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1 roliferation in Lin(-) cells and led to more mixed lineage colonies from transduced KI BM cells.
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
4                        Here we show that the mixed-lineage dual leucine zipper kinase (DLK) is an ess
5                      MLK4 is a member of the mixed-lineage family of kinases that regulate the JNK, p
6 ferentiated prematurely, and often adopted a mixed lineage fate.
7 e show that this analysis captured prevalent mixed-lineage intermediates that manifested concurrent e
8                     This analysis identified mixed lineage kinase 3 (MLK3) as a putative NS5A interac
9                                              Mixed lineage kinase 3 (MLK3) deficiency reduces macroph
10                                              Mixed lineage kinase 3 (MLK3) functions in migration and
11 on in the kinase activity of a pro-apoptotic mixed lineage kinase 3 (MLK3) in HER2-positive (HER2+) b
12                                Inhibition of mixed lineage kinase 3 (MLK3) is a potential strategy fo
13  noted that the activity of the proapoptotic mixed lineage kinase 3 (MLK3) kinase was relatively high
14                                              Mixed lineage kinase 3 (MLK3), a MAP3K member has been e
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
17                                              Mixed lineage kinase 3 (MLK3), also known as MAP3K11, wa
18                         Here, we report that mixed lineage kinase 4 (MLK4) is overexpressed in MES bu
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
23                 Characterization of infected mixed lineage kinase domain-like (MLKL) and tumor necros
24 ion of the necroptotic effector pseudokinase Mixed Lineage Kinase Domain-Like (MLKL) by the upstream
25                             The pseudokinase Mixed Lineage Kinase Domain-Like (MLKL) is an essential
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
29              Total levels of RIP1, RIP3, and mixed lineage kinase domain-like (MLKL) proteins were in
30 tor-interacting protein kinase-3 (RIPK3) and mixed lineage kinase domain-like (MLKL) proteins.
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
34                                              Mixed Lineage Kinase domain-Like (MLKL), a key player in
35  effector implicated in MSU crystal killing, mixed lineage kinase domain-like (MLKL), did not prevent
36  protein kinase 3 (RIPK3) and its substrate, mixed lineage kinase domain-like (MLKL).
37 nd its downstream effector, the pseudokinase mixed lineage kinase domain-like (MLKL).
38 e-3, eventually leading to the activation of mixed lineage kinase domain-like and plasma membrane per
39                   Blocking necroptosis using mixed lineage kinase domain-like deficient mice or necro
40          HFD did not increase phosphorylated mixed lineage kinase domain-like in RIP3(-/-) mice.
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
45                      The expression level of mixed lineage kinase domain-like protein (MLKL), a key d
46                  This approach revealed that mixed lineage kinase domain-like protein (MLKL), a key t
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
49 nery in the CNS, including RIPK1, RIPK3, and mixed lineage kinase domain-like protein (MLKL).
50 eracting protein kinase 1 (RIPK1), RIPK3 and mixed lineage kinase domain-like protein (MLKL).
51                                          The mixed lineage kinase domain-like protein MLKL is a funct
52 RIP1 and RIP3 and their interaction with the mixed lineage kinase domain-like protein MLKL.
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
56 ptosis, assessed by levels of phosphorylated mixed lineage kinase domain-like protein.
57 lving receptor-interacting protein 1 and the mixed lineage kinase domain-like protein.
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,
64 ous scaffolds that lead to the activation of mixed lineage kinase domain-like pseudokinase.
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-
67 croptosis, and the downstream effector MLKL (Mixed Lineage Kinase Domain-Like).
68 or of necroptosis, as well as phosphorylated mixed lineage kinase domain-like, an effector of necropt
69         Here we report the identification of mixed lineage kinase domain-like, MLKL, as a key RIP3 do
70 eficiency, cells develop sensitivity to RIP3-mixed lineage kinase domain-like-mediated necroptosis as
71 , which eventually lead to the activation of mixed lineage kinase domain-like.
72              In this paper, we show that the mixed lineage kinase dual leucine zipper kinase (DLK) se
73 ring Kinase (LZK/MAP3K13) is a member of the mixed lineage kinase family with high sequence identity
74                                          The mixed lineage kinase MLK3 plays a crucial role in compro
75 ceptor-interacting protein kinase-3 (RIPK3), mixed lineage kinase-like (MLKL) and NADPH oxidase.
