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GLIS family zinc finger 2

NKL, GLIS2
This gene is a member of the GLI-similar zinc finger protein family and encodes a nuclear transcription factor with five C2H2-type zinc finger domains. The protein encoded by this gene is widely expressed at low levels in the neural tube and peripheral nervous system and likely promotes neuronal differentiation. It is abundantly expressed in the kidney and may have a role in the regulation of kidney morphogenesis. p120 regulates the expression level of this protein and induces the cleavage of this protein's C-terminal zinc finger domain. This protein also promotes the nuclear translocation of p120. Mutations in this gene cause nephronophthisis (NPHP), an autosomal recessive kidney disease characterized by tubular basement membrane disruption, interstitial lymphohistiocytic cell infiltration, and development of cysts at the corticomedullary border of the kidneys.[provided by RefSeq, Jan 2010] (from NCBI)
Top mentioned proteins: CAN, NKG2D, Interleukin-2, MHC, OUT
Papers using NKL antibodies
Confined lateral diffusion of membrane receptors as studied by single particle tracking (nanovid microscopy). Effects of calcium-induced differentiation in cultured epithelial cells.
Supplier
Pockley Graham, In PLoS ONE, 1992
... NKL cells were pre-incubated with the following inhibitors for 30 min at 37°C, where indicated: 0.5 and 10 µM Latrunculin B (BIOMOL International L.P, Plymouth Meeting, ...
Papers on NKL
TSC-22 Promotes Interleukin-2-Deprivation Induced Apoptosis in T-Lymphocytes.
New
Biola-Vidamment et al., Châtenay-Malabry, France. In J Cell Biochem, Feb 2016
In the human NKL cell line deprived of IL-2, TSC-22 showed the same effect and thus may represent a potent repressor of GILZ expression in IL-2-dependent cells, independently of the cell type or the stimulus, leading to an increase of IL-2-deprived T-cells apoptosis.
Sphingosine kinase inhibitors decrease viability and induce cell death in natural killer-large granular lymphocyte leukemia.
New
Loughran et al., State College, United States. In Cancer Biol Ther, Jan 2016
SKI-II and SKI-178 restored the sphingolipid balance by increasing ceramide and decreasing S1P in leukemic NKL cells.
NK Cell Proliferation Induced by IL-15 Transpresentation Is Negatively Regulated by Inhibitory Receptors.
New
Long et al., Rockville, United States. In J Immunol, Dec 2015
Similarly, proliferation of the NKG2A(+) cell line NKL induced by IL-15 transpresentation was inhibited by HLA-E.
The C175R mutation alters nuclear localization and transcriptional activity of the nephronophthisis NPHP7 gene product.
New
Walz et al., Freiburg, Germany. In Eur J Hum Genet, Oct 2015
The zinc-finger protein GLIS2/NPHP7 represents an exception as it has been implicated in transcriptional regulation; only two families with GLIS2/NPHP7 mutations and typical NPH manifestations have been identified so far.
The biology of pediatric acute megakaryoblastic leukemia.
Review
New
Downing et al., Memphis, United States. In Blood, Sep 2015
CBFA2T3-GLIS2 is the most frequent chimeric oncogene identified to date in this subset of patients and confers a poor prognosis.
CAR-Engineered NK Cells Targeting Wild-Type EGFR and EGFRvIII Enhance Killing of Glioblastoma and Patient-Derived Glioblastoma Stem Cells.
Yu et al., Columbus, United States. In Sci Rep, 2014
We transduced human NK cell lines NK-92 and NKL, and primary NK cells with a lentiviral construct harboring a second generation CAR targeting both wtEGFR and EGFRvIII and evaluated the anti-GB efficacy of EGFR-CAR-modified NK cells.
Novel Human Embryonic Stem Cell Regulators Identified by Conserved and Distinct CpG Island Methylation State.
De Sousa et al., Edinburgh, United Kingdom. In Plos One, 2014
Knockdown of candidate transcriptional regulators (HMGA1, GLIS2, PFDN5) induced differentiation in hESCs, whereas ectopic expression in fibroblasts modulated iPSC colony formation.
