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anti-Human MERTK Antikörper:
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Mouse (Murine) Polyclonal MERTK Primary Antibody für CyTOF, FACS - ABIN4899759
Nascimento, Huang, Smith, Everts, Lam, Bassity, Gautier, Randolph, Pearce: Ly6Chi monocyte recruitment is responsible for Th2 associated host-protective macrophage accumulation in liver inflammation due to schistosomiasis. in PLoS pathogens 2014
Show all 26 Pubmed References
Human Polyclonal MERTK Primary Antibody für CM, ICC - ABIN2746864
Keating, Salzberg, Sather, Liang, Nickoloff, Anwar, Deryckere, Hill, Joung, Sawczyn, Park, Curran-Everett, McGavran, Meltesen, Gore, Johnson, Graham: Lymphoblastic leukemia/lymphoma in mice overexpressing the Mer (MerTK) receptor tyrosine kinase. in Oncogene 2006
Show all 16 Pubmed References
Mouse (Murine) Polyclonal MERTK Primary Antibody für FACS, WB - ABIN5012952
Ikarashi, Nakashima, Kinoshita, Sato, Nakashima, Miyazaki, Nishiyama, Yamamoto, Seki: Distinct development and functions of resident and recruited liver Kupffer cells/macrophages. in Journal of leukocyte biology 2014
Show all 10 Pubmed References
Human Polyclonal MERTK Primary Antibody für CyTOF, FACS - ABIN4899963
Eken, Martin, Sadallah, Treves, Schaller, Schifferli: Ectosomes released by polymorphonuclear neutrophils induce a MerTK-dependent anti-inflammatory pathway in macrophages. in The Journal of biological chemistry 2010
Show all 10 Pubmed References
Human Polyclonal MERTK Primary Antibody für CM, ICC - ABIN2746860
Wu, Singh, Georgescu, Birge: A role for Mer tyrosine kinase in alphavbeta5 integrin-mediated phagocytosis of apoptotic cells. in Journal of cell science 2005
Show all 9 Pubmed References
Human Monoclonal MERTK Primary Antibody für FACS - ABIN4895670
Graham, Salzberg, Kurtzberg, Sather, Matsushima, Keating, Liang, Lovell, Williams, Dawson, Schell, Anwar, Snodgrass, Earp: Ectopic expression of the proto-oncogene Mer in pediatric T-cell acute lymphoblastic leukemia. in Clinical cancer research : an official journal of the American Association for Cancer Research 2006
Show all 6 Pubmed References
Mouse (Murine) Monoclonal MERTK Primary Antibody für FACS - ABIN4896617
Stijlemans, Cnops, Naniima, Vaast, Bockstal, De Baetselier, Magez: Development of a pHrodo-based assay for the assessment of in vitro and in vivo erythrophagocytosis during experimental trypanosomosis. in PLoS neglected tropical diseases 2015
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Human Monoclonal MERTK Primary Antibody für ELISA, WB - ABIN969283
McGough, Cummings: Coeliac disease: a diverse clinical syndrome caused by intolerance of wheat, barley and rye. in The Proceedings of the Nutrition Society 2005
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Human Polyclonal MERTK Primary Antibody für CM, ICC - ABIN2750536
Mahajan, Earp: An SH2 domain-dependent, phosphotyrosine-independent interaction between Vav1 and the Mer receptor tyrosine kinase: a mechanism for localizing guanine nucleotide-exchange factor action. in The Journal of biological chemistry 2004
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Human Monoclonal MERTK Primary Antibody für CyTOF, ELISA (Capture) - ABIN4899148
Shiozawa, Pedersen, Taichman: GAS6/Mer axis regulates the homing and survival of the E2A/PBX1-positive B-cell precursor acute lymphoblastic leukemia in the bone marrow niche. in Experimental hematology 2010
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Three novel loss-of-function mutations in MERTK gene were identified in Chinese patients with retinitis pigmentosa.
Axl and Tyro3, but not Mertk, have an important role in platelet activation and thrombus formation
Authors report that SAV1, a Hippo signaling component, inhibits Akt, a function independent of its role in Hippo signaling. Binding to a proline-tyrosine motif in the Akt-PH domain, SAV1 suppresses Akt activation by blocking Akt's movement to plasma membrane. Authors further identify cancer-associated SAV1 mutations with impaired ability to bind Akt, leading to Akt hyperactivation.