76                            The activation of mixed lineage kinase-like (MLKL) by receptor-interacting
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 (
83                                          The mixed-lineage kinase 3 (MLK-3) inhibitor URMC-099 provid
84                                              Mixed-lineage kinase 3 (MLK3) activates mitogen-activate
85  goal of this study was to determine whether mixed-lineage kinase 3 (MLK3) mediates the initial, ASK1
86                     Here we demonstrate that mixed-lineage kinase 3 (MLK3), a MAP3K family member, ph
87 in-penetrant inhibitor with activity against mixed-lineage kinase 3 (MLK3), named URMC-099.
88 ts initiated by FGD1 that involves the MAP3K mixed-lineage kinase 3 (MLK3).
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
94 kinases RIPK1/RIPK3 and the effector protein mixed-lineage kinase domain-like protein (MLKL).
95 teracting protein kinase-3 and its substrate mixed-lineage kinase domain-like protein play a crucial
96                                              Mixed-lineage kinase-3 (MLK3) is a mammalian mitogen-act
97 l death dependent on RIPK-1, RIPK-3, and the mixed-lineage kinase-like protein (MLKL).
98                  CD40L induced activation of mixed-lineage-kinase-3 and JNK, leading to the subsequen
99                 Here we demonstrate that the mixed lineage kinases (MLK1-4) are MEK kinases that reac
100                                              Mixed lineage kinases (MLKs) have been implicated in cyt
101 tivation of the MAPK-kinase-kinases (MAP3Ks) mixed lineage kinases (MLKs)-2 and -3.
102             One is CEP-1347, an inhibitor of mixed lineage kinases that elicits neuroprotective and a
103               Similar to the closely related mixed-lineage kinases, LRRK2 can undergo autophosphoryla
104  kinase domain based on sequence homology to mixed-lineage kinases.
105                                The conserved Mixed Lineage Leukaemia (MLL) complex deposits activatin
106        This modification is catalyzed by the mixed lineage leukaemia (MLL) family of histone methyltr
107                                          The mixed lineage leukaemia (MLL) family of proteins (includ
108 ent chromosomal translocations involving the mixed lineage leukaemia (MLL) gene initiate aggressive f
109  and MEIS1 have essential oncogenic roles in mixed lineage leukaemia (MLL)-rearranged leukaemia.
110                    Menin also interacts with mixed lineage leukaemia protein 1 (MLL1), a histone H3 l
111 ted or myelodysplasia-related AML (n=12), or mixed-lineage leukaemia (n=14) were enrolled at eight ce
112      Here we show that the trxG member Mll1 (mixed-lineage leukaemia 1) is required for neurogenesis
113  216 patients with AML, excluding those with mixed-lineage leukaemia.
114                                              Mixed lineage leukemia (MLL) and its metazoan Trithorax
115                    c-Myb, GATA-3, Menin, and mixed lineage leukemia (MLL) bound to CGRE in human prim
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
118                                              Mixed lineage leukemia (MLL) family histone methyltransf
119  The oncoprotein Ash2L is a component of the mixed lineage leukemia (MLL) family members 1-4, Setd1A,
120                    Although misregulation of mixed lineage leukemia (MLL) family proteins has been as
121                                              Mixed lineage leukemia (MLL) fusion genes arise from chr
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
128                                              Mixed lineage leukemia (MLL) fusion-driven acute leukemi
129            Chromosomal translocations of the mixed lineage leukemia (MLL) gene are a common cause of
130 ith chromosomal translocations involving the mixed lineage leukemia (MLL) gene are usually associated
131      Chromosome translocations involving the mixed lineage leukemia (MLL) gene fuse it in frame with
132  first identified as a fusion partner of the mixed lineage leukemia (MLL) gene in acute myeloid leuke
133                                          The mixed lineage leukemia (MLL) gene is also frequently inv
134                        Translocations of the mixed lineage leukemia (MLL) gene occur in 60% to 80% of
135            Chromosomal rearrangements of the mixed lineage leukemia (MLL) gene occur in ~10% of B-cel
136                                          The mixed lineage leukemia (MLL) gene plays a critical role
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
140  to be a drug target for acute leukemia with mixed lineage leukemia (MLL) gene translocations.
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
145                                              Mixed lineage leukemia (MLL) is a key epigenetic regulat
146                The histone methyltransferase Mixed Lineage Leukemia (MLL) is essential to maintain he
147 ome translocations, most often involving the mixed lineage leukemia (MLL) locus at 11q23.
