Pages that link to "Q36690799"
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The following pages link to Four of the seven zinc fingers of the Evi-1 myeloid-transforming gene are required for sequence-specific binding to GA(C/T)AAGA(T/C)AAGATAA. (Q36690799):
Displayed 50 items.
- Phosphorylation of the leukemic oncoprotein EVI1 on serine 196 modulates DNA binding, transcriptional repression and transforming ability (Q21133010) (← links)
- Evi-1 transforming and repressor activities are mediated by CtBP co-repressor proteins (Q24291175) (← links)
- A novel EVI1 gene family, MEL1, lacking a PR domain (MEL1S) is expressed mainly in t(1;3)(p36;q21)-positive AML and blocks G-CSF-induced myeloid differentiation (Q24305753) (← links)
- Sequence-specific transcriptional repression by an MBD2-interacting zinc finger protein MIZF (Q24306708) (← links)
- Pbx1 is a downstream target of Evi-1 in hematopoietic stem/progenitors and leukemic cells (Q24317653) (← links)
- Staf, a novel zinc finger protein that activates the RNA polymerase III promoter of the selenocysteine tRNA gene (Q24598763) (← links)
- Gfi-1 encodes a nuclear zinc finger protein that binds DNA and functions as a transcriptional repressor (Q24648833) (← links)
- An emerging role for prdm family genes in dorsoventral patterning of the vertebrate nervous system (Q26779384) (← links)
- Identification of binding sites of EVI1 in mammalian cells (Q28260755) (← links)
- SMYD3 encodes a histone methyltransferase involved in the proliferation of cancer cells (Q28270360) (← links)
- Zinc fingers 1-7 of EVI1 fail to bind to the GATA motif by itself but require the core site GACAAGATA for binding (Q28273005) (← links)
- The Ikaros gene encodes a family of functionally diverse zinc finger DNA-binding proteins (Q28513108) (← links)
- Mutations in MECOM, Encoding Oncoprotein EVI1, Cause Radioulnar Synostosis with Amegakaryocytic Thrombocytopenia (Q33427657) (← links)
- RUNX1-ETO and RUNX1-EVI1 Differentially Reprogram the Chromatin Landscape in t(8;21) and t(3;21) AML. (Q33759034) (← links)
- Acetylation of lysine 564 adjacent to the C-terminal binding protein-binding motif in EVI1 is crucial for transcriptional activation of GATA2. (Q33883148) (← links)
- The oncoprotein EVI1 and the DNA methyltransferase Dnmt3 co-operate in binding and de novo methylation of target DNA. (Q33939478) (← links)
- The KLHL1-antisense transcript ( KLHL1AS) is evolutionarily conserved (Q34120940) (← links)
- Transcription factors and translocations in lymphoid and myeloid leukemia (Q34173877) (← links)
- Aberrant DNA hypermethylation signature in acute myeloid leukemia directed by EVI1. (Q34568861) (← links)
- Designed transcription factors as tools for therapeutics and functional genomics (Q34816185) (← links)
- Mice carrying a hypomorphic Evi1 allele are embryonic viable but exhibit severe congenital heart defects (Q35107227) (← links)
- Ecotopic viral integration site 1 (EVI1) regulates multiple cellular processes important for cancer and is a synergistic partner for FOS protein in invasive tumors (Q35750824) (← links)
- Sox4 cooperates with Evi1 in AKXD-23 myeloid tumors via transactivation of proviral LTR. (Q35849315) (← links)
- EVI1 acts as an inducible negative-feedback regulator of NF-κB by inhibiting p65 acetylation (Q36016473) (← links)
- EVI1 is critical for the pathogenesis of a subset of MLL-AF9-rearranged AMLs. (Q36057626) (← links)
- Expression of the zinc finger gene EVI-1 in ovarian and other cancers (Q36136599) (← links)
- The DNA-binding and enhancer-blocking domains of the Drosophila suppressor of Hairy-wing protein (Q36560581) (← links)
- Targeting a DNA binding motif of the EVI1 protein by a pyrrole-imidazole polyamide (Q36749396) (← links)
- Molecular and cytogenetic abnormalities in acute myeloid leukaemia and myelodysplastic syndromes (Q36810168) (← links)
- Leukemogenesis of the EVI1/MEL1 gene family (Q36812700) (← links)
- The C2H2-ZF transcription factor Zfp335 recognizes two consensus motifs using separate zinc finger arrays (Q37104703) (← links)
- Pathogenetic significance of ecotropic viral integration site-1 in hematological malignancies (Q37455180) (← links)
- Evi-1 as a critical regulator of leukemic cells (Q37763616) (← links)
- PRDM proteins: important players in differentiation and disease (Q37949547) (← links)
- Protein-DNA binding: complexities and multi-protein codes (Q38163510) (← links)
- EVI1 promotes tumor growth via transcriptional repression of MS4A3. (Q38299701) (← links)
- Enhanced sensitivity to hydrogen peroxide-induced apoptosis in Evi1 transformed Rat1 fibroblasts due to repression of carