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anti-Human 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 Activity as Regulated by Sufu in Drosophila and Mammalian Hedgehog Response
Sufu can sequester Ci/Gli in the cytoplasm through binding to an N-terminal site while inhibiting Ci/Gli activity in the nucleus depending on a C-terminal Sufu-interacting site.
Drosophila Hedgehog 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 binding and inhibited by Hh treatment, whereas the 'open' state of Sufu is promoted by Gli-dissociation and Hh signaling.
Su(fu) causes the Rdx switch between two mchanisms of Cubitus interruptus regulation.
Suppressor of Fused represses Gli-mediated transcription by recruiting the SAP18-mSin3 corepressor complex.
Differential Hh target gene regulation can be accomplished by differential sensitivity of Cos2 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.
This protein, a component of the Ci signaling complex, functions to block nuclear import of Ci.
Sufu may act as a common regulator of Hh and Wnt signaling and contribute to intertwining the two pathways.
Germline SUFU mutations are associated with medulloblastoma.
establishes the dual role of SUFU inSonic Hedgehog medulloblastoma (MB) and provides mechanistic insights into transcriptional regulation underlying Gli2-mediated SHH MB tumorigenesis
MiR-423-5p enriched exosomes could be internalized into gastric cancer cells, which enhanced cell proliferation and migration both in vitro and in vivo. Mechanistically, miR-423-5p inhibited the expression of suppressor of fused protein (SUFU) to enhance the proliferation and migration of gastric cancer cells. The expression levels of SUFU were significantly decreased in gastric cancer cells and the tumor tissues.
A novel SUFU splice site deleterious genetic variant in cutaneous cancer predisposition syndrome.
miR-194 was highly expressed in gastric cancer (GC) tissues, whereas SUFU was downregulated in GC tissues and cell lines, thus suggesting that miR-194 may be a carcinogenic miRNA, whereas SUFU may act as a tumor suppressor.
Down-regulation of microRNA-224 inhibits growth and epithelial-to-mesenchymal transition phenotype via modulating SUFU expression in bladder cancer cells.
Itch/beta-arrestin2 complex binds SuFu and induces its Lys63-linked polyubiquitylation without affecting its stability.
Patients with SUFU pathogenic variants were significantly more likely to develop a medulloblastoma, a meningioma or an ovarian fibroma, but were less likely to develop a jaw cyst.
Nek2A 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 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-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 signaling, at least in part, via suppression of SUFU.
SUFU's role in Hedgehog signaling, tumor progression, and highlight a way in which BCCs can arise
In summary, these findings reveal Fbxl17 as a novel regulator of the Hedgehog signaling pathway and highlight the perturbation of the Fbxl17-Sufu axis in the pathogenesis of medulloblastoma.
there was a positive correlation between VDR status and the expression of Suppressor of fused gene (SuFu), a hedgehog pathway inhibitor. miR-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 inhibited the alkaline phosphatase activity and the expression of the transcription factor DLX3, but the depletion of PTHrP did not support the differentiation of DFCs.We showed that SUFU (Suppressor Of Fused Homolog) was not regulated during the osteogenic differentiation in DFCs
This study uncovers a previously unappreciated miR-214-Sufu pathway in controlling EMT and metastasis of lung adenocarcinoma.
A germline SUFU mutation was present in a patient with MHIBCC, and additional acquired SUFU mutations underlie the development of infundibulocystic basal cell carcinomas
Through regulation of su(fu), miR-214 enables precise specification of muscle cell types by sharpening cellular responses to Hedgehog.
Study found that miR-423 targets the 3'-untranslated region (UTR) of Sufu, and the expression of Sufu can be inhibited by the overexpression of miR-423, indicating that Sufu could be the target of miR-423.
Together, our results show that SuFu promotes cerebellar radial precursor differentiation to neurons. SuFu function is mediated in part by GLI3R and down-regulation of Fgf15 expression.
beta-Arrestin2 increases the Itch-mediated ubiquitylation of SuFu.
tissue development is differentially affected in response to the reduced SUFU levels.
Suppressor of Fused restraint of Hedgehog activity level is critical for osteogenic proliferation and differentiation during calvarial bone development
Sufu is upregulated in active Shh responding tissues and accompanies Gli activators translocating into and Gli repressors out of the nucleus.
Sufu deletion early in embryogenesis resulted in unstable Gli2 and Gli3 activity, leading to the ectopic activation of Shh signaling.
Thus, we provide evidence that Sufu is involved in the genetic network that restricts the posterior expression of Gli2/3/Hand2 and Gremlin/Fgf in limb bud patterning.
Results showed that the Thr396 residue of Sufu is specifically required for regulation of Gli3 but not Gli2 implying a novel Sufu-mediated mechanism in which Gli2 activator and Gli3 repressor are differentially regulated.
findings demonstrate that perturbations of Sufu and Kif7 affect Gli 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 proteins in the nucleus, highlighting critical functions of Sufu in the nucleus.
Data suggest nuclear entry of GLI1 (glioma-associated oncogene homolog, a zinc finger protein) is regulated by unique mechanism via mutually exclusive binding by its nuclear import factor IMB1 (importin B1) and SuFu (suppressor of fused protein).
Differential regulation of Gli proteins by Sufu in the lung affects PDGF signaling and myofibroblast development.
Evc silencing in Sufu(-/-) cells attenuated the output of the Hh pathway, suggesting that Evc/Evc2 also promote Hh signaling in the absence of Sufu
Sufu acts universally as a negative regulator of Hedgehog signaling.
These studies establish Sufu and Kif7 as crucial components in the regulation of Gli2 localization and activity, and illustrate their overlapping functions in skin development and tumor suppression.
Pthlh regulates chondrocyte differentiation and Gli activity in a Sufu-dependent manner, with Sufu acting as a molecular switch in its regulation of differentiation.
mechanism of action on Hedgehog signaling by a suppressor of fused carboxy terminal variant
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