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anti-Human SUFUH Antikörper:
anti-Mouse (Murine) SUFUH Antikörper:
anti-Rat (Rattus) SUFUH Antikörper:
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Human Polyclonal SUFUH Primary Antibody für WB - ABIN871409
Zimmern, Kobashi, Lemack: Outcome measure for stress urinary incontinence treatment (OMIT): results of two society of urodynamics and female urology (SUFU) surveys. in Neurourology and urodynamics 2010
Show all 3 Pubmed References
A Comparison of Ci/Gli (zeige GLI1 Antikörper) Activity as Regulated by Sufu in Drosophila and Mammalian Hedgehog (zeige SHH Antikörper) Response
Sufu can sequester Ci/Gli (zeige GLI1 Antikörper) in the cytoplasm through binding to an N-terminal site while inhibiting Ci/Gli (zeige GLI1 Antikörper) activity in the nucleus depending on a C-terminal Sufu-interacting site.
Drosophila Hedgehog (zeige SHH Antikörper) signaling promotes downregulation of Su(fu) through its target protein HIB (Hh-induced BTB protein).
Suppressor of fused (Sufu) opposes Trn-mediated Ci nuclear import by masking its PY-nuclear localization sequence.
The 'closed' form of Sufu is stabilized by Gli (zeige GLI1 Antikörper) binding and inhibited by Hh treatment, whereas the 'open' state of Sufu is promoted by Gli (zeige GLI1 Antikörper)-dissociation and Hh signaling.
Su(fu) causes the Rdx (zeige RDX Antikörper) switch between two mchanisms of Cubitus interruptus regulation.
Suppressor of Fused represses Gli (zeige GLI1 Antikörper)-mediated transcription by recruiting the SAP18 (zeige SAP18 Antikörper)-mSin3 corepressor complex.
Differential Hh target gene regulation can be accomplished by differential sensitivity of Cos2 (zeige KIF7 Antikörper) and Su(Fu) to Hh.
Su(fu) protein levels and isoforms are crucial for the modulation of the different Ci states that control Hh target gene expression.
Sufu may act as a common regulator of Hh and Wnt (zeige WNT2 Antikörper) signaling and contribute to intertwining the two pathways.
Nek2A (zeige NEK2 Antikörper) is found to stabilize SuFu at least partly depending on its kinase activity, thereby triggering phosphorylation of the SuFu protein.
Extra-mitochondrial prosurvival BCL-2 (zeige BCL2 Antikörper) proteins regulate gene transcription by inhibiting the SUFU tumour suppressor.
Missense mutation in SUFU gene is associated with Joubert Syndrome with Cranio-facial and Skeletal Defects.
In conclusion, this study showed the potential of miR (zeige MLXIP Antikörper)-342-3p as a therapeutic target to promote bone regeneration by modulating expression of Sufu in UCMSCs.
miRNA-194 is oncogenic and promotes gastric cancer cell proliferation and migration by activating Wnt (zeige WNT2 Antikörper) signaling, at least in part, via suppression of SUFU.
SUFU's role in Hedgehog (zeige SHH Antikörper) signaling, tumor progression, and highlight a way in which BCCs can arise
In summary, these findings reveal Fbxl17 (zeige FBXL17 Antikörper) as a novel regulator of the Hedgehog (zeige SHH Antikörper) signaling pathway and highlight the perturbation of the Fbxl17 (zeige FBXL17 Antikörper)-Sufu axis in the pathogenesis of medulloblastoma.
there was a positive correlation between VDR (zeige CYP27B1 Antikörper) status and the expression of Suppressor of fused gene (SuFu), a hedgehog (zeige SHH Antikörper) pathway inhibitor. miR (zeige MLXIP Antikörper)-214 on the other hand suppressed SuFu protein expression.
The data indicate that there exists a novel transcript variant of SUFU which can be transcribed and translated into corresponding protein and its transcription is related with metastasis of lymph nodes in pancreatic ductal adenocarcinoma.
We showed that the supplementation of the osteogenic differentiation medium with PTHrP (zeige PTHLH Antikörper) inhibited the alkaline phosphatase activity and the expression of the transcription factor DLX3 (zeige DLX3 Antikörper), but the depletion of PTHrP (zeige PTHLH Antikörper) did not support the differentiation of DFCs.We showed that SUFU (Suppressor Of Fused Homolog) was not regulated during the osteogenic differentiation in DFCs
Through regulation of su(fu), miR (zeige MYLIP Antikörper)-214 enables precise specification of muscle cell types by sharpening cellular responses to Hedgehog (zeige SHH Antikörper).
tissue development is differentially affected in response to the reduced SUFU levels.
Suppressor of Fused restraint of Hedgehog (zeige SHH Antikörper) activity level is critical for osteogenic proliferation and differentiation during calvarial bone development
Sufu is upregulated in active Shh (zeige SHH Antikörper) responding tissues and accompanies Gli (zeige GLI1 Antikörper) activators translocating into and Gli (zeige GLI1 Antikörper) repressors out of the nucleus.
Sufu deletion early in embryogenesis resulted in unstable Gli2 (zeige GLI2 Antikörper) and Gli3 (zeige GLI3 Antikörper) activity, leading to the ectopic activation of Shh (zeige SHH Antikörper) signaling.
Thus, we provide evidence that Sufu is involved in the genetic network that restricts the posterior expression of Gli2 (zeige GLI2 Antikörper)/3/Hand2 (zeige HAND2 Antikörper) and Gremlin (zeige GREM1 Antikörper)/Fgf in limb bud patterning.
Results showed that the Thr396 residue of Sufu is specifically required for regulation of Gli3 (zeige GLI3 Antikörper) but not Gli2 (zeige GLI2 Antikörper) implying a novel Sufu-mediated mechanism in which Gli2 (zeige GLI2 Antikörper) activator and Gli3 (zeige GLI3 Antikörper) repressor are differentially regulated.
findings demonstrate that perturbations of Sufu and Kif7 (zeige KIF7 Antikörper) affect Gli (zeige GLI1 Antikörper) activity and recapitulate the full spectrum of vertebrate limb defects, ranging from severe truncation to polydactyly.
Hh signaling results in reduced Sufu protein levels and Sufu dissociation from Gli (zeige GLI1 Antikörper) proteins in the nucleus, highlighting critical functions of Sufu in the nucleus.
Data suggest nuclear entry of GLI1 (glioma-associated oncogene homolog (zeige GLI1 Antikörper), a zinc finger protein) is regulated by unique mechanism via mutually exclusive binding by its nuclear import factor IMB1 (zeige KPNB1 Antikörper) (importin B1) and SuFu (suppressor of fused protein).
The Hedgehog signaling pathway plays an important role in early human development. The pathway is a signaling cascade that plays a role in pattern formation and cellular proliferation during development. This gene encodes a negative regulator of the hedgehog signaling pathway. Defects in this gene are a cause of medulloblastoma. Alternative splicing results in multiple transcript variants.
, suppressor of fused
, suppressor of fused homolog