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The expression of MerTK and AxlTK varied according to the deposition of immunoglobulin and complements on glomeruli. Both MerTK and AxlTK expressions were increased on glomeruli and varied according to pathological classifications.
Study identified the Gas6 (show GAS6 Proteins)/TAM (show CCNA1 Proteins) receptor pathway with Tyro3 (show TYRO3 Proteins) and Mer as novel targets in colorectal cancer.
MERTK is frequently overexpressed in head and neck squamous cell carcinoma and plays an important role in tumor cell motility.
these data suggest that endogenous GAS6 (show GAS6 Proteins) and Mer receptor signaling contribute to the establishment of prostate cancer stem cells in the bone marrow microenvironment
Sequence analysis revealed that the proband was a compound heterozygote with two independent mutations in MERTK, a novel nonsense mutation (c.2179C > T) and a previously reported missense variant (c.2530C > T). The proband's affected brother also had both mutations
this study shows that viral infection sensitizes fetal membranes by MERTK Inhibition
Knockdown of MERTK by shRNA in prostate cancer cells induced a decreased ratio of P-Erk1/2 to P-p38, increased expression of p27, NR2F1, SOX2, and NANOG, induced higher levels of histone H3K9me3 and H3K27me3, and induced a G1/G0 arrest, all of which are associated with dormancy.
MERTK G > A variant affects liver disease, nutrient oxidation and glucose metabolism in NAFLD.
Monocyte-induced MerTK cleavage on proreparative MHCII(LO) cardiac macrophages is a novel contributor to myocardial ischemic reperfusion injury.
Patients with macroalbuminuria diabetes had higher circulating levels of sMer and more urinary soluble Tyro3 (show TYRO3 Proteins) and sMer than normoalbuminuric diabetics. Increased clearance of sTyro3 and sMer was associated with loss of tubular Tyro3 (show TYRO3 Proteins) and Mer expression in diabetic nephropathy tissue. During in vitro diabetes, human kidney cells had down-regulation of Tyro3 (show TYRO3 Proteins) and Mer mRNA and increased shedding of sTyro3 and sMer.
GC B (show NPR2 Proteins) cell-intrinsic sensing of self-RNA, but not self-DNA, from dead cells in GCs (show UGCG Proteins) drives enhanced GC responses in Mer (show ERH Proteins)(-/-) mice. Mer (show ERH Proteins) loss in dendritic cells promotes enhanced T cell activation and proinflammatory cytokine production. Mer (show ERH Proteins) immunoregulatory signaling in APCs (show APCS Proteins) regulates B cell selection and autoimmunity. The phagocytic and immunomodulatory functions of Mer (show ERH Proteins) regulate GC responses preventing autoimmunity.
evidence that proteolytic cleavage of the macrophage efferocytosis receptor c-Mer tyrosine kinase (show TYRO3 Proteins) (MerTK) reduces efferocytosis and promotes plaque necrosis and defective resolution.
these results suggest, for the first time, that MerTK is an intracellular negative feedback regulator that inhibits the inflammatory response of lipoteichoic acid -stimulated macrophages
the reciprocal activation of Axl (show AXL Proteins) and Mer (show ERH Proteins) receptor tyrosine kinases has a major impact on the outcome of renal inflammation.
Reduced transcription of Mertk, rather than differences in MERTK protein structure, determines the reduced efficiency of apoptotic cell clearance in the Aath4a(DBA/DBA (show RPS19 Proteins)) mice, which, in turn, contributes to their increased susceptibility to atherosclerosis.
Axl (show AXL Proteins), Mertk and Tyro3 (show TYRO3 Proteins) receptors are not required for Zika virus entry and infection.
Signaling through the Mer (show ERH Proteins) proto-oncogene (show RAB1A Proteins) tyrosine kinase (show TYRO3 Proteins) (MerTK) receptor in cultured macrophages and in sterile inflammation in vivo promotes specialized proresolving mediator (SPM (show NPC1 Proteins)) biosynthesis by a mechanism involving an increase in the cytoplasmic:nuclear ratio of a key SPM (show NPC1 Proteins) biosynthetic enzyme, 5-lipoxygenase (show ALOX5 Proteins).
These studies define the clearance of infected, apoptotic neutrophils by dendritic cells and Mer (show ERH Proteins) receptor signaling as central to the early immune evasion strategies of L. major.
This gene is a member of the MER/AXL/TYRO3 receptor kinase family and encodes a transmembrane protein with two fibronectin type-III domains, two Ig-like C2-type (immunoglobulin-like) domains, and one tyrosine kinase domain. Mutations in this gene have been associated with disruption of the retinal pigment epithelium (RPE) phagocytosis pathway and onset of autosomal recessive retinitis pigmentosa (RP).
, tyrosine-protein kinase Mer
, c-mer proto-oncogene tyrosine kinase
, MER receptor tyrosine kinase
, tyrosine-protein kinase Mer-like
, STK kinase
, proto-oncogene c-Mer
, receptor tyrosine kinase MerTK
, Tyro 12
, proto-oncogene tyrosine-protein kinase Mer
, Receptor tyrosine tinase gene probably the gene for Rdy
, proto-oncogene tyrosine-protein kinase MER
, retinal dystrophy