The present study provides a meaningfully negative result demonstrating that rare variants in MERTK are not associated with AMD. The study also demonstrates the role of large sample size genetic studies utilizing whole-genome sequencing as a powerful tool that can resolve clinically relevant questions regarding the genetic basis of ophthalmic disease.
cooperation between CD14 and MerTK may foster the clearance of apoptotic neutrophils by human monocytes/macrophages
Patients with retinitis pigmentosa (RP) in this study were carriers of two novel allelic mutations in the MERTK gene, a missense variant in exon 17 and an approximate 91 kb genomic deletion. Mapping of the deletion breakpoints allowed molecular testing of a cohort of patients with RP with allele-specific PCR.
The targeted NGS strategy employed provides an efficient tool for RP pathogenic gene detection. This study identified a new autosomal recessive mutation in the RP-related gene MERTK, which expands the spectrum of RP disease-causing mutations
We observed that the frequency for the wild-type haplotype was higher in the control group, compared to that in the group of patients with COPD, in the subgroup analysis of current smokers, although the difference was not statistically significant
Study describes a novel cellular pathway involved in diabetic efferocytosis, wherein diabetes-induced decrease in miR-126 expression results in upregulation of ADAM9 expression that in-turn leads proteolytic cleavage of MerTK and formation of inactive soluble Mer. Decrease in MerTK phosphorylation leads to reduced downstream cytoskeletal signaling required for engulfment and thus decreases efferocytosis.
Phosphatidylserine mediated hyperactivation of Mertk.MERTK promotes epithelial cell efferocytosis in a tyrosine kinase-dependent manner.MERTK role in AKT-dependent drug resistance.
STK 11 testing can confirm those at risk of Peutz-Jeghers syndrome, who require lifelong surveillance, and possibly release those with a simple dermatosis, such as Laugier-Hunziker syndrome, from invasive and thus potentially harmful surveillance.
The broad-spectrum activity mediated by UNC2025 in leukemia patient samples and xenograft models, alone or in combination with cytotoxic chemotherapy, supports continued development of MERTK inhibitors for treatment of leukemia
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/TAM receptor pathway with Tyro3 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 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.
Tyro3/Axl/Mertk-deficient mice develop bone marrow edema which is an early pathological marker in rheumatoid arthritis.
Mer-LXRalpha signaling plays an important role in the differentiation and maintenance of marginal zone macrophages.
MerTK-deficient macrophages have defective microparticle clearance resulting in lung inflammation and injury.
These results suggest that MerTK inhibition impaired phagocytic function of the retina
MerTK does not play an essential role in the phagocytosis of S. aureus but attenuates inflammation induced by staphylococcal LTA through blocking NF-kappaB activation.
Tumor macrophage expression of Mertk is a therapeutic target to prevent tumor recurrence following radiation therapy.
Hypercapnic Acidosis Regulates Mer Tyrosine Kinase Receptor Shedding and Activity.
GC B cell-intrinsic sensing of self-RNA, but not self-DNA, from dead cells in GCs drives enhanced GC responses in Mer(-/-) mice. Mer loss in dendritic cells promotes enhanced T cell activation and proinflammatory cytokine production. Mer immunoregulatory signaling in APCs regulates B cell selection and autoimmunity. The phagocytic and immunomodulatory functions of Mer regulate GC responses preventing autoimmunity.
Monocyte-induced MerTK cleavage on proreparative MHCII(LO) cardiac macrophages is a novel contributor to myocardial ischemic reperfusion injury.
evidence that proteolytic cleavage of the macrophage efferocytosis receptor c-Mer tyrosine kinase (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 and Mer 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) mice, which, in turn, contributes to their increased susceptibility to atherosclerosis.
Axl, Mertk and Tyro3 receptors are not required for Zika virus entry and infection.
Signaling through the Mer proto-oncogene tyrosine kinase (MerTK) receptor in cultured macrophages and in sterile inflammation in vivo promotes specialized proresolving mediator (SPM) biosynthesis by a mechanism involving an increase in the cytoplasmic:nuclear ratio of a key SPM biosynthetic enzyme, 5-lipoxygenase.
These studies define the clearance of infected, apoptotic neutrophils by dendritic cells and Mer receptor signaling as central to the early immune evasion strategies of L. major.
Tyro3 gene dosage modulates Mertk-associated retinal degeneration, provide strong evidence for a direct role for TYRO3 in RPE phagocytosis, and suggest that an eQTL can modify a recessive Inherited photoreceptor degenerations.
Activation of Mertk synergized with interferon-beta to tighten cell junctions and prevent virus transit across brain microvascular endothelial cells.
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).
MER receptor tyrosine kinase
, STK kinase
, proto-oncogene c-Mer
, receptor tyrosine kinase MerTK
, tyrosine-protein kinase Mer
, 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
, c-eyk proto-oncogene
, c-mer proto-oncogene tyrosine kinase
, tyrosine-protein kinase Mer-like