コーパス検索結果 (1語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
2 mixed population, as a minority give rise to mixed-lineage colonies while the majority of cells are t
3 tor-interacting protein kinase 3 (RIPK3) and mixed lineage domain-like protein (MLKL), targeting necr
7 e show that this analysis captured prevalent mixed-lineage intermediates that manifested concurrent e
11 on in the kinase activity of a pro-apoptotic mixed lineage kinase 3 (MLK3) in HER2-positive (HER2+) b
13 noted that the activity of the proapoptotic mixed lineage kinase 3 (MLK3) kinase was relatively high
15 possible cross-talk between beta-catenin and mixed lineage kinase 3 (MLK3), a MAPK kinase kinase memb
16 protein (merlin/schwannomin) associates with mixed lineage kinase 3 (MLK3), a mitogen-activated prote
19 e mutational analyses have revealed that the mixed lineage kinase 4 (MLK4) protein kinase is frequent
20 ce did not occur via apoptosis, but required Mixed Lineage Kinase Domain Like (MLKL) and activation o
21 ptor-interacting protein kinase 3 (RIPK3) or mixed lineage kinase domain like (MLKL), two core protei
22 acting serine-threonine kinase 3 (RIPK3) and mixed lineage kinase domain-like (MLKL) and generally ma
24 ion of the necroptotic effector pseudokinase Mixed Lineage Kinase Domain-Like (MLKL) by the upstream
26 with subsequent RIP3-dependent activation of mixed lineage kinase domain-like (MLKL) leading to necro
27 grammed form of necrosis, is executed by the mixed lineage kinase domain-like (MLKL) protein, which i
28 ontaining protein-3 (NLRP3) inflammasome and mixed lineage kinase domain-like (MLKL) protein-dependen
31 interacting protein kinase 3 (RIPK3) and the mixed lineage kinase domain-like (MLKL) pseudokinase.
32 r RIP3 activation and phosphorylation of the mixed lineage kinase domain-like (MLKL) pseudokinase.
33 ylates and activates the downstream effector mixed lineage kinase domain-like (MLKL) to induce necrop
35 effector implicated in MSU crystal killing, mixed lineage kinase domain-like (MLKL), did not prevent
38 e-3, eventually leading to the activation of mixed lineage kinase domain-like and plasma membrane per
41 kinase activity, but it remains dependent on mixed lineage kinase domain-like protein (MLKL) downstre
42 events in two forms of programmed necrosis [mixed lineage kinase domain-like protein (MLKL) in necro
43 is is not involved in APAP toxicity by using mixed lineage kinase domain-like protein (MLKL) knockout
44 her et al. demonstrate that the pseudokinase mixed lineage kinase domain-like protein (MLKL) particip
47 , we have demonstrated that the pseudokinase mixed lineage kinase domain-like protein (MLKL), which p
48 g virus infections, RIPK3 phosphorylates the mixed lineage kinase domain-like protein (MLKL), which t
53 es receptor-interacting proteins 1 and 3 and mixed lineage kinase domain-like protein necroptotic sig
54 ing serine/threonine-protein kinase 3)-MLKL (mixed lineage kinase domain-like protein)-dependent prog
55 RIPK1 or RIPK3, but not the RIPK3 substrate mixed lineage kinase domain-like protein, attenuated TNF
58 ce and detect increased RIPK1 expression and mixed lineage kinase domain-like pseudokinase (MLKL) act
59 wn to require the formation of a RIPK1-RIPK3-mixed lineage kinase domain-like pseudokinase (MLKL) sig
60 3 (RIPK3)-mediated pathways of apoptosis and mixed lineage kinase domain-like pseudokinase (MLKL)-dep
61 either IFN-alpha/beta receptor signaling or mixed lineage kinase domain-like pseudokinase (MLKL)-dep
62 rylation and plasma membrane localization of mixed lineage kinase domain-like pseudokinase (MLKL).
63 eceptor-interacting protein kinase-1), MLKL (mixed lineage kinase domain-like pseudokinase) protein,
65 ivated, RIP3 kinase targets the pseudokinase mixed lineage kinase domain-like to drive cell lysis.
