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GLI family zinc finger 3

This gene encodes a protein which belongs to the C2H2-type zinc finger proteins subclass of the Gli family. They are characterized as DNA-binding transcription factors and are mediators of Sonic hedgehog (Shh) signaling. The protein encoded by this gene localizes in the cytoplasm and activates patched Drosophila homolog (PTCH) gene expression. It is also thought to play a role during embryogenesis. Mutations in this gene have been associated with several diseases, including Greig cephalopolysyndactyly syndrome, Pallister-Hall syndrome, preaxial polydactyly type IV, and postaxial polydactyly types A1 and B. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: CAN, ACID, HAD, Gli, Shh
Papers using Gli3 antibodies
Getting more from less: algorithms for rapid protein identification with multiple short peptide sequences
Grzeschik Karl-Heinz et al., In BMC Developmental Biology, 2001
... GLI3 Selected for Functional Analysis in Transgenic mice assay.
Papers on Gli3
Evaluating a 4-marker signature of aggressive prostate cancer using time-dependent AUC.
Mucci et al., Boston, United States. In Prostate, 31 Dec 2015
METHODS: Using data from the initial study, we fit survival models for men with prostate cancer who were participants in the Physicians' Health Study (PHS; n = 276).
GLI3 mutations in syndromic and non-syndromic polydactyly in two Indian families.
Ali et al., Benares, India. In Congenit Anom (kyoto), 27 Nov 2015
The present study reports two cases: first, a familial case of Greig Cephalopolysyndactyly Syndrome (GCPS); second one is a sporadic case with both postaxial polydactyly (PAP) type A and B. Resequencing of GLI3 gene reveals a previously reported nonsense truncation mutation g.42007251G>A (p.R792X; rs121917714) in the GCPS family and a novel single nucleotide insertion g.42004239_42004240insA (p.E1478X) in the sporadic case of postaxial polydactyly (PAP).
PLANT VOLATILES. Biosynthesis of monoterpene scent compounds in roses.
Baudino et al., Saint-Étienne, France. In Science, Aug 2015
Monoterpenes represent up to 70% percent of the scent content in some cultivars, such as the Papa Meilland rose.
[Diagnosis and Clinical Examination of Autoinflammatory Syndrome].
Ida, In Rinsho Byori, May 2015
The main monogenic autoinflammatory syndromes are familial Mediterranean fever (FMF), TNF receptor-associated periodic syndrome (TRAPS), mevalonate kinase deficiency (MKD), cryopyrin-associated periodic syndrome (CAPS), Blau syndrome, and pyogenic arthritis, pyoderma gangrenosum, and acne (PAPA) syndrome.
Dinitrosyl iron complexes (DNICs): from biomimetic synthesis and spectroscopic characterization toward unveiling the biological and catalytic roles of DNICs.
Liaw et al., Taiwan. In Acc Chem Res, May 2015
In addition, Fe/S K-edge X-ray absorption spectroscopy of tetrahedral DNICs deduced the qualitative assignment of Fe/NO oxidation states of {Fe(NO)2}(9) DNICs as a resonance hybrid of {Fe(II)((•)NO)(NO(-))}(9) and {Fe(III)(NO(-))2}(9) electronic states; the quantitative NO oxidation states of [(PhS)3Fe(NO)](-), [(PhS)2Fe(NO)2](-), and [(PhO)2Fe(NO)2](-) were further achieved by newly developed valence to core Fe Kβ X-ray emission spectroscopy as -0.58 ± 0.18, -0.77 ± 0.18, and -0.95 ± 0.18, respectively.
A common immunopathogenesis mechanism for infectious diseases: the protein-homeostasis-system hypothesis.
Lee, Seoul, South Korea. In Infect Chemother, Mar 2015
The author proposes that this network is controlled by the protein homeostasis system (PHS), and that the immune system is one part of the PHS of the host.
The Hedgehog pathway as targetable vulnerability with 5-azacytidine in myelodysplastic syndrome and acute myeloid leukemia.
Bogenberger et al., Scottsdale, United States. In J Hematol Oncol, Dec 2014
Several genes within the hedgehog pathway (HhP), specifically SHH, SMO, and GLI3, were identified as 5-Aza sensitizing hits.
Pallister-Hall syndrome has gone the way of modern medical genetics.
Hall, In Am J Med Genet C Semin Med Genet, Dec 2014
Genotype/phenotype correlations have led to fine mapping of GLI3 and the recognition that PHS is caused by dominant negative mutations in the middle third of the gene.
