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Human Monoclonal MPL Primary Antibody pour FACS, ELISA - ABIN969542
Marty, Chaligné, Lacout, Constantinescu, Vainchenker, Villeval: Ligand-independent thrombopoietin mutant receptor requires cell surface localization for endogenous activity. dans The Journal of biological chemistry 2009
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Human Polyclonal MPL Primary Antibody pour IF (p) - ABIN2177733
Maekawa, Osawa, Izumi, Nagao, Takano, Okada, Tachi, Teramoto, Kawamura, Horiuchi, Saga, Kato, Yamamura, Watanabe, Kobayashi, Kobayashi, Sato, Hashimoto, Suzu, Kimura: Myeloproliferative leukemia protein activation directly induces fibrocyte differentiation to cause myelofibrosis. dans Leukemia 2017
Human Monoclonal MPL Primary Antibody pour FACS - ABIN4896876
Baker, Nederveen, Parise: Aerobic exercise in humans mobilizes HSCs in an intensity-dependent manner. dans Journal of applied physiology (Bethesda, Md. : 1985) 2017
The S505A MPL mutation is associated with childhood hereditary thrombocytosis and essential thrombocythemia.
Frameshift mutation in the MPL gene is associated with congenital amegakaryocytic thrombocytopenia.
positive CD110 expression in PDAC was associated with poor prognosis and liver metastasis of human PDAC samples
MPL, CALR and JAK2 are considered driver mutations in myeloproliferative neoplasms.The occurrence of two driver mutations in the same patient was determined and the clinical presentation and disease progression were compared with those in patients with only one driver mutation. Co-occurrence of 2 driver mutations affects the presentation or evolution of MPN, especially essential thrombocythemia.
JAK2, CALR, MPL and ASXL1 mutational status correlates with distinct histological features in Philadelphia chromosome-negative myeloproliferative neoplasms
Insights into the mechanism of the pathogenic mutant CALR-MPL interaction in myeloproliferative neoplasms.
This study explored the relationship between mutations in the Janus kinase 2 gene ( JAK2), MPL, and the calreticulin gene ( CALR) in Uygur and Han Chinese patients with BCR-ABL fusion gene-negative myeloproliferative neoplasms.
JAK2V617F mutation was found in 37 (61.7%) patients with ET. Among 23 patients without JAK2V617F mutation, 7 (11.7%) had CALR mutation and 1 (1.7%) had MPL mutation. Fifteen (25.0%) patients were negative for all 3 mutations: JAK2V617F(-), CALR(-), and MPL(-).
Comprehensive genomic characterization identified distinct genetic subgroups and provided a classification of myeloproliferative neoplasms on the basis of causal biologic mechanisms. Mutations in JAK2, CALR, or MPL being the sole abnormality in 45% of the patients.
MPL and CALR genotypes show a similar clinical picture at essential thrombocythaemia diagnosis. Bone marrow histology in MPL-mutated ET is characterized by prominent megakaryocytic proliferation.
These results indicate that lusutrombopag acts on human TPOR to upregulate differentiation and proliferation of megakaryocytic cells, leading to platelet production.
The expression of TPO and c-Mpl was significantly decreased in the cITP group compared to the nITP group, suggesting that TPO and its receptor may play important roles in childhood cITP pathogenesis.
In 94.9% of PV, 85.5% ET and 85.2% PMF, authors found mutations in JAK2, MPL or CALR. 74.9% carried JAK2V617F, 12.3% CALR mutations, 2.1% MPL mutations and 10.7% were triple negative.
A novel germ-line mutation of c-mpl gene in a sporadic case of essential thrombocythemia.
In 136 patients with myelofibrosis and a median age of 58 years who underwent allogeneic stem cell transplantation (AHSCT) for molecular residual disease, the percentage of molecular clearance on day 100 was higher in CALR-mutated patients (92%) in comparison with MPL- (75%) and JAKV617F-mutated patients (67%).
This study demonstrated that absence of MPL mutation in stroke.
MPL mutations and splenomegaly are risk factors for essential thrombocythemia progression into primary nyelofibrosis.
goals were: (i) to identify other MPL mutations that should be tested in MPN patients by mutation-specific PCR; and (ii) to determine the amino acid requirements at position 515 to prevent TpoR self-activation
Concurrent MPL W515L and Y591D mutations in a patient with myelofibrosis.
