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Concurrent MPL W515L and Y591D mutations in a patient with myelofibrosis.
MPL is up regulated in JAK2 (show JAK2 Proteins)(V617F) ECs and contributes to the maintenance/expansion of the JAK2 (show JAK2 Proteins)(V617F) clone over JAK2 (show JAK2 Proteins)(WT) clone in vitro
In tumor cell cultures, exogenous expression of MPL led to constitutive activation of STAT3 (show STAT3 Proteins) and 5, ERK1/2, and AKT (show AKT1 Proteins), cytokine-independent growth, and reduction of apoptosis similar to the effects seen in the spontaneously outgrown cells.
Essential Thrombocythemia and Primary Myelofibrosis patients with MPL mutations are at high risk for Thrombotic Events.
Results show that mutant CALR (show CALR Proteins) induces autocrine, but not paracrine activation of MPL in myeloproliferative neoplasm. [review]
these results demonstrate that MPL P106L is a receptor with an incomplete defect in trafficking.
Coexisting mutations of the JAK2 (show JAK2 Proteins), CALR (show CALR Proteins), and MPL genes in myeloproliferative neoplasms suggest that CALR (show CALR Proteins) and MPL should be analyzed not only in JAK2 (show JAK2 Proteins)-negative patients but also in low V617F mutation patients.
identification of a higher frequency of co-existing JAK2 (show JAK2 Proteins) exon-12 or MPL exon-10 mutations in patients with myeloproliferative neoplasms with a low JAK2V617F allelic burden compared to those with a higher allelic burden.
A newborn girl with congenitcal amegakaryocytic thrombocytopenia had a homozygous missense Trp154-to- Arg mutation in exon 4 of c-MPL. The same heterozygote mutation was detected in her mother, father, and 2 siblings.
Mutation status of JAK2 (show JAK2 Proteins), CALR (show CALR Proteins), and MPL in essential thrombocythemia and primary myelofibrosis defines clinical outcome.
C-Mpl is expressed on osteoblasts and osteoclasts and is important in regulating skeletal homeostasis.
CALR (show CALR Proteins) mutants are sufficient to induce thrombocytosis through MPL activation.
Thrombopoietin receptor activation by myeloproliferative neoplasm associated calreticulin (show CALR Proteins) mutants.
The interaction between Mpl and Atp5d (show ATP5D Proteins) 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 (show BABAM1 Proteins) deficiency triggers hypersensitivity to Tpo (show THPO Proteins) stimulation and the stem cell phenotypes are abrogated on a background null for the Tpo (show THPO Proteins) receptor Mpl.
OTT1 regulates the alternative splicing of Mpl-TR, a truncated isoform of c-Mpl, which modulates Thrombopoietin (show THPO Proteins)-mediated signaling.
Mpl expression, but not Tpo (show THPO Proteins), is fundamental in the development of JAK2V617F(+) myeloproliferative neoplasms
Thrombopoietin (show THPO Proteins)/MPL signaling confers growth and survival capacity to CD41-positive cells in a mouse model of Evi1 (show MECOM Proteins) leukemia.
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