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1                                              MERTK also regulated T cell arrest in melanoma tumors.
2                                              MERTK and AXL are members of the TAM (TYRO3, AXL, MERTK)
3                                              MERTK expression (mean fluorescence intensity) correlate
4                                              MERTK expression and activity in mononuclear phagocytes
5                                              MERTK expression and lipid peroxidation in synaptoneuros
6                                              MERTK expression was highest in metastatic melanomas, fo
7                                              MERTK has an essential role in phagocytosis, one of the
8                                              MERTK inhibition via shRNA reduced MERTK-mediated downst
9                                              MERTK inhibitors restore production of inflammatory cyto
10                                              MERTK is expressed in macrophages.
11                                              MERTK missense variants identified by single-strand conf
12                                              MERTK, expressed in retinal pigment epithelia, is a rece
13                                              MERTK-dependent regulation led to reduced T cell activat
14 nt study, we evaluated whether delivery of a MERTK transgene using a tyrosine-mutant AAV8 capsid coul
15 enotype, migration, and functional analyses, MERTK-expressing monocytes migrate across the endothelia
16 hrough the receptor tyrosine kinases AXL and MERTK led to the production of interleukin-10 (IL-10) by
17 e, loss of receptor tyrosine kinases AXL and MERTK reduced efferocytosis of eryptotic erythrocytes an
18    The TAM receptor family of TYRO3, AXL and MERTK regulates tissue and immune homeostasis.
19                      The TAM (TYRO3, AXL and MERTK) family receptor tyrosine kinases (RTKs) are poten
20 ts selectively targeting the TYRO3, AXL, and MERTK (TAM) family tyrosine kinases.
21          Stimulation of TAM (TYRO3, AXL, and MERTK) receptor tyrosine kinases promotes tumor progress
22  a ligand for TAM receptors (TYRO3, AXL, and MERTK).
23 AM receptor tyrosine kinases-TYRO3, AXL, and MERTK-as an emerging class of innate immune checkpoints
24 ptor tyrosine kinases (RTKs)-TYRO3, AXL, and MERTK-together with their cognate agonists GAS6 and PROS
25 MHCIIlow), correlating with higher CD206 and MERTK expression.
26 stasis with cell-type specific functions and MERTK blockade represents an osteoanabolic therapy with
27 st listed, the early-onset RP genes LRAT and MERTK were added).
28 flammatory MERTK(low)CD48(+) macrophages and MERTK + LYVE1 + MRC1+ macrophages enriched for negative
29 eloping and adult brain, identify MEGF10 and MERTK as critical proteins in the synapse remodelling un
30 synapse elimination, requires the MEGF10 and MERTK phagocytic pathways, and is strongly dependent on
31  coordinate targeting of IGFBP2, PITPNC1 and MERTK--novel pro-angiogenic genes and biomarkers of huma
32                               Dual TYRO3 and MERTK inhibition may be advantageous for treatment of di
33                                    TYRO3 and MERTK inhibitory activities were confirmed by NanoBRET a
34 ognate ligands GAS6 and PROS1 (for TYRO3 and MERTK) are secreted by host immune cells, an interaction
35 ant protein expression was assayed with anti-MERTK and anti-phosphotyrosine antibodies.
36 nt in adjuvant renal cell carcinoma, such as MERTK and TDO2.
37 AS6) is a soluble agonist of the TYRO3, AXL, MERTK (TAM) family of receptor tyrosine kinases identifi
38                         The TAM (TYRO3, AXL, MERTK) family of receptor tyrosine kinases has roles in
39  and AXL are members of the TAM (TYRO3, AXL, MERTK) family of receptor tyrosine kinases that are aber
40 therapeutic agents activate TAM (TYRO3, AXL, MERTK) kinases to augment Akt and ERK signaling facilita
41 specific 6 (GAS6), a ligand of the TYRO3-AXL-MERTK (TAM) receptor family, in regulating oral mucosal
42 ytosis of eryptotic erythrocytes through AXL/MERTK as a critical mechanism modulating macrophage phen
43  overexpression/activation of TAM (TYRO3/AXL/MERTK) receptors (TAMs) and overexpression/release of li
44 re also confirmed by NanoBRET and cell-based MERTK and AXL phosphorylation assays.
