{Models}
| Symbol: {Links}
|
Flybase ID: {Flybase_ID} |
| Synonyms: {Name}
|
{GadFly} |
| Function: {Short_Function} |
{LocusLink} |
| Keywords: {Keywords} |
{Interactive_Fly} |
{Summary}
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- Mediation of Sonic Hedgehog–Induced Expression of COUP-TFII by
a Protein Phosphatase (Krishnan et al., 1997)
- They indicate that there is a different transcription factor other
than Gli that binds to their Shh dependent element.
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- ShhN internalized by Ptc1 accumulated to much higher levels with leupeptin
treatment (Incardona,
2002), consistent with observations on endogenous Shh in embryonic
neural tissue (Incardona, 2000)
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- Shh upregulates hptc and Gli1
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- In the absenceof leupeptin, the small amount of internalized
ShhN detected was localized to LBPA+ late endosomes, and,
in the presence of leupeptin, ShhN and Ptc1 accumulated highly in LAMP-1+
vesicles.
- Double labeling for Ptc1 and LBPA was precluded by a requirement for
Triton X-100 permeabilization to expose Ptc1HA immunoreactivity, which
extracts LBPA. Concanamycin A treatment resulted in the accumulation
of Ptc1 and ShhN in transferrin early endosomes, and ShhN did not colocalize
with LBPA. Ptc1+ early endosomes appeared with similar kinetics
(data not shown) and degree with or without ligand, indicating that
Ptc1 reaches endosomes from the cell surface rather than by another
route. (Incardona,
2002)
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