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1 NIMA (never in mitosis arrest)-related kinase 2 (Nek2) i
2 NIMA appears to be particularly important.
3 NIMA expression also induces Ser-10 phosphorylation inap
4 NIMA is also required for TINA, a NIMA-interacting prote
5 NIMA promotes entry into mitosis in late G2 by some mech
6 NIMA promotes NPC disassembly in a spatially regulated m
7 NIMA protein instability during S phase and G2 was also
8 NIMA(d)-exposed splenocytes exhibited bystander suppress
9 NIMA, as well as its most closely related human ortholog
10 NIMA-exposed neonates also developed vigorous primary an
11 NIMA-related protein kinase 2 (Nek2), which regulates ce
12 NIMA-specific Tregs expand during pregnancies sired by m
14 and a majority (61%) of adults; nursing by a NIMA+ mother was essential for preserving MMc into adult
18 equences from this region identified Nek1, a NIMA (never in mitosis A)-related kinase as a candidate
19 of jck mutation on the expression of Nek8, a NIMA-related (never in mitosis A) kinase, and polycystin
20 terminal noncatalytic tail of Nercc1/Nek9, a NIMA family protein kinase that is activated in mitosis.
23 k7, a member of the Never in Mitosis Gene A (NIMA) kinase family, as a regulator of telomere integrit
24 homology with the Never In Mitosis, gene A (NIMA) kinase from the filamentous fungus Aspergillus nid
25 suppression of the Never in Mitosis Gene A (NIMA)-related protein kinase gene NEK4 disrupted timely
26 NEK2, which encodes the never in mitosis A (NIMA)-related kinase, by 5aza-dC is context-specific as
28 duced cell cycle oscillations require active NIMA, because a nimA5 + bimA1(APC3) double mutant arrest
31 ental exposure to noninherited maternal Ags (NIMA) results in alloantigen-specific natural and adapti
32 the hypothesized direction of effect for all NIMA in women, indicating that increased body iron statu
34 compatibility, parent-of-origin effects, and NIMA effects at DRB1 are unlikely to play a role in SLE.
36 ctivities of maturation promotion factor and NIMA are coincidentally regulated in A. nidulans and sug
37 esized directions of effect between iron and NIMA, except for rs651007, associated with decreased fer
39 1, the physical interaction between PINA and NIMA is primarily dependent upon the prolylisomerase dom
42 two nuclear pore complex (NPC) proteins and NIMA is required for mitotic localization of the Cdk1 ki
45 ission rates (noninherited maternal antigen [NIMA] effects) in other autoimmune diseases have been re
46 ffect of noninherited maternal HLA antigens (NIMA) and double-unit cord blood transplantation (CBT).
48 we investigated the functions of Arabidopsis NIMA-related kinase 6 (NEK6), which regulates microtubul
51 whose products interact with the Aspergillus NIMA cell cycle regulatory protein kinase, reveals that
52 on-invasive measurements of atherosclerosis (NIMA), i.e., presence of plaque, intima media thickness
55 Specifically, phosphorylation of Sid4 by NIMA(Fin1) reduces Sid4 affinity for its SPB anchor, Ppc
59 hymena thermophila contains 39 loci encoding NIMA-related kinases (NRKs), an extraordinarily large nu
61 phatase (PP1) from the spindle pole by Fin1 (NIMA) kinase ensures switch-like activation of Cyclin B-
66 ne H3 kinase, perhaps helping to explain how NIMA promotes chromatin condensation in A. nidulans and
69 -negative breast cancer cells, we identified NIMA (never in mitosis gene A)-related kinase 9 (NEK9) a
70 substrates of CDK5, casein kinases I and II, NIMA, calmodulin-dependent kinases, Erk1, and phosphoryl
71 To investigate this possibility, we imaged NIMA-green fluorescent protein (GFP) using four-dimensio
73 A/2 heart transplant, but were controlled in NIMA(d)-exposed mice by T(R) cells to varying degrees.
74 ing of a peptidyl-prolyl cis-trans isomerase NIMA-interacting 1 (PIN1) to p53-RS, but not the p53 for
77 tein (Pin2) that can bind the mitotic kinase NIMA and suppress its ability to induce mitotic catastro
81 nt kinases, polo kinases and Aurora kinases, NIMA-related kinases are emerging as critical regulators
82 Furthermore, when overexpressed, MLK3, like NIMA, localizes to the centrosomal region, induces profo
83 udy of endogenous MLK3 and report that, like NIMA, MLK3 phosphorylation and activity are enhanced dur
85 racterization of human Nek8, a new mammalian NIMA-related kinase, and its candidate substrate Bicd2.
