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A Comparison of Ci/Gli (show GLI1 ELISA Kits) Activity as Regulated by Sufu in Drosophila and Mammalian Hedgehog (show SHH ELISA Kits) Response
Sufu can sequester Ci/Gli (show GLI1 ELISA Kits) in the cytoplasm through binding to an N-terminal site while inhibiting Ci/Gli (show GLI1 ELISA Kits) activity in the nucleus depending on a C-terminal Sufu-interacting site.
Drosophila Hedgehog (show SHH ELISA Kits) 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 (show GLI1 ELISA Kits) binding and inhibited by Hh treatment, whereas the 'open' state of Sufu is promoted by Gli (show GLI1 ELISA Kits)-dissociation and Hh signaling.
Su(fu) causes the Rdx (show RDX ELISA Kits) switch between two mchanisms of Cubitus interruptus regulation.
Suppressor of Fused represses Gli (show GLI1 ELISA Kits)-mediated transcription by recruiting the SAP18 (show SAP18 ELISA Kits)-mSin3 corepressor complex.
Differential Hh target gene regulation can be accomplished by differential sensitivity of Cos2 (show KIF7 ELISA Kits) 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 (show WNT2 ELISA Kits) signaling and contribute to intertwining the two pathways.
Extra-mitochondrial prosurvival BCL-2 (show BCL2 ELISA Kits) 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 (show MLXIP ELISA Kits)-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 (show WNT2 ELISA Kits) signaling, at least in part, via suppression of SUFU.
SUFU's role in Hedgehog (show SHH ELISA Kits) signaling, tumor progression, and highlight a way in which BCCs can arise
In summary, these findings reveal Fbxl17 (show FBXL17 ELISA Kits) as a novel regulator of the Hedgehog (show SHH ELISA Kits) signaling pathway and highlight the perturbation of the Fbxl17 (show FBXL17 ELISA Kits)-Sufu axis in the pathogenesis of medulloblastoma.
there was a positive correlation between VDR (show CYP27B1 ELISA Kits) status and the expression of Suppressor of fused gene (SuFu), a hedgehog (show SHH ELISA Kits) pathway inhibitor. miR (show MLXIP ELISA Kits)-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 (show PTHLH ELISA Kits) inhibited the alkaline phosphatase activity and the expression of the transcription factor DLX3 (show DLX3 ELISA Kits), but the depletion of PTHrP (show PTHLH ELISA Kits) 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 (show MLXIP ELISA Kits)-214-Sufu pathway in controlling EMT (show ITK ELISA Kits) and metastasis of lung adenocarcinoma.
Through regulation of su(fu), miR (show MYLIP ELISA Kits)-214 enables precise specification of muscle cell types by sharpening cellular responses to Hedgehog (show SHH ELISA Kits).
tissue development is differentially affected in response to the reduced SUFU levels.
Suppressor of Fused restraint of Hedgehog (show SHH ELISA Kits) activity level is critical for osteogenic proliferation and differentiation during calvarial bone development
Sufu is upregulated in active Shh (show SHH ELISA Kits) responding tissues and accompanies Gli (show GLI1 ELISA Kits) activators translocating into and Gli (show GLI1 ELISA Kits) repressors out of the nucleus.
Sufu deletion early in embryogenesis resulted in unstable Gli2 (show GLI2 ELISA Kits) and Gli3 (show GLI3 ELISA Kits) activity, leading to the ectopic activation of Shh (show SHH ELISA Kits) signaling.
Thus, we provide evidence that Sufu is involved in the genetic network that restricts the posterior expression of Gli2 (show GLI2 ELISA Kits)/3/Hand2 (show HAND2 ELISA Kits) and Gremlin (show GREM1 ELISA Kits)/Fgf in limb bud patterning.
Results showed that the Thr396 residue of Sufu is specifically required for regulation of Gli3 (show GLI3 ELISA Kits) but not Gli2 (show GLI2 ELISA Kits) implying a novel Sufu-mediated mechanism in which Gli2 (show GLI2 ELISA Kits) activator and Gli3 (show GLI3 ELISA Kits) repressor are differentially regulated.
findings demonstrate that perturbations of Sufu and Kif7 (show KIF7 ELISA Kits) affect Gli (show GLI1 ELISA Kits) 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 (show GLI1 ELISA Kits) proteins in the nucleus, highlighting critical functions of Sufu in the nucleus.
Data suggest nuclear entry of GLI1 (glioma-associated oncogene homolog (show GLI1 ELISA Kits), a zinc finger protein) is regulated by unique mechanism via mutually exclusive binding by its nuclear import factor IMB1 (show KPNB1 ELISA Kits) (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