66 nase 1) and RIPK3, and a pseudo-kinase MLKL (Mixed Lineage Kinase domain-Like) associated in a multi-
68 or of necroptosis, as well as phosphorylated mixed lineage kinase domain-like, an effector of necropt
70 eficiency, cells develop sensitivity to RIP3-mixed lineage kinase domain-like-mediated necroptosis as
73 ring Kinase (LZK/MAP3K13) is a member of the mixed lineage kinase family with high sequence identity
77 eceptor-interacting protein kinase 3 (RIPK3)-mixed lineage kinase-like (MLKL) signaling pathway in eo
78 eptor-interacting protein kinase-3 (RIPK3)-a mixed lineage kinase-like (MLKL) signaling pathway in ne
79 g aberrant caspase-8-dependent apoptosis and mixed lineage kinase-like (MLKL)-dependent necroptosis.
80 ic cells also expose PS after phosphorylated mixed lineage kinase-like (pMLKL) translocation to the m
81 rotein kinase 1 (RIP1), RIP3, phosphorylated mixed lineage kinase-like protein (MLKL), phosphoglycera
82 e the endogenous dp5, its induction requires mixed-lineage kinase (MLK) and c-Jun N-terminal kinase (
85 goal of this study was to determine whether mixed-lineage kinase 3 (MLK3) mediates the initial, ASK1
89 is study we investigated the contribution of Mixed-Lineage Kinase 4 (MLK4) to aggressive phenotype of
90 r-interacting protein kinase (RIPK) 1/3- and mixed-lineage kinase domain-like (MLKL)-dependent necrop
91 ng protein kinase 3 (RIP3) and its substrate mixed-lineage kinase domain-like protein (MLKL) are core
92 The effector of necroptosis, phosphorylated mixed-lineage kinase domain-like protein (MLKL), was det
93 protein kinase-3 (RIPK3) phosphorylation of mixed-lineage kinase domain-like protein (MLKL), which r
95 teracting protein kinase-3 and its substrate mixed-lineage kinase domain-like protein play a crucial
108 ent chromosomal translocations involving the mixed lineage leukaemia (MLL) gene initiate aggressive f
111 ted or myelodysplasia-related AML (n=12), or mixed-lineage leukaemia (n=14) were enrolled at eight ce
116 nic fusions of the Trithorax-related protein mixed lineage leukemia (MLL) can initiate aggressive leu
117 allosteric changes that transcription factor mixed lineage leukemia (MLL) causes to the interactions
119 The oncoprotein Ash2L is a component of the mixed lineage leukemia (MLL) family members 1-4, Setd1A,
122 ne 79 (K79) on histone H3 and is involved in Mixed Lineage Leukemia (MLL) fusion leukemogenesis; howe
123 unctions and in leukemogenesis driven by the mixed lineage leukemia (MLL) fusion oncogene MLL-AF9.
124 ough menin acts as an oncogenic cofactor for mixed lineage leukemia (MLL) fusion protein-mediated his
125 polymerase-associated factor complex (PAFc), mixed lineage leukemia (MLL) fusion proteins activate ge
126 unctions as a critical oncogenic cofactor of mixed lineage leukemia (MLL) fusion proteins in the deve
127 The interaction between menin and oncogenic mixed lineage leukemia (MLL) fusion proteins is required
130 ith chromosomal translocations involving the mixed lineage leukemia (MLL) gene are usually associated
132 first identified as a fusion partner of the mixed lineage leukemia (MLL) gene in acute myeloid leuke
137 Chromosomal translocations involving the Mixed Lineage Leukemia (MLL) gene produce chimeric prote
138 of infants with ALL, particularly those with mixed lineage leukemia (MLL) gene rearrangements, is onl
139 Chromosomal translocations targeting the mixed lineage leukemia (MLL) gene result in MLL fusion p
141 kemia (B-ALL) harboring rearrangement of the mixed lineage leukemia (MLL) gene with CD19 CAR-T cells.