Advances in the molecular genetics of non-syndromic polydactyly.
Yuan et al., Changsha, China. In Expert Rev Mol Med, Dec 2014
To date, in human, at least ten loci and four disease-causing genes, including the GLI3 gene, the ZNF141 gene, the MIPOL1 gene and the PITX1 gene, have been identified.
Context-dependent signal integration by the GLI code: the oncogenic load, pathways, modifiers and implications for cancer therapy.
Ruiz I Altaba et al., Salzburg, Austria. In Semin Cell Dev Biol, Sep 2014
In humans, the three GLI factors encode context-dependent activities with GLI1 being mostly an activator and GLI3 often a repressor.
Whole-genome sequencing and comprehensive molecular profiling identify new driver mutations in gastric cancer.
Leung et al., San Diego, United States. In Nat Genet, Jun 2014
We identified previously known (TP53, ARID1A and CDH1) and new (MUC6, CTNNA2, GLI3, RNF43 and others) significantly mutated driver genes.
Mutant PTEN in Cancer: Worse Than Nothing.
den Hertog et al., Utrecht, Netherlands. In Cell, May 2014
Papa et al.
[Sonic Hedgehog signaling pathway and regulation of inner ear development].
Cao et al., Nanjing, China. In Yi Chuan, 2013
In humans, diseases accompanied by hearing disorders caused by abnormal Shh signaling include Greig cephalopolysyndactyly syndrome (GCPS), Pallister-Hall syndrome (PHS), Waardenburg syndrome (WS) and medulloblastoma, etc.
Monogenic autoinflammatory syndromes: state of the art on genetic, clinical, and therapeutic issues.
Cantarini et al., Padova, Italy. In Int J Rheumatol, 2012
To date, there are twelve known MAISs: familial Mediterranean fever, tumor necrosis factor receptor-associated periodic syndrome, familial cold urticaria syndrome, Muckle-Wells syndrome, CINCA syndrome, mevalonate kinase deficiency, NLRP12-associated autoinflammatory disorder, Blau syndrome, early-onset sarcoidosis, PAPA syndrome, Majeed syndrome, and deficiency of the interleukin-1 receptor antagonist.
Limb anterior-posterior polarity integrates activator and repressor functions of GLI2 as well as GLI3.
Joyner et al., New York City, United States. In Dev Biol, 2012
Establishment of a complete range of anterior-posterior positional identities in the embryonic limb requires integration of the spatial distribution, timing, and dosage of GLI2 and GLI3 activators and repressors.
Forward genetics uncovers Transmembrane protein 107 as a novel factor required for ciliogenesis and Sonic hedgehog signaling.
Weatherbee et al., New Haven, United States. In Dev Biol, 2012
Data show that Transmembrane protein 107 (Tmem107) is required for normal Sonic hedgehog (Shh) signaling in the neural tube and acts in combination with Gli2 and Gli3 to pattern ventral and intermediate neuronal cell types.
Novel AKT1-GLI3-VMP1 pathway mediates KRAS oncogene-induced autophagy in cancer cells.
Fernandez-Zapico et al., Rochester, United States. In J Biol Chem, 2012
AKT1-GLI3-VMP1 pathway mediates KRAS oncogene-induced autophagy in cancer cells.
Prevention of premature fusion of calvarial suture in GLI-Kruppel family member 3 (Gli3)-deficient mice by removing one allele of Runt-related transcription factor 2 (Runx2).
Rice et al., Helsinki, Finland. In J Biol Chem, 2012
a novel role for Gli3 in regulating calvarial suture development by controlling canonical Bmp-Smad signaling, which integrates a Dlx5/Runx2-II cascade
[Possible role of GLI3 gene in the pathogenesis of idiopathic congenital talipes equinovarus].
Jin et al., Shenyang, China. In Zhonghua Yi Xue Yi Chuan Xue Za Zhi, 2012
No expression of GLI3 gene was detected in the flexor hallucis longus of ICTEV patients or normal controls.
KIF7 mutations cause fetal hydrolethalus and acrocallosal syndromes.
Attié-Bitach et al., Paris, France. In Nat Genet, 2011
Consistent with a role of KIF7 in Hedgehog signaling, we show deregulation of most GLI transcription factor targets and impaired GLI3 processing in tissues from individuals with KIF7 mutations.
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