MPL is up regulated in JAK2(V617F) ECs and contributes to the maintenance/expansion of the JAK2(V617F) clone over JAK2(WT) clone in vitro
Authors demonstrate that thrombopoietin and its receptor MPL are critical for the human JAK2V617F-bearing MK-induced myeloproliferation in mice, both by directly affecting the quantity and quality of MKs and by altering the MK-endothelial interaction and vascular niche function.
These results indicate that c-MPL is a candidate LSC surface marker that may serve as a therapeutic target for the elimination of LSCs.
these findings indicate that c-MPL deficiency is associated with abnormal maturation of neonatal megakaryocytes and developmental stage-specific defects in platelet function
these results demonstrate that MPL P106L is a receptor with an incomplete defect in trafficking.
C-Mpl is expressed on osteoblasts and osteoclasts and is important in regulating skeletal homeostasis.
CALR mutants are sufficient to induce thrombocytosis through MPL activation.
Thrombopoietin receptor activation by myeloproliferative neoplasm associated calreticulin mutants.
The interaction between Mpl and Atp5d was confirmed by the yeast two-hybrid system, mammalian two-hybrid assay, pull-down experiment, and co-immunoprecipitation study in vivo and in vitro.
Mouse prenatal platelet-forming lineages share a core transcriptional program but divergent dependence on MPL.
MERIT40 deficiency triggers hypersensitivity to Tpo stimulation and the stem cell phenotypes are abrogated on a background null for the Tpo receptor Mpl.
OTT1 regulates the alternative splicing of Mpl-TR, a truncated isoform of c-Mpl, which modulates Thrombopoietin-mediated signaling.
Mpl expression, but not Tpo, is fundamental in the development of JAK2V617F(+) myeloproliferative neoplasms
Thrombopoietin/MPL signaling confers growth and survival capacity to CD41-positive cells in a mouse model of Evi1 leukemia.
These studies show the importance of the c-Mpl membrane-distal cytokine receptor homology module to thrombopoietin-binding and suggest that mutations within this CRM that perturb TPO binding could give rise to Congenital Amegakaryocytic Thrombocytopenia.
Mpl expression on megakaryocytes and platelets is essential to prevent megakaryocytosis and myeloproliferation.
IL-17A and its downstream cytokines are important regulators and synergistic factors for the physiologic function of TPO/c-mpl on hematopoiesis.
These experiments define a novel VEGF-miR-1-Mpl-P-selectin effector pathway in lung Th2 inflammation and herald the utility of miR-1 and Mpl as potential therapeutic targets for asthma.
Gene-corrected Mpl(-/-) cells had increased long-term repopulating potential, with a marked increase in lineage(-)Sca1(+)cKit(+) cells and early progenitor populations in reconstituted mice.
Data indicate that Mpl is an active player during the first steps of definitive hematopoiesis establishment through direct regulation of the expression of transcription factors or genes important for the self-renewal, proliferation and apoptosis of HSCs.
Data locate Mpl expression to neurons at different subdivisions of the spinal cord, rhombencephalon, midbrain and prosencephalon; besides neuronal cells Mpl protein is also expressed in Purkinje cells of the adult cerebellum.
In 1990 an oncogene, v-mpl, was identified from the murine myeloproliferative leukemia virus that was capable of immortalizing bone marrow hematopoietic cells from different lineages. In 1992 the human homologue, named, c-mpl, was cloned. Sequence data revealed that c-mpl encoded a protein that was homologous with members of the hematopoietic receptor superfamily. Presence of anti-sense oligodeoxynucleotides of c-mpl inhibited megakaryocyte colony formation. The ligand for c-mpl, thrombopoietin, was cloned in 1994. Thrombopoietin was shown to be the major regulator of megakaryocytopoiesis and platelet formation. The protein encoded by the c-mpl gene, CD110, is a 635 amino acid transmembrane domain, with two extracellular cytokine receptor domains and two intracellular cytokine receptor box motifs . TPO-R deficient mice were severely thrombocytopenic, emphasizing the important role of CD110 and thrombopoietin in megakaryocyte and platelet formation. Upon binding of thrombopoietin CD110 is dimerized and the JAK family of non-receptor tyrosine kinases, as well as the STAT family, the MAPK family, the adaptor protein Shc and the receptors themselves become tyrosine phosphorylated.
, myeloproliferative leukemia protein
, proto-oncogene c-Mpl
, thrombopoietin receptor
, myeloproliferative leukemia virus oncogene
, thrombopoietin receptor-like
, cytokine receptor
, myeloproliferative leukemia virus oncogene, like
, thrombopoietin receptor c-mpl