Interferon-β Modulates the Innate Immune Response against Glioblastoma Initiating Cells.
Eisele et al., Zürich, Switzerland. In Plos One, 2014
In 3 out of 5 GIC lines tested we found a net immune stimulating effect of IFN-β in cytotoxicity assays using NKL cells as effectors.
The Genetic Deletion of 6q21 and PRDM1 and Clinical Implications in Extranodal NK/T Cell Lymphoma, Nasal Type.
Li et al., Beijing, China. In Biomed Res Int, 2014
Similarly, heterozygous codeletion of 6q21 and PRDM1 was identified in NK92 and NKL cells.
An Inv(16)(p13.3q24.3)-encoded CBFA2T3-GLIS2 fusion protein defines an aggressive subtype of pediatric acute megakaryoblastic leukemia.
Impact
Downing et al., Memphis, United States. In Cancer Cell, 2012
Our analysis identified a cryptic chromosome 16 inversion (inv(16)(p13.3q24.3)) in 27% of pediatric cases, which encodes a CBFA2T3-GLIS2 fusion protein.
NKL homeobox genes in leukemia.
Review
Meijerink et al., Rotterdam, Netherlands. In Leukemia, 2012
NK-like (NKL) homeobox genes code for transcription factors, which can act as key regulators in fundamental cellular processes.
Identification of nuclear localization, DNA binding, and transactivating mechanisms of Kruppel-like zinc finger protein Gli-similar 2 (Glis2).
GeneRIF
Jetten et al., United States. In J Biol Chem, 2011
Glis2 can function as a transcriptional activator and that post-translational modification within its DNA-binding domain can regulate its transcriptional activity
Gli-similar (Glis) Krüppel-like zinc finger proteins: insights into their physiological functions and critical roles in neonatal diabetes and cystic renal disease.
Review
Jetten et al., United States. In Histol Histopathol, 2010
Mutations in GLIS2 have been linked to nephronophthisis, an autosomal recessive cystic kidney disease.
Kruppel-like zinc finger protein Glis2 is essential for the maintenance of normal renal functions.
GeneRIF
Jetten et al., United States. In Mol Cell Biol, 2008
Deficiency in Glis2 expression leads to tubular atrophy & progressive fibrosis, similar to nephronophthisis, that ultimately results in renal failure. Glis2 plays a critical role in the maintenance of normal kidney architecture and functions.
Loss of GLIS2 causes nephronophthisis in humans and mice by increased apoptosis and fibrosis.
Impact
GeneRIF
Treier et al., Ann Arbor, United States. In Nat Genet, 2007
Study identified Glis2 as a transcription factor mutated in Nephronophthisis and demonstrate its essential role for the maintenance of renal tissue architecture through prevention of apoptosis and fibrosis.
The transcriptional repressor Glis2 is a novel binding partner for p120 catenin.
GeneRIF
Fujita et al., London, United Kingdom. In Mol Biol Cell, 2007
identification of Gli-similar 2 (Glis2) as a novel binding protein for p120 catenin
The Krüppel-like zinc finger protein Glis2 functions as a negative modulator of the Wnt/beta-catenin signaling pathway.
GeneRIF
Jetten et al., United States. In Febs Lett, 2007
Glis2 functions as a negative modulator of beta-catenin/TCF-mediated transcription.
Hmx homeobox gene function in inner ear and nervous system cell-type specification and development.
Review
Lufkin et al., New York City, United States. In Exp Cell Res, 2005
The Hmx homeobox gene family is comprised of three members in mammals, Hmx1, Hmx2, and Hmx3, which are conserved across the animal kingdom and are part of the larger NKL clustered family of homeobox genes.
Beyond the Hox: how widespread is homeobox gene clustering?
Review
Holland, Reading, United Kingdom. In J Anat, 2001
Contrary to this view, however, two clusters of non-Hox homeobox genes have been reported: the amphioxus ParaHox gene cluster and the Drosophila 93D/E cluster (referred to here as the NKL cluster).
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