Key features and details
- Rabbit polyclonal to SUFU
- Suitable for: IP, WB
- Reacts with: Mouse, Human
- Isotype: IgG
Product nameAnti-SUFU antibody
See all SUFU primary antibodies
DescriptionRabbit polyclonal to SUFU
Tested applicationsSuitable for: IP, WBmore details
Species reactivityReacts with: Mouse, Human
Synthetic peptide within Human SUFU aa 434-484. The exact sequence is proprietary. NP_057253.2
Database link: Q9UMX1
- WB: HeLa, HEK-293T and NIH/3T3 whole cell lysate. IP: SUFU IP in HeLa whole cell lysate.
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Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term. Avoid freeze / thaw cycle.
Storage bufferpH: 6.8
Preservative: 0.09% Sodium azide
Constituents: Tris buffered saline, 0.1% BSA
Concentration information loading...
PurityImmunogen affinity purified
Purification notesab245428 was affinity purified using an epitope specific to SUFU immobilized on solid support.
Our Abpromise guarantee covers the use of ab245428 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|IP||Use at 2-5 µg/mg of lysate.|
|WB||1/2000 - 1/10000.|
FunctionNegative regulator in the hedgehog signaling pathway. Down-regulates GLI1-mediated transactivation of target genes (PubMed:15367681, PubMed:24311597, PubMed:24217340). Down-regulates GLI2-mediated transactivation of target genes (PubMed:24311597, PubMed:24217340). Part of a corepressor complex that acts on DNA-bound GLI1. May also act by linking GLI1 to BTRC and thereby targeting GLI1 to degradation by the proteasome. Sequesters GLI1, GLI2 and GLI3 in the cytoplasm, this effect is overcome by binding of STK36 to both SUFU and a GLI protein (PubMed:10806483, PubMed:24217340). Negative regulator of beta-catenin signaling. Regulates the formation of either the repressor form (GLI3R) or the activator form (GLI3A) of the full length form of GLI3 (GLI3FL). GLI3FL is complexed with SUFU in the cytoplasm and is maintained in a neutral state. Without the Hh signal, the SUFU-GLI3 complex is recruited to cilia, leading to the efficient processing of GLI3FL into GLI3R. When Hh signaling is initiated, SUFU dissociates from GLI3FL and the latter translocates to the nucleus, where it is phosphorylated, destabilized, and converted to a transcriptional activator (GLI3A). Required for normal embryonic development. Required for the proper formation of hair follicles and the control of epidermal differentiation.
Tissue specificityUbiquitous in adult tissues. Detected in osteoblasts of the perichondrium in the developing limb of 12-week old embryos. Isoform 1 is detected in fetal brain, lung, kidney and testis. Isoform 2 is detected in fetal testis, and at much lower levels in fetal brain, lung and kidney.
Involvement in diseaseMedulloblastoma
Sequence similaritiesBelongs to the SUFU family.
Cellular localizationCytoplasm. Nucleus.
- Information by UniProt
- OTTHUMP00000020374 antibody
- OTTHUMP00000020377 antibody
- OTTHUMP00000020379 antibody
All lanes : Anti-SUFU antibody (ab245428) at 0.04 µg/ml
Lane 1 : HeLa (Human epithelial cell line from cervix adenocarcinoma) whole cell lysate at 50 µg
Lane 2 : HeLa whole cell lysate at 15 µg
Lane 3 : HeLa whole cell lysate at 5 µg
Lane 4 : HEK-293T (Human epithelial cell line from embryonic kidney transformed with large T antigen) whole cell lysate at 50 µg
Lane 5 : NIH/3T3 (Mouse embryo fibroblast cell line) whole cell lysate at 50 µg
Exposure time: 30 seconds
SUFU was immunoprecipitated from HeLa (Human epithelial cell line from cervix adenocarcinoma) whole cell lysate (1 mg per IP reaction; 20% of IP loaded).
ab245428 used for IP at 3 µg/mg lysate. For WB 1 µg/ml.
Lane 1: ab245428 IP in HeLa whole cell lysate.
Lane 2: Control IgG in HeLa whole cell lysate.
Chemiluminescence detection: 10 seconds.
To our knowledge, customised protocols are not required for this product. Please try the standard protocols listed below and let us know how you get on.
ab245428 has not yet been referenced specifically in any publications.