Mouse Gli1 mutants are viable but have defects in SHH signaling in combination with a Gli2 mutation.

By H. Park, C. Bai, K. Platt, M. Matise, A. Beeghly, C. Hui, M. Nakashima, Alexandra L. Joyner. Development, 2000

766 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/af3346b3fcabaa7a6175afee2378cca75fc903a5

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Citations in the corpus

The Hedgehog and Wnt signalling pathways in cancer (2001, background): “For example, the transcriptional regulatory functions of Ci seem to be executed by Gli3, primarily a repressor, and Gli1 and Gli2, primarily activator”
Chromatin Potential Identified by Shared Single-Cell Profiling of RNA and Chromatin (2020, background): “Interestingly, we also identified highly connected transcriptional repressors (TFs that negatively correlate with DORC activity levels), including Gli3 and Tcf12, associated with the Sonic hedgehog (Shh) signaling pathway (Park et al., 2000; Mill et al., 2003).”
Gli proteins in development and disease. (2011, background): “518 Control of Gli Transcription Factors at the Chromatin Level . . . . . . . . . 519 GLI PROTEIN MODIFICATION AND REGULATION. . . . . . . . . . . . . 520 Gli Repressor Is Generated by the Proteasome Through Partial Degradation . . . . . . . . . . . . . . . . . . . . 520 Control of Gli Activity by M”
Hedgehog signalling within airway epithelial progenitors and in small-cell lung cancer (2003, background): “We indeed observed that stable expression of a Flag-tagged Gli1 protei”
Gli2 and Gli3 Localize to Cilia and Require the Intraflagellar Transport Protein Polaris for Processing and Function (2005, background): “mice is sufficient to produce ectopic digits [10,11].”
Hedgehog signaling in animal development: paradigms and principles. (2001, background): “Gli1/Gli2 compound mutants are reported to have a similar phenotype to Gli2 mutants (Park and Bai 2000).”
Pattern formation in the vertebrate neural tube: a sonic hedgehog morphogen-regulated transcriptional network (2008, background): “This suggests that Gli2 is required to generate the highest Shh signaling response, consistent with the notion that Gli2 acts predominately as an activator (Ding et al., 1998; Matise et al., 1999; Park et al., 2000).”
Hedgehog Signaling in Development and Cancer (2008, unknown): “It is also worth noting that, while Gli1 and Gli2 are dispensable for digit patterning (Park et al., 2000), they may contribute to limb development in Gli3 P1-4/ D 699 mice.”
Gli2, but not Gli1, is required for initial Shh signaling and ectopic activation of the Shh pathway. (2002, methodology): “…Gli1zfd mutant mice are phenotypically normal, reducing the level of Gli2 in Gli1 homozygous mutant mice (Gli1zfd/zfd;Gli2zfd/+) results in multiple defects including a partial loss of the floor plate, failure of notochord regression, aberrant lung development and lethality (Park et al., 2000).”
Hedgehog: functions and mechanisms. (2008, background): “1998), GLI1 is dispensable for normal development (Park et al. 2000).”
Evidence for an expansion-based temporal Shh gradient in specifying vertebrate digit identities. (2004, background): “Thus, cells remember prior exposure to Shh. for normal limb morphogenesis (Park et al., 2000), theearly limb bud, including Ptc1 (Marigo et al., 1996a; Goodrich et al., 1996), Ptc2 (Pearse et al., 2001), Bmp2 functional significance of its downregulation in the pos- terior limb is unclear.”