protein
| binding to CREBBP with SHH to regulate many processes in cells |
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bind to ZIC3 through the GLI consensus binding site (GLIBS) |
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Zic |
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Ski |
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betaTrCP |
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MED12 |
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KIF7 |
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SUFU |
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PIAS1-dependent SUMOylation influences GLI1, GLI2, GLI3 protein activity and thereby identifies SUMOylation as a post-translational mechanism that regulates the hedgehog signaling pathway |
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IFT122 leads to accumulation of GLI2 and GLI3 at cilia tips while blocking the ciliary localization of the antagonist TULP3 |
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unappreciated function of HOXD13 in regulating digit number through its interaction with GLI3 |
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potentially, upon Hedgehog input, GLI1 functions collectively with GLI2 and GLI3 in osteogenesis |
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TMEM107 acts in combination with GLI2 and GLI3 to pattern ventral and intermediate neuronal cell types |
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EVC2 promotes recruitment of GLI3 to the tips of cilia |
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role for enzymatically active CDK8 in suppression of GLI3 transactivation activity |
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enzymatically active CDK8 is responsible for suppression of GLI3 transactivation activity, and further, MED12 most likely contributes to this suppression through its role as an anchor for CDK8 in Mediator |
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PKDCC and GlI3 synergize to control the temporal kinetics of chondrocyte differentiation during long bone development |
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PKDCC and GLI3 cooperate to regulate long bone development by modulating the temporal kinetics of establishing columnar and hypertrophic chondrocyte domains |
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DZIP1 interacts with GLI3, a transcriptional regulator for Hedgehog signaling, and prevents GLI3 from entering the nucleus |
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SOST and its paralog SOSTDC1 coordinate digit number in a GLI3-dependent manner |
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STK36 ubiquitination and cleavage is one of the key elements connecting the MID1-PPP2CA protein complex with GLI3 activity control |
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GLI1, GLI2, GLI3 interacts synergistically with KIFAP3 and KIF3A |
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activated NOTCH1 leads to pronounced accumulation of SMO within primary cilia and elevated levels of full-length GLI3 |
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SPOP targets GLI2 and GLI3 for degradation and negatively regulates Hedgehog (Hh) signaling |
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SUFU controls cerebellar neuronal differentiation in a manner modulated by GLI3 repressor and FGF19 |
| Shh(-/-) Gli3(-/-) limbs are distally complete and polydactylous, but completely lack wild-type digit identities | |
Gli3-mutant mice displayed a central polydactyly, a wide range of developmental abnormalities encompassing almost all of the common PHS features, including imperforate anus, gastrointestinal, epiglottis and larynx defects, abnormal kidney development, and absence of adrenal glands |
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Gli3Xt-J/Xt-J mice, which represent a Gli3-null allele, exhibit craniosynostosis of the lambdoid sutures accompanied by increased osteoprogenitor proliferation and differentiation |