The mitotic inhibitor docetaxel (DTX) is often used to treat
25 bly checkpoint complex, Mad2B, and the early mitotic inhibitor Emi1.
26                  We have discovered an early mitotic inhibitor, Emi1, which regulates mitosis by inhi
27           MK-1775 (also known as AZD1775), a mitotic inhibitor, has been demonstrated to enhance the
28 ible drug-tolerant persister state following mitotic inhibitors in advanced patient-derived breast ca
29 s to evaluate the activity of ON 01910.Na, a mitotic inhibitor, in in vitro and in vivo models of pan
30                                  Emi1 (early mitotic inhibitor) inhibits APC/C (anaphase-promoting co
31      Targeting AKT in combination with WEE1 (mitotic inhibitor kinase) seems to have potential to mak
32                                      WEE1, a mitotic inhibitor kinase, regulates the DNA damage repai
33  Mutation of several E3s with sensitivity to mitotic inhibitors led to increased aberrant mitoses, su
34 entry and exit and allow the suggestion that mitotic inhibitors may have selective effects in tumors
35                  Groups A and B received the mitotic inhibitor monocrotaline, followed by male F344 (
36 is lower than on hard even in the absence of mitotic inhibitors normally used to temper the astrocyte
37 kpoint proteins, formation of interphase and mitotic inhibitors of Cdc20, and correction of faulty mi
38                                    The novel mitotic inhibitor, ON 01910.Na, showed activity in precl
39 inoblastoma, and decreased expression of the mitotic inhibitor p21.
40 nt kinase (Cdk)-2 and -4, high levels of the mitotic inhibitors, p21Waf1 and p27Kipl, and decreased c
41 -like growth factor-I receptor (IGF-IR), and mitotic inhibitors, respectively, clustered with others
42  Finally, cells chronically treated with the mitotic inhibitor retinoic acid displayed a selective do
43                                          The mitotic inhibitor Skb1 localizes to a set of cortical no
44 mergence is essential for degradation of the mitotic inhibitor, Swe1.
45 d size would cause G2 arrest enforced by the mitotic inhibitor Swe1p, explaining previous findings th
46      Mitotic delay is due to the Wee1 family mitotic inhibitor Swe1p, whose degradation is linked to
47                     Here we describe a novel mitotic inhibitor that acts during Drosophila gastrulati
48  enabling them to survive in the presence of mitotic inhibitors, which is a characteristic of mature
49 ere discovered as proapoptotic molecules and mitotic inhibitors with potencies at low nanomolar conce