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
150                                          The mixed lineage leukemia (MLL) protein and its Drosophila
151 e Men1 gene product menin interacts with the mixed lineage leukemia (MLL) protein, a histone H3 lysin
152                      Inhibition of the menin-mixed lineage leukemia (MLL) protein-protein interaction
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
156                                          The mixed lineage leukemia (MLL) proto-oncogene is a recurre
157 third plant homeodomain (PHD3) finger of the mixed lineage leukemia (MLL) proto-oncoprotein and a pol
158                                              Mixed lineage leukemia (MLL) represents a genetically di
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
166 the c-Myb/GATA-3 complex contained Menin and mixed lineage leukemia (MLL).
167  partner of both de novo and therapy-induced mixed lineage leukemia (MLL).
168 , we identify the histone-remodelling enzyme mixed lineage leukemia (MLL)3 as a clock-controlled fact
169 gulated in the pathophysiology of rearranged mixed lineage leukemia (MLL-r).
170                    They demonstrate that the mixed lineage leukemia (MLL1) gene acts independently fr
171                                              Mixed Lineage Leukemia (MLL1) translocations encode fusi
172 F23, and NUP98-TOP1 physically interact with mixed lineage leukemia 1 (MLL1) and the non-specific let
173            Acute myeloid leukemia (AML) with mixed lineage leukemia 1 (MLL1) gene rearrangement is ch
174                                              Mixed lineage leukemia 1 (MLL1) is a histone H3 lysine 4
175                     The epigenetic activator Mixed lineage leukemia 1 (MLL1) is paramount for embryon
176 rotein-protein interaction between menin and mixed lineage leukemia 1 (MLL1) plays a critical role in
177                             We show that the mixed lineage leukemia 1 (MLL1) protein, a histone methy
178 Menin is an essential oncogenic cofactor for mixed lineage leukemia 1 (MLL1)-mediated leukemogenesis
179 ulated by MOZ, mixed lineage leukemia 1, and mixed lineage leukemia 1 cofactor menin.
180 leukemia cell lines harboring the rearranged mixed lineage leukemia 1 gene.
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
183                                    The MLL1 (mixed lineage leukemia 1) protein, which is often disrup
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,
188                                    The MLL3 (mixed lineage leukemia 3) protein is a member of the hum
189                         H3.3 is repressed by mixed lineage leukemia 5 (MLL5) in self-renewing GBM cel
190                                Taspase1, the mixed lineage leukemia and TFIIAalpha-beta cleaving prot
191 ias that harbor translocations involving the mixed lineage leukemia gene (MLL) possess unique biologi
192                                              Mixed lineage leukemia gene (MLL) rearrangements (MLL-r)
193         Chromosomal translocations affecting mixed lineage leukemia gene (MLL) result in acute leukem
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
197                                          The mixed lineage leukemia protein MLL1 contains four highly
198                                          The mixed lineage leukemia protein-1 (MLL1) belongs to the S
199                                              Mixed lineage leukemia protein-1 (MLL1) is a member of t
200                                          The mixed lineage leukemia protein-1 (MLL1) is a member of 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
204 e a drug target for acute leukemia with MLL (mixed lineage leukemia) gene translocations.
205                            AMLs bearing MLL (mixed lineage leukemia) rearrangements are associated wi
206                                          The mixed lineage leukemia-1 (MLL1) core complex predominant
207                                          The mixed lineage leukemia-1 (MLL1) enzyme is a histone H3 l
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
211                       A notable exception is mixed lineage leukemia-rearranged infant ALL, where vene
212 ole and is a potential therapeutic target in mixed lineage leukemia.
213 sociated with infant acute lymphoblastic and mixed lineage leukemia.
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,
218 g to a single surface of the KIX domain, the mixed-lineage leukemia (MLL) binding surface.
219 his targeting strategy does not affect other mixed-lineage leukemia (MLL) family histone methyltransf
220                   A subgroup of leukemogenic mixed-lineage leukemia (MLL) fusion proteins (MFPs) incl
221                        LEDGF associates with mixed-lineage leukemia (MLL) fusion proteins and menin a
222                                              Mixed-lineage leukemia (MLL) fusion proteins are potent
223                                              Mixed-lineage leukemia (MLL) fusions are potent oncogene
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
228                                          The mixed-lineage leukemia (MLL) gene often fuses with ENL a
229            Chromosomal translocations of the mixed-lineage leukemia (MLL) gene with various partner g
230 t B-ALL is chromosomal rearrangements of the mixed-lineage leukemia (MLL) gene.
