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SHH can promote cell growth and cell osteoblastic/cementoblastic differentiation via BMP pathway
These studies reveal a postnatal cell population with transient Shh signaling that contributes to oligodendrogenesis during corpus callosum myelination, and gives rise to cells that continue to proliferate in adulthood and contribute to corpus callosum remyelination
These results support a model whereby mutations in Cdon (show CDON Proteins) and prenatal ethanol exposure increase Septo-optic dysplasia risk through spatiotemporal perturbations in Shh signaling activity.
Results report the identification of a novel long-range enhancer for Shh-Shh-brain-enhancer-6 (SBE6)-that is located 100 kb upstream of Shh and that is required for the proper induction of Shh expression during this differentiation program.
neuroectodermal Shh expression, dorsal/ventral patterning, and amount of proliferation in the ventral neuroectoderm was not changed in Wnt1 (show WNT1 Proteins)-Cre;Kif3a (show KIF3A Proteins)(fl/fl (show FLT3LG Proteins)) mutants; however, tissue polarity and directional cell division were disrupted.
The authors find that cholesterol, an important component of the cell membrane, directly binds to Smoothened and changes its shape so that it can activate Hedgehog signaling components inside cells.
Embryonal tumors with multilayered rosettes (ETMRs) are characterized by a parallel activation of Shh and Wnt (show WNT2 Proteins) signaling. Co-activation of these pathways in mouse neural precursors is sufficient to induce ETMR-like tumors in vivo that resemble their human counterparts on the basis of histology and global gene-expression analyses, and that point to apical radial glia cells as the possible tumor cell of origin.
reactivating SHH signaling in mutant lungs rescued the tip dilation phenotype and attenuated FGF signaling. Importantly, the reduced SHH signaling activity did not appear to be caused by decreased Shh expression or protein stability; instead, biologically active form of SHH proteins were reduced in both the Ext1 (show EXT1 Proteins) mutant epithelium and surrounding wild type mesenchymal cells.
provide compelling evidence that epidermal YAP (show YAP1 Proteins) and Hedgehog/GLI2 signalling undergo positive regulatory interactions in the control of normal epidermal homeostasis and in basal cell carcinoma (BCC) development, which in the large majority of cases is caused by aberrant Hedgehog signalling activity
conditional deletion of Shh in the anterior hypothalamus results in a fully penetrant phenotype characterised by a complete arrest of (Rathke's pouch) RP development, with lack of Lhx3 (show LHX3 Proteins)/Lhx4 (show LHX4 Proteins) expression in RP epithelium.
Findings suggest that oral squamous cell carcinoma (OSCC)derived sonic hedgehog protein (SHH) stimulates angiogenesis at the tumor invasive front.
Expression of SHH and GLI1 (show GLI1 Proteins) may be useful prognostic markers of Merkel cell carcinoma because increased expression was associated with better prognosis.
High SHH expression is associated with esophageal squamous cell carcinoma.
Studies suggest significance of other signaling aside from hedgehog in the pathogenesis of basal cell carcinoma (BCC) of the skin.
Gorlin syndrome-derived induced pluripotent stem cells (iPSCs) expressed lower basal levels than control iPSCs of the genes encoding the Hh ligands Indian Hedgehog (IHH (show IHH Proteins)) and Sonic Hedgehog (SHH).
SHH activation is associated with Rhabdomyosarcoma.
Studies suggest that embryonic signaling pathways, the likes of Notch (show NOTCH1 Proteins), Wnt (show WNT2 Proteins), and Hedgehog and tumor marker Oct-4 (show POU5F1 Proteins) offer targets for cascade-specific molecular inhibition as they are fundamental to (cancer and normal) stem cell maintenance and growth.
Methylation at K436 and K595 respectively by Set7 (show SETD7 Proteins) increases the stability and DNA binding ability of Gli3 (show GLI3 Proteins), resulting in an enhancement of Shh signaling activation.
Altogether, these data suggested that curcumin inhibited the activities of BCSCs through suppressing Shh pathway, which might be an effective chemopreventive agent for bladder cancer intervention.
Data indicate that sonic hedgehog is expressed exclusively in the notochord but not in the spinal cord of the regenerate.
Dzip1 (show DZIP1 Proteins)-dependent stabilization of Spop (show SPOP Proteins)/HIB is evolutionarily conserved and essential for proper regulation of Gli (show GLI1 Proteins)/Ci proteins in the Hh pathway.