142 lso interacts with translocation partners of Mixed Lineage Leukemia (MLL) gene, which is commonly tra
143 receptors (ERs) and ER coregulators such as mixed lineage leukemia (MLL) histone methylases (MLL2 an
144 ights into the role of the Trithorax protein mixed lineage leukemia (MLL) in maintaining cancer stem
148 plex (DotCom), which includes several of the mixed lineage leukemia (MLL) partners in leukemia such a
149 -protein interaction (PPI) between menin and mixed lineage leukemia (MLL) plays a critical role in ac
151 e Men1 gene product menin interacts with the mixed lineage leukemia (MLL) protein, a histone H3 lysin
153 WD repeat domain 5 (WDR5) and block the WDR5-mixed lineage leukemia (MLL) protein-protein interaction
154 ENL, and AF9, is recruited by HIV-1 Tat and mixed lineage leukemia (MLL) proteins to activate the ex
155 Aven stimulates the mRNA translation of the mixed lineage leukemia (MLL) proto-oncogene in an argini
157 third plant homeodomain (PHD3) finger of the mixed lineage leukemia (MLL) proto-oncoprotein and a pol
159 sents the most common leukemogenic fusion of mixed lineage leukemia (MLL) to a cytoplasmic partner pr
160 regulator in the expression of HOX genes in mixed lineage leukemia (MLL)-based hematological maligna
161 d the miRNAs are aberrantly overexpressed in mixed lineage leukemia (MLL)-rearranged acute leukemias.
162 regulator CDK6 as a promising new target in mixed lineage leukemia (MLL)-rearranged acute myeloid le
163 hylation (H3K27me3/2) and inhibits growth of mixed lineage leukemia (MLL)-rearranged leukemia cells.
164 rates for pediatric patients suffering from mixed lineage leukemia (MLL)-rearranged leukemia remain
165 ranslocations, that approximately 43% of all mixed lineage leukemia (MLL)-rearranged leukemias are EV
168 , we identify the histone-remodelling enzyme mixed lineage leukemia (MLL)3 as a clock-controlled fact
172 F23, and NUP98-TOP1 physically interact with mixed lineage leukemia 1 (MLL1) and the non-specific let
176 rotein-protein interaction between menin and mixed lineage leukemia 1 (MLL1) plays a critical role in
178 Menin is an essential oncogenic cofactor for mixed lineage leukemia 1 (MLL1)-mediated leukemogenesis
181 of acute leukemias arise from fusion of the mixed lineage leukemia 1 protein (MLL) N terminus to a v
182 oregulators such as histone methylases MLL1 (mixed lineage leukemia 1) and MLL3 and CREB-binding prot
184 gnificant overlap in genes regulated by MOZ, mixed lineage leukemia 1, and mixed lineage leukemia 1 c
185 Lpt) is the N-terminal homolog of mammalian Mixed Lineage Leukemia 2 (MLL2/ALR), a core component of
186 transferases such as enhancer of zeste 2 and mixed lineage leukemia 2, histone demethylases including
187 ximately 50% reduction in gene dosage of the mixed lineage leukemia 3 (MLL3) gene, located on 7q36.1,
191 ias that harbor translocations involving the mixed lineage leukemia gene (MLL) possess unique biologi
194 5 (WDR5) is a common component of mammalian mixed lineage leukemia methyltransferase family members
195 h an aberrant histone methyltransferase, the mixed lineage leukemia partial tandem duplication (MLL-P
196 ct the WD repeat-containing protein 5 (WDR5)-mixed lineage leukemia protein 1 (MLL1) complex across t
201 DPY-30), a complex that is part of the MLL1 (mixed lineage leukemia protein-1) core complex but that
202 y, although PTIP and PA1 associate with MLL (mixed lineage leukemia) complexes and participate in tra
203 ves as a critical oncogenic cofactor of MLL (mixed lineage leukemia) fusion proteins in acute leukemi
208 Translocations and amplifications of the mixed lineage leukemia-1 (MLL1) gene are associated with
209 3 (IGF2BP3) is specifically overexpressed in mixed lineage leukemia-rearranged (MLL-rearranged) B-acu
210 nd its receptor (IL-17RB) in human and mouse mixed lineage leukemia-rearranged AML cells, which were
214 impaired reconstitution of stem cell-derived mixed-lineage leukemia (MLL) AML, which represents an ag
215 isordered transcription factors, such as the mixed-lineage leukemia (MLL) and c-Myb peptides, at isol
216 more, we observed that SALL4 interacted with mixed-lineage leukemia (MLL) and co-occupied the HOXA9 p
217 t multiple MLL-fusion proteins implicated in mixed-lineage leukemia (MLL) associate with AFF4, ELLs,
219 his targeting strategy does not affect other mixed-lineage leukemia (MLL) family histone methyltransf
224 ary acute myelogenous leukemia involving the mixed-lineage leukemia (MLL) gene (11q23) translocations
225 hromosomal translocation that juxtaposes the mixed-lineage leukemia (MLL) gene and the AF4 gene.
