The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Purity70 - 90% by HPLC.
- First try to dissolve a small amount of peptide in either water or buffer. The more charged residues on a peptide, the more soluble it is in aqueous solutions. - If the peptide doesn’t dissolve try an organic solvent e.g. DMSO, then dilute using water or buffer. - Consider that any solvent used must be compatible with your assay. If a peptide does not dissolve and you need to recover it, lyophilise to remove the solvent. - Gentle warming and sonication can effectively aid peptide solubilisation. If the solution is cloudy or has gelled the peptide may be in suspension rather than solubilised. - Peptides containing cysteine are easily oxidised, so should be prepared in solution just prior to use.
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Preparation and Storage
Stability and Storage
Shipped at 4°C. Upon delivery aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles.
Information available upon request.
Methylcytosine dioxygenase TET2
Probable methylcytosine dioxygenase TET2
Protein Ayu17 449
Tet methylcytosine dioxygenase 2
Tet oncogene 2
Tet oncogene family member 2
FunctionCatalyzes the conversion of methylcytosine (5mC) to 5-hydroxymethylcytosine (hmC). Plays an important role in myelopoiesis. The clear function of 5-hydroxymethylcytosine (hmC) is still unclear but it may influence chromatin structure and recruit specific factors or may constitute an intermediate component in cytosine demethylation.
Tissue specificityBroadly expressed. Highly expressed in hematopoietic cells; highest expression observed in granulocytes. Expression is reduced in granulocytes from peripheral blood of patients affected by myelodysplastic syndromes.
Involvement in diseaseNote=TET2 is frequently mutated in myeloproliferative disorders (MPD). These constitute a heterogeneous group of disorders, also known as myeloproliferative diseases or myeloproliferative neoplasms (MPN), characterized by cellular proliferation of one or more hematologic cell lines in the peripheral blood, distinct from acute leukemia. Included diseases are: essential thrombocythemia, polycythemia vera, primary myelofibrosis (chronic idiopathic myelofibrosis). Bone marrow samples from patients display uniformly low levels of hmC in genomic DNA compared to bone marrow samples from healthy controls as well as hypomethylation relative to controls at the majority of differentially methylated CpG sites. Defects in TET2 are a cause of polycythemia vera (PV) [MIM:263300]. A myeloproliferative disorder characterized by abnormal proliferation of all hematopoietic bone marrow elements, erythroid hyperplasia, an absolute increase in total blood volume, but also by myeloid leukocytosis, thrombocytosis and splenomegaly. Note=TET2 is frequently mutated in systemic mastocytosis; also known as systemic mast cell disease. A condition with features in common with myeloproliferative diseases. It is a clonal disorder of the mast cell and its precursor cells. The clinical symptoms and signs of systemic mastocytosis are due to accumulation of clonally derived mast cells in different tissues, including bone marrow, skin, the gastrointestinal tract, the liver, and the spleen. Note=TET2 is frequently mutated in myelodysplastic syndromes, a heterogeneous group of closely related clonal hematopoietic disorders. All are characterized by a hypercellular or hypocellular bone marrow with impaired morphology and maturation, dysplasia of the myeloid, megakaryocytic and/or erythroid lineages, and peripheral blood cytopenias resulting from ineffective blood cell production. Included diseases are: refractory anemia (RA), refractory anemia with ringed sideroblasts (RARS), refractory anemia with excess blasts (RAEB), refractory cytopenia with multilineage dysplasia and ringed sideroblasts (RCMD-RS). Chronic myelomonocytic leukemia (CMML) is a myelodysplastic/myeloproliferative disease. Myelodysplastic syndromes are considered a premalignant condition in a subgroup of patients that often progresses to acute myeloid leukemia (AML). Bone marrow samples from patients display uniformly low levels of hmC in genomic DNA compared to bone marrow samples from healthy controls as well as hypomethylation relative to controls at the majority of differentially methylated CpG sites.