45 in-mediated cell-matrix interactions between MERTK+ macrophages and pro-resolving DKK3+ and POSTN+ fi
46 d 43 had low-nanomolar activity against both MERTK and AXL and good selectivity over TYRO3 and FLT3.
47 istance; this mechanism of Akt regulation by MERTK/SAV1 provides yet another complexity in an extensi
48                            In contrast, C844 MERTK was expressed at low levels and did not stimulate
49                 The loss of function of C844 MERTK is probably due to decreased protein stability.
50  In addition, the relative stability of C844 MERTK was significantly less than wt in assays of protei
51 expression cassette between shoulder capsule MERTK+ macrophages and a respective population enriched
52                           In a model of CAV, MERTK deficiency accelerated allograft rejection and inc
53 d, treatment with MRX-2843, a first-in-class MERTK kinase inhibitor, resensitized GAS6-treated NSCLC
54 iation between rare functionally deleterious MERTK variants and Parkinson's disease in one of the coh
55 d native proteins, western analysis detected MERTK interactions with GRB2, PIK3R1 (P85alpha), VAV3, a
56 romote allograft injury, in part, by driving MERTK proteolysis.
57                                         Dual MERTK and AXL inhibition could provide antitumor action
58 o discover a novel class of macrocyclic dual MERTK/AXL inhibitors.
59  manner with MRX-2843, a small molecule dual MERTK and FLT3 kinase inhibitor currently in clinical te
60 he binding of its ligand GAS6 to endothelial MERTK receptors.
61                        This work establishes MERTK as a therapeutic target in melanoma and provides a
62 atory monocytes and macrophages that express MERTK and suppress the innate immune response to microbe
63  of monocytes and macrophages that expressed MERTK was greatly increased in the circulation, livers,
64 scribed to be a direct consequence of failed MERTK-mediated phagocytosis of photoreceptor outer segme
65 group compared to control groups (except for MERTK, which was significantly different only for stage
66 ells treated with OSI, suggesting a role for MERTK activation in OSI resistance.
67                                 Furthermore, MERTK and/or its ligands were dramatically upregulated i
68 also identify the IGFBP2/IGF1/IGF1R and GAS6/MERTK signalling pathways as regulators of cancer-mediat
69 ere linked to the functionally related genes MERTK and TULP1, which encode factors involved in phagoc
70      An AAV8 Y733F vector expressing a human MERTK cDNA driven by a RPE-selective promoter was admini
71 kinase, perhaps including mutations in human MERTK.
72 dy was to evaluate the interactions of human MERTK with SH2-domain proteins present in the RPE.
73                          These data identify MERTK as a driver of bypass signaling in treatment-naive
74              Together, our findings identify MERTK as a critical regulator of macrophage efferocytosi
75 is of human foetal shoulder tissues identify MERTK + LYVE1 + MRC1+ macrophages and DKK3+ and POSTN+ f
76 Other pathogenic variants were identified in MERTK (c.2194C > T, p.Arg732Ter), RHO (c.448G > A, p.Glu
77              Despite a small upregulation in MERTK mRNA expression in nigral microglia from Parkinson
78 entosa associated with biallelic variants in MERTK.
