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Results show that mutant CALR (显示 CALR ELISA试剂盒) 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 (显示 JAK2 ELISA试剂盒), CALR (显示 CALR ELISA试剂盒), and MPL genes in myeloproliferative neoplasms suggest that CALR (显示 CALR ELISA试剂盒) and MPL should be analyzed not only in JAK2 (显示 JAK2 ELISA试剂盒)-negative patients but also in low V617F mutation patients.
identification of a higher frequency of co-existing JAK2 (显示 JAK2 ELISA试剂盒) 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 (显示 JAK2 ELISA试剂盒), CALR (显示 CALR ELISA试剂盒), and MPL in essential thrombocythemia and primary myelofibrosis defines clinical outcome.
Normal FLT3 (显示 FLT3 ELISA试剂盒) and negative expression of CD34 (显示 CD34 ELISA试剂盒) and cMPL may predict a longer overall survival in aute myeloid leukemia (显示 BCL11A ELISA试剂盒).
we show that the positive charge of the CALR (显示 CALR ELISA试剂盒) mutant C-terminus is necessary to transform hematopoietic cells by enabling binding between mutant CALR (显示 CALR ELISA试剂盒) and the thrombopoietin receptor MPL.
Anagrelide proved effective among all molecular subsets, indicating that JAK2 (显示 JAK2 ELISA试剂盒)/CALR (显示 CALR ELISA试剂盒)/MPL mutational status does not seem to represent a major determinant of choice of cytoreductive treatment among essential thrombocythemia therapies.
In essential thrombocythemia, MPL mutations might be associated with a higher risk of fibrotic transformation and the presence of JAK2 (显示 JAK2 ELISA试剂盒)/MPL mutations with higher risk of thrombosis.
C-Mpl is expressed on osteoblasts and osteoclasts and is important in regulating skeletal homeostasis.
CALR (显示 CALR ELISA试剂盒) mutants are sufficient to induce thrombocytosis through MPL activation.
Thrombopoietin receptor activation by myeloproliferative neoplasm associated calreticulin (显示 CALR ELISA试剂盒) mutants.
The interaction between Mpl and Atp5d (显示 ATP5D ELISA试剂盒) 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 (显示 BABAM1 ELISA试剂盒) deficiency triggers hypersensitivity to Tpo (显示 THPO ELISA试剂盒) stimulation and the stem cell phenotypes are abrogated on a background null for the Tpo (显示 THPO ELISA试剂盒) receptor Mpl.
OTT1 regulates the alternative splicing of Mpl-TR, a truncated isoform of c-Mpl, which modulates Thrombopoietin (显示 THPO ELISA试剂盒)-mediated signaling.
Mpl expression, but not Tpo (显示 THPO ELISA试剂盒), is fundamental in the development of JAK2V617F(+) myeloproliferative neoplasms
Thrombopoietin (显示 THPO ELISA试剂盒)/MPL signaling confers growth and survival capacity to CD41-positive cells in a mouse model of Evi1 (显示 MECOM ELISA试剂盒) 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