ライフサイエンスコーパス: MERTK

1 MERTK expression (mean fluorescence intensity) correlate

2 MERTK expression and lipid peroxidation in synaptoneuros

3 MERTK expression was highest in metastatic melanomas, fo

4 MERTK has an essential role in phagocytosis, one of the

5 MERTK inhibition via shRNA reduced MERTK-mediated downst

6 MERTK inhibitors restore production of inflammatory cyto

7 MERTK missense variants identified by single-strand conf

8 nt study, we evaluated whether delivery of a MERTK transgene using a tyrosine-mutant AAV8 capsid coul

9 enotype, migration, and functional analyses, MERTK-expressing monocytes migrate across the endothelia

10 e, loss of receptor tyrosine kinases AXL and MERTK reduced efferocytosis of eryptotic erythrocytes an

11 AM receptor tyrosine kinases-TYRO3, AXL, and MERTK-as an emerging class of innate immune checkpoints

12 ptor tyrosine kinases (RTKs)-TYRO3, AXL, and MERTK-together with their cognate agonists GAS6 and PROS

13 st listed, the early-onset RP genes LRAT and MERTK were added).

14 eloping and adult brain, identify MEGF10 and MERTK as critical proteins in the synapse remodelling un

15 synapse elimination, requires the MEGF10 and MERTK phagocytic pathways, and is strongly dependent on

16 coordinate targeting of IGFBP2, PITPNC1 and MERTK--novel pro-angiogenic genes and biomarkers of huma

17 ant protein expression was assayed with anti-MERTK and anti-phosphotyrosine antibodies.

18 AS6) is a soluble agonist of the TYRO3, AXL, MERTK (TAM) family of receptor tyrosine kinases identifi

19 specific 6 (GAS6), a ligand of the TYRO3-AXL-MERTK (TAM) receptor family, in regulating oral mucosal

20 ytosis of eryptotic erythrocytes through AXL/MERTK as a critical mechanism modulating macrophage phen

21 In contrast, C844 MERTK was expressed at low levels and did not stimulate

22 The loss of function of C844 MERTK is probably due to decreased protein stability.

23 In addition, the relative stability of C844 MERTK was significantly less than wt in assays of protei

24 d native proteins, western analysis detected MERTK interactions with GRB2, PIK3R1 (P85alpha), VAV3, a

25 he binding of its ligand GAS6 to endothelial MERTK receptors.

26 This work establishes MERTK as a therapeutic target in melanoma and provides a

27 atory monocytes and macrophages that express MERTK and suppress the innate immune response to microbe

28 of monocytes and macrophages that expressed MERTK was greatly increased in the circulation, livers,

29 also identify the IGFBP2/IGF1/IGF1R and GAS6/MERTK signalling pathways as regulators of cancer-mediat

30 ere linked to the functionally related genes MERTK and TULP1, which encode factors involved in phagoc

31 An AAV8 Y733F vector expressing a human MERTK cDNA driven by a RPE-selective promoter was admini

32 kinase, perhaps including mutations in human MERTK.

33 dy was to evaluate the interactions of human MERTK with SH2-domain proteins present in the RPE.

34 entosa associated with biallelic variants in MERTK.

35 Of note, the receptor tyrosine kinase MERTK and the pyrimidine kinase UCK1 were both found to

36 The receptor tyrosine kinase MERTK plays an essential role in the phagocytic uptake o

37 ving the MER proto-oncogene tyrosine kinase (MERTK) and discovered a clinical occurrence and cell lin

38 C-MER proto-oncogene tyrosine kinase (MERTK) is a receptor tyrosine kinase with oncogenic prop

39 MER receptor tyrosine kinase (MERTK) is expressed by monocytes and macrophages and con

40 helial cells; whereas c-Mer tyrosine kinase (MERTK) receptor cleaved from metastatic cells promotes e

41 Strikingly, all three RAF family members, MERTK, and NTRK2 drove the formation of bone and viscera

42 ment of melanoma cells with UNC1062, a novel MERTK-selective small-molecule tyrosine kinase inhibitor

43 ntification and functional analysis of novel MERTK mutations to provide information regarding whether

44 sine kinase inhibitor, reduced activation of MERTK-mediated downstream signaling, induced apoptosis i

45 a rationale for the continued development of MERTK-targeted therapies.

46 sults, together with the recent discovery of MERTK mutations in individuals with retinitis pigmentosa

47 Expression of MERTK reduced the response of cultured monocytes to lipo

48 ed with down-regulation of the expression of MERTK.

49 cultured RPE by inducing gene expression of MERTK/AXL/TYRO3.

50 ysaccharide, with or without an inhibitor of MERTK (UNC569).

51 also decreased the mRNA and protein level of MERTK, as well as the ox-POS phagocytosis.

52 microscopy were used to determine levels of MERTK in bone marrow, liver, and lymph node tissues.

53 n shedding of soluble-Mer (sMER) and loss of MERTK function.

54 ntly homozygous loss-of-function mutation of MERTK (2q14.1) in a second retinal dystrophy patient.

55 tion of the SH2-domain signaling partners of MERTK is an important step toward further defining the m

56 lving reduction to homoallelism for RPE65 or MERTK loss-of-function alleles.

57 er half of melanoma cell lines overexpressed MERTK compared with normal human melanocytes; however, o

58 tion of R844C, the first putative pathogenic MERTK missense mutation that results in severe retinal d

59 und that the phagocytosis-associated protein MERTK was significantly reduced in CERKL-/- zebrafish.

60 through the inhibition of the TAM receptor, MERTK, and activation of the inflammasome.

61 MERTK inhibition via shRNA reduced MERTK-mediated downstream signaling, reduced colony form

62 and microarray analyses, we demonstrate that MERTK expression correlates with disease progression.

63 These findings suggest that MERTK signaling in the RPE involves a cohort of SH2-doma

64 The MERTK deficiency in this individual results from a nonse

65 The MERTK intracellular domain was expressed as a 6xHis-fusi

66 Mutations in the MERTK gene are responsible for retinal degeneration in t

67 l results from a nonsense variant and so the MERTK-RPE cells were subsequently treated with two trans

68 Stimulation of melanoma cells with the MERTK ligand GAS6 resulted in the activation of several

69 Three MERTK sequence variants were identified in a patient wit

70 fected HEK293Tcells, wild-type (wt) and W865 MERTK were expressed at equivalent levels and present in

71 We investigated whether MERTK expression is altered on monocytes from patients w

72 romise for the treatment of individuals with MERTK-associated RP.