231                                          The mixed-lineage leukemia (MLL) H3K4 methyltransferase prot
232 ost cell factor 1 (HCF1), a component of the mixed-lineage leukemia (MLL) histone methyltransferase c
233                               It is fused to mixed-lineage leukemia (MLL) in leukemia, and missense m
234                                              Mixed-lineage leukemia (MLL) is a proto-oncogene frequen
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
238                   The t(4;11)(q21;q23) fuses mixed-lineage leukemia (MLL) to AF4, the most common MLL
239 gements involving the H3K4 methyltransferase mixed-lineage leukemia (MLL) trigger aberrant gene expre
240                                              Mixed-lineage leukemia (MLL), an epigenetic regulator, p
241                                              Mixed-lineage leukemia (MLL)-AF4 fusion arises prenatall
242                          Myeloid/lymphoid or mixed-lineage leukemia (MLL)-family genes encode histone
243 t to chromatin as an effective treatment for mixed-lineage leukemia (MLL)-fusion leukemia' by Dawson
244 k the progression of certain cancers such as mixed-lineage leukemia (MLL)-rearranged leukemias.
245              In contrast, leukemia driven by mixed-lineage leukemia (MLL, encoded by KMT2A) fusions w
246                                              Mixed-lineage leukemia (MLL; also known as myeloid/lymph
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
249            Chromosomal translocations of the Mixed-lineage leukemia 1 (MLL1) gene generate MLL chimer
250            Further, using a myeloid-specific mixed-lineage leukemia 1 (MLL1) knockout (Mll1(f/f)Lyz2(
251                           Here, we show that mixed-lineage leukemia 1 (MLL1) protein is a key determi
252           Ash1l cooperated functionally with mixed-lineage leukemia 1 (Mll1), as combined loss of Ash
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
256 ultiprotein complex essential for activating mixed-lineage leukemia 1 (MLL1).
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
262 umonji C family of proteins, associates with mixed-lineage leukemia 3/4 complexes.
263                                              Mixed-lineage leukemia 4 (MLL4/KMT2D) is a major enhance
264                                              Mixed-lineage leukemia 4 (MLL4; also called MLL2 and ALR
265                                    The human mixed-lineage leukemia 5 (MLL5) protein mediates hematop
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
270                MEN1 and its coactivator, the mixed-lineage leukemia histone methyltransferase, are re
271 ize the biology and optimal therapy of acute mixed-lineage leukemia in children, we reviewed the path
272                 Here we demonstrate that the mixed-lineage leukemia protein (MLL) complex, a well-kno
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
275                                          The mixed-lineage leukemia protein MLL1 is a transcriptional
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
279                                     The MLL (mixed-lineage leukemia) proto-oncogene encodes a histone
280                                              Mixed-lineage leukemia-1 (MLL1) has been shown to direct
281                The histone methyltransferase mixed-lineage leukemia-4 (MLL4) is a transcriptional coa
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
284 ing response to therapy, of 35 patients with mixed-lineage leukemia.
285                                              Mixed lineage leukemias (MLLs) are human histone H3 lysi
286 key roles of ERs in the recruitment of these mixed lineage leukemias into the HOXC6 promoter.
287 DM2 activates chk1 phosphorylation, elevates mixed lineage lymphoma histone methyl transferase levels
288 volved in T-cell signaling, and give rise to mixed-lineage lymphoma in vivo.
289  secreted signalling molecule Wnt1 generates mixed-lineage mammary tumours composed of basal and lumi
290 ts exhibited varied morphology, suggesting a mixed-lineage origin of tumor-initiating cells.
291  well as bipotential intermediates, manifest mixed-lineage patterns of gene expression at a single-ce
292 ete differentiation but often also display a mixed lineage phenotype.
293                     Moreover, we uncovered a mixed-lineage population of cells that may reflect molec
294 tification of transcriptomes from individual mixed lineage progenitor cells in the chick as these cel
295             We report that disruption of the mixed-lineage protein kinase (MLK) - cJun NH2-terminal k
296 e Rac/Cdc42 interaction site (CRIB motif) on mixed-lineage protein kinases (MLKs).
297                              We propose that mixed-lineage states are obligatory during cell-fate spe
298                                         Such mixed-lineage states may reflect the molecular priming o
299               The proposed method is a novel mixed lineage tree/sequence based method to detect withi
300 ting cells (TICs), which proliferate to form mixed-lineage tumors.

 
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