Notch (show NOTCH1 Proteins) signaling promotes floor plate and hypochord fates over notochord, but has variable effects on Shh expression in the midline.
These results indicate that electrical activity and second-messenger signaling mediate Shh action in embryonic spinal neurons.
Connective tissue-specific expression of BMP-4 (show BMP4 Proteins) mRNA is up-regulated by sonic hedgehog.
In an examination of signaling pathways in developing Xenopus lung, shh but not ihh (show IHH Proteins) was expressed in the very anterior part of early lung epithelium.
Data propose that Shh serves as a ventral optic tract repellent that helps to define the caudal boundary for retinal axons in the diencephalon, and that this signaling is also required for initial target recognition at the optic tectum.
The forebrain of Xenopus revealed a largely conserved pattern of Shh expression among tetrapods.
Hedgehog regulates superficial slow muscle fibres in Xenopus and tetrapod trunk myogenesis
Results suggest that 7-dehydrocholesterol reductase (show DHCR7 Proteins) and Sonic Hedgehog are co-expressed during midline development in Xenopus embryos
study shows evolutionary alteration of a Ptch1 (show PTCH1 Proteins) cis (show CISH Proteins)-regulatory module, which no longer responds to graded SHH signalling during bovine handplate development
Mutation of hmgcs1 (show HMGCS1 Proteins) had no effect on Shh signaling at 2 and 3 days post fertilization (dpf), but did result in a decrease in the expression of gli1 (show GLI1 Proteins), a known Shh target gene, at 4 dpf, after morphological deficits in craniofacial development and chondrocyte differentiation were observed in hmgcs1 (show HMGCS1 Proteins) mutants.
Shha/Smo is functionally dedicated to ray branching during fin regeneration.
Shh and Rx3 govern formation of a distinct progenitor domain that elaborates patterning through its anisotropic growth and differentiation.
Time-lapse imaging revealed that knockdown of miR (show MYLIP Proteins)-219 function accelerates the growth of primary cilia, revealing a possible mechanistic link between miR (show MYLIP Proteins)-219-mediated regulation of apical Par (show AFG3L2 Proteins) proteins and Shh signaling.
Shh is not essential for the early activation of has2 (show HAS2 Proteins), but supports proper chondrogenic differentiation.
Opposing Shh and Fgf signals initiate nasotemporal patterning of the zebrafish retina.
Hedgehog signaling has a role in dental papilla formation and tooth size during zebrafish odontogenesis
Data indicate that the transgenic lines report Hedgehog pathway state in individual cells and with high sensitivity.
We further demonstrate that the elevated Hedgehog signaling in Sox11 (show SOX11 Proteins)-deficient zebrafish was caused by a large increase in shha transcription; indeed, suppressing Shha expression rescued the ocular phenotypes of sox11 (show SOX11 Proteins) morphants.
Pax6 (show PAX6 Proteins) has an evolutionarily conserved function in establishing the temporospatial expression of Shh in the mid-diencephalic organizer in vertebrates.
This gene encodes a protein that is instrumental in patterning the early embryo. It has been implicated as the key inductive signal in patterning of the ventral neural tube, the anterior-posterior limb axis, and the ventral somites. Of three human proteins showing sequence and functional similarity to the sonic hedgehog protein of Drosophila, this protein is the most similar. The protein is made as a precursor that is autocatalytically cleaved\; the N-terminal portion is soluble and contains the signalling activity while the C-terminal portion is involved in precursor processing. More importantly, the C-terminal product covalently attaches a cholesterol moiety to the N-terminal product, restricting the N-terminal product to the cell surface and preventing it from freely diffusing throughout the developing embryo. Defects in this protein or in its signalling pathway are a cause of holoprosencephaly (HPE), a disorder in which the developing forebrain fails to correctly separate into right and left hemispheres. HPE is manifested by facial deformities. It is also thought that mutations in this gene or in its signalling pathway may be responsible for VACTERL syndrome, which is characterized by vertebral defects, anal atresia, tracheoesophageal fistula with esophageal atresia, radial and renal dysplasia, cardiac anomalies, and limb abnormalities. Additionally, mutations in a long range enhancer located approximately 1 megabase upstream of this gene disrupt limb patterning and can result in preaxial polydactyly.
sonic hedgehog protein
, sonic hedgehog
, hemimelic extra toes
, short digits
, sonic hedgehog homolog
, sonic hedgehog protein A