79 , and not CD4+ or naive CD8+ T cells, induce MERTK cleavage on macrophages, leading to reduced effero
80 -cell analysis, we identify pro-inflammatory MERTK(low)CD48(+) macrophages and MERTK + LYVE1 + MRC1+
81                             In human islets, MERTK-expressing cells were increased in remaining insul
82        Of note, the receptor tyrosine kinase MERTK and the pyrimidine kinase UCK1 were both found to
83                 The receptor tyrosine kinase MERTK plays an essential role in the phagocytic uptake o
84 ving the MER proto-oncogene tyrosine kinase (MERTK) and discovered a clinical occurrence and cell lin
85  phagocytic receptors c-Mer tyrosine kinase (MERTK) and triggering receptor expressed on myeloid cell
86        C-MER proto-oncogene tyrosine kinase (MERTK) is a receptor tyrosine kinase with oncogenic prop
87                MER receptor tyrosine kinase (MERTK) is expressed by monocytes and macrophages and con
88 helial cells; whereas c-Mer tyrosine kinase (MERTK) receptor cleaved from metastatic cells promotes e
89 naling toward Rac1 and focal adhesion kinase/MERTK, and with MERTK directly, additionally inhibiting
90 gical inhibition of MerTK and siRNA-mediated MERTK knockdown both caused a decreased rate of alpha-sy
91    Strikingly, all three RAF family members, MERTK, and NTRK2 drove the formation of bone and viscera
92  proto-oncogene tyrosine-protein kinase MER (MERTK), a key anti-inflammatory receptor on macrophages,
93  Proto-oncogene tyrosine-protein kinase MER (MERTK), and growth arrest-specific protein 6 (GAS6) were
94 s6541998 (OR = 1.53, 95% CI = 1.37-1.74 near MERTK), rs10184573 (OR = 1.43, 95% CI = 1.26-1.61 near A
95                   LAB mice with noncleavable MERTK in WT BM showed improvements in necrotic core and
96 ment of melanoma cells with UNC1062, a novel MERTK-selective small-molecule tyrosine kinase inhibitor
97 ntification and functional analysis of novel MERTK mutations to provide information regarding whether
98 sine kinase inhibitor, reduced activation of MERTK-mediated downstream signaling, induced apoptosis i
99 hies was assessed through burden analysis of MERTK variants and analysis of MerTK expression in patie
100 ast biology: Osteoblast-targeted deletion of MERTK promotes increased bone mass in healthy mice and m
101 a rationale for the continued development of MERTK-targeted therapies.
102 sults, together with the recent discovery of MERTK mutations in individuals with retinitis pigmentosa
103                                Expression of MERTK reduced the response of cultured monocytes to lipo
104 ed with down-regulation of the expression of MERTK.
105  cultured RPE by inducing gene expression of MERTK/AXL/TYRO3.
106 r the first time, we reveal the formation of MERTK/TYRO3 heterocomplexes in meningioma and schwannoma
107                                Inhibition of MERTK kinase activity blocked PROS1-mediated suppression
108 ysaccharide, with or without an inhibitor of MERTK (UNC569).
109             Functionally, the interaction of MERTK with its ligand PROS1 negatively regulates osteobl
110  tumour types, as well as interdependency of MERTK and AXL expression in meningioma.
111                 We utilized our knowledge of MERTK inhibitors and a structure-based drug design appro
112 also decreased the mRNA and protein level of MERTK, as well as the ox-POS phagocytosis.
113  microscopy were used to determine levels of MERTK in bone marrow, liver, and lymph node tissues.
114 n shedding of soluble-Mer (sMER) and loss of MERTK function.
115 ntly homozygous loss-of-function mutation of MERTK (2q14.1) in a second retinal dystrophy patient.
116 tion of the SH2-domain signaling partners of MERTK is an important step toward further defining the m
117 9435 has 46-fold and 120-fold selectivity of MERTK over AXL and FLT3, respectively, and selectively a
118 tal cells, suggesting acquired dependence on MERTK signaling.
119 he dependence of AXL and TYRO3 expression on MERTK in both tumour types, as well as interdependency o
120 lving reduction to homoallelism for RPE65 or MERTK loss-of-function alleles.
121 er half of melanoma cell lines overexpressed MERTK compared with normal human melanocytes; however, o
122 istent with induction of autocrine/paracrine MERTK activation.