226 OF REVIEW: Leukemia carrying mutation of the mixed-lineage leukemia (MLL) gene is particularly refrac
227 Chromosomal rearrangements involving the mixed-lineage leukemia (MLL) gene occur in primary and t
232 ost cell factor 1 (HCF1), a component of the mixed-lineage leukemia (MLL) histone methyltransferase c
235 t mutations such as FLT3 internal-tandem and mixed-lineage leukemia (MLL) partial-tandem duplications
236 Histone lysine methylation, mediated by mixed-lineage leukemia (MLL) proteins, is now known to b
237 determined that MSI2 directly maintains the mixed-lineage leukemia (MLL) self-renewal program by int
239 gements involving the H3K4 methyltransferase mixed-lineage leukemia (MLL) trigger aberrant gene expre
243 t to chromatin as an effective treatment for mixed-lineage leukemia (MLL)-fusion leukemia' by Dawson
247 down (KD) of a writer, the methyltransferase mixed-lineage leukemia 1 (Mll1) (n = 26), and an eraser,
248 tivators CREB-binding protein (CBP)/p300 and mixed-lineage leukemia 1 (MLL1) critically regulate circ
253 f the H3K4-specific methyltransferase, Kmt2a/Mixed-lineage leukemia 1 (Mll1), in mouse postnatal fore
254 expression of the histone methyltransferase, mixed-lineage leukemia 1 (MLL1), which specifically trim
255 onal identity in the murine brain requires a mixed-lineage leukemia 1 (Mll1)-dependent epigenetic mem
257 istone-methyltransferase myeloid/lymphoid or mixed-lineage leukemia 2 (mll2/kmt2b) gene in adult fore
258 s identified were all of the subunits of the mixed-lineage leukemia 3 (Mll3) and 4 (Mll4) complexes,
259 The histone H3-lysine-4 methyltransferase mixed-lineage leukemia 3 (MLL3) and its closest homolog,
260 Although PTIP is a unique component of the mixed-lineage leukemia 3 (MLL3)/MLL4 chromatin-modifying
261 deficient in the PTIP component of the MLL3 (mixed-lineage leukemia 3)-MLL4 complex display impaired
266 ragile sites, and breakpoints, including the mixed-lineage leukemia breakpoint cluster region (MLL BC
267 Chromosome rearrangements involving the mixed-lineage leukemia gene (MLL) create MLL-fusion prot
268 adults as a result of rearrangements to the mixed-lineage leukemia gene (MLL) located on chromosome
269 atient-derived xenografts (PDX) of pediatric mixed-lineage leukemia gene (MLL)-rearranged ALL were es
271 ize the biology and optimal therapy of acute mixed-lineage leukemia in children, we reviewed the path
273 its promoter, and p300, myeloid/lymphoid or mixed-lineage leukemia protein 4 (MLL4), and RNA polymer
274 ith the transcriptional activation domain of mixed-lineage leukemia protein leads to an enhancement o
276 in leukemogenesis driven by a subset of MLL (mixed-lineage leukemia) fusion proteins raises the possi
277 to as MLL to denote the gene associated with mixed-lineage leukemia) generate MLL fusion proteins tha
278 horax family member MLL (myeloid/lymphoid or mixed-lineage leukemia) is presumed to activate Hox expr
282 eptor NKp44 (NKp44L), a novel isoform of the mixed-lineage leukemia-5 protein, as a cellular ligand f
283 effectively treats aggressive AML, including mixed-lineage leukemia-driven AML, and outperforms stand
287 DM2 activates chk1 phosphorylation, elevates mixed lineage lymphoma histone methyl transferase levels
289 secreted signalling molecule Wnt1 generates mixed-lineage mammary tumours composed of basal and lumi
291 well as bipotential intermediates, manifest mixed-lineage patterns of gene expression at a single-ce
294 tification of transcriptomes from individual mixed lineage progenitor cells in the chick as these cel