86 of NEK7, a member of the family of mammalian NIMA-related kinases (NEK proteins), as an NLRP3-binding
88 rin beta3-binding protein (ITGB3BP), MAP3K8, NIMA-related kinase (NEK2), and SHC-transforming protein
91 nd Nek6 represent a novel cascade of mitotic NIMA family protein kinases whose combined function is i
94 Hec1 (highly expressed in cancer 1) or Nek2 (NIMA-related kinase 2) is often overexpressed in cancers
102 ctive CaMK also results in the appearance of NIMA kinase activity within 1 h of the germinating signa
104 maternal cells that promote conservation of NIMA and enforce cross-generational reproductive benefit
105 hat partial NPC disassembly under control of NIMA and Cdk1 in A. nidulans may represent a new mechani
106 kinases, and accumulation and degradation of NIMA, which all coordinately cycle multiple times withou
107 s that received a transplant of low doses of NIMA-like alloantigens develop vigorous memory cytotoxic
108 l, we conclude that exposure to low doses of NIMA-like alloantigens induces robust in vivo cytotoxic
110 n of p34cdc2 allows precocious expression of NIMA during S-phase arrest, and lack of BIME then allows
111 condensation, activation and inactivation of NIMA and p34(cdc2) kinases, and accumulation and degrada
116 suggest that early exposure to low levels of NIMA may lead to long-term immunologic priming of all ar
117 flects differences in the relative levels of NIMA-specific T regulatory (T(R)) versus T effector (T(E
122 ertebrate systems as a negative regulator of NIMA, a Ser/Thr protein kinase that regulates the G(2)/M
127 les expressing alloantigens with overlapping NIMA specificity, thereby averting fetal wastage trigger
128 e mutations in the Schizosaccharomyces pombe NIMA homologue, Fin1, blocked spindle formation at 37 de
132 h PINA is essential and positively regulates NIMA function, A. nidulans is most sensitive to a reduct
136 ain homology to NIMA, none of these resemble NIMA within its extensive noncatalytic region, a region
138 Here, we show that another APC/C substrate, NIMA-related kinase 2A (Nek2A), is also destroyed in pro
139 rnal cells and/or soluble MHC Ags suppresses NIMA-allospecific T cells of the offspring, predisposing
140 ecipitation assays, we demonstrate here that NIMA (never in mitosis gene A)-related kinase 2 (NEK2) i
142 histone H3 Ser-10 in vitro, suggesting that NIMA is a mitotic histone H3 kinase, perhaps helping to
147 tion between the two elements by MPF and the NIMA kinase Fin1 blocked PP1(Dis2) recruitment, thereby
148 leoporins SONA(GLE2) and SONB(NUP98) and the NIMA kinase interact and regulate nuclear accumulation o
155 -ATRIP, we found that a single member of the NIMA (never in mitosis A)-related kinase family, Nek1, i
158 d a mutation affecting NEK2, a member of the NIMA-like serine-threonine kinase family, in a patient w
159 Nek5 is a poorly characterized member of the NIMA-related kinase family, other members of which play
162 a bifurcation in a signaling cascade of the NIMA-related kinases (Neks) Nek6, Nek7, and Nek9 that is
164 ns encodes a protein that interacts with the NIMA mitotic protein kinase in a cell cycle-specific man
165 we identify a new pathway that acts through NIMA-related kinase 6 (Nek6) and Hsp72 to promote centro
169 ed that anti-K(b) thymocytes were exposed to NIMA and became activated during fetal life but were not
173 identified with catalytic domain homology to NIMA, none of these resemble NIMA within its extensive n
174 n amino-terminal catalytic domain related to NIMA, an Aspergillus kinase involved in the control of s
175 t, which was accompanied by sensitization to NIMA in some offspring, indicating a role of oral exposu
176 In addition, we observed that tolerance to NIMA K(b) was abrogated via depletion of CD4(+) but not
181 es during the cell cycle and associates with NIMA-related kinase 2 (NEK2), which is able to phosphory
182 lates mitosis presumably by interacting with NIMA and attenuating its mitosis-promoting activity.
183 is-trans isomerase (PPIase) interacting with NIMA-1 (Pin1) catalyzes the cis-trans isomerization of p
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