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Product Name
SETBP1 antibody
- Documents
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Description
SETBP1 Rabbit Polyclonal antibody. Positive WB detected in HeLa cells. Observed molecular weight by Western-blot: 145-150 kDa
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Tested applications
ELISA, WB
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Species reactivity
Human,Mouse,Rat; other species not tested.
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Alternative names
DKFZp666J1210 antibody; KIAA0437 antibody; SEB antibody; SET binding protein antibody; SET binding protein 1 antibody; SETBP1 antibody
- Immunogen
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Isotype
Rabbit IgG
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Preparation
This antibody was obtained by immunization of SETBP1 recombinant protein (Accession Number: NM_001130110). Purification method: Antigen affinity purified.
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Clonality
Polyclonal
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Formulation
PBS with 0.02% sodium azide and 50% glycerol pH 7.3.
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Storage instructions
Store at -20℃. DO NOT ALIQUOT
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Applications
Recommended Dilution:
WB: 1:200-1:1000
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Validations
HeLa cells were subjected to SDS PAGE followed by western blot with Catalog No:115220(SETBP1 Antibody) at dilution of 1:300
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Background
SETBP1 is initially found to interact with SET, which is a small protein inhibitor for tumor suppressors PP2A and NM23-H1. There are existing two isoforms of SETBP1 and the molecular weight of isoform one is 170 kDa and another is 26 kDa. SET is fused with another gene CAN through chromosome translocation in a case of acute undifferentiated leukemia. SETBP1 may involve in chromosome translocation in a case of acute T-cell leukemia [PMID:17569777]. SETBP1 can cooperate with BCR/ABL to transform committed myeloid progenitors normally lacking self-renewal capability into LSCs and cause development of myeloid leukemias resembling human CML myeloid blast crisis [PMID:22566606]. SETBP1 was shown to form a complex with SET and PP2A, enhancing the stability of SET and its inhibition of PP2A.
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References
- Oakley K, Han Y, Vishwakarma BA. Setbp1 promotes the self-renewal of murine myeloid progenitors via activation of Hoxa9 and Hoxa10. Blood. 119(25):6099-108. 2012.
- Makishima H, Yoshida K, Nguyen N. Somatic SETBP1 mutations in myeloid malignancies. Nature genetics. 45(8):942-6. 2013.
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