123 tion of R844C, the first putative pathogenic MERTK missense mutation that results in severe retinal d
124                  Consequently, pharmacologic MERTK blockade by the small molecule inhibitor R992 incr
125 reast cancer models, we identified the PROS1/MERTK axis within BMDMs as a potent regulator of adaptiv
126 und that the phagocytosis-associated protein MERTK was significantly reduced in CERKL-/- zebrafish.
127 ophages expressed the efferocytosis receptor MERTK and displayed engulfment of NeuN+ and cleaved casp
128 ted expression of the efferocytosis receptor MERTK mediated by the transcription factor KLF4.
129 sis, which was recognized by the PS receptor MERTK.
130  through the inhibition of the TAM receptor, MERTK, and activation of the inflammasome.
131             Here, we show that TAM receptors MERTK and TYRO3 exert reciprocal effects in osteoblast b
132 cholesterol metabolism, scavenger receptors, MERTK, and complement.
133           MERTK inhibition via shRNA reduced MERTK-mediated downstream signaling, reduced colony form
134 hogenic variants in six genes (ABCA4, RPE65, MERTK, USH2A, SPATA7, TULP1) in 10 consanguineous Irania
135        Therapeutic approaches that stabilize MERTK or TREM2 could promote plaque stabilization, espec
136                                  In summary, MERTK and TYRO3 represent potent regulators of bone home
137 sease remission, supporting the concept that MERTK+ macrophages mediate resolution of inflammation an
138 and microarray analyses, we demonstrate that MERTK expression correlates with disease progression.
139                       We also determine that MERTK phosphorylates Akt1-Y26, releasing SAV1 binding an
140                     These data indicate that MERTK signaling in mononuclear phagocytes drives T cell
141                                 We show that MERTK and AXL contribute to increased proliferation and
142                        Our data suggest that MERTK activity protects against CAV progression and that
143                  These findings suggest that MERTK signaling in the RPE involves a cohort of SH2-doma
144 of type 1 diabetic patients, suggesting that MERTK protects islets from autoimmune destruction.
145                                          The MERTK deficiency in this individual results from a nonse
146                                          The MERTK intracellular domain was expressed as a 6xHis-fusi
147                                          The MERTK ligand GAS6 promoted downstream oncogenic signalin
148 1 and BRK variants impair efferocytosis, the MERTK-mediated anti-inflammatory response to apoptotic c
149                             Mutations in the MERTK gene are responsible for retinal degeneration in t
150 l results from a nonsense variant and so the MERTK-RPE cells were subsequently treated with two trans
151 cells, which we inhibited in vitro using the MERTK/FLT3 inhibitor UNC2025 and the AXL inhibitor BGB32
152       Stimulation of melanoma cells with the MERTK ligand GAS6 resulted in the activation of several
153                                        Three MERTK sequence variants were identified in a patient wit
154 C variant was detected novel, whereas TULP1, MERTK, and MYO7A variants were detected rare and first t
155                         Salivary AXL, TYRO3, MERTK, and GAS6 levels were significantly elevated in pe
156                UNC9435 also inhibited TYRO3, MERTK, and downstream oncogenic signaling in cancer cell
157 the discovery of the first potent dual TYRO3/MERTK inhibitor, UNC9435 (44).
158    This work provides a mechanism underlying MERTK-mediated Akt activation and survival signaling in
159 n anti-inflammatory signaling in the RPE via MERTK or the related TYRO3 is lacking, catastrophic infl
160 fected HEK293Tcells, wild-type (wt) and W865 MERTK were expressed at equivalent levels and present in
161                      We investigated whether MERTK expression is altered on monocytes from patients w
162 c1 and focal adhesion kinase/MERTK, and with MERTK directly, additionally inhibiting RhoA/ROCK and th
163 toreceptor (PR) degeneration associated with MERTK mutations is thought to result from failed phagocy
164 romise for the treatment of individuals with MERTK-associated RP.
165  and found predominantly among patients with MERTK (n = 3 [20%]) and RDH5 (n = 2 [13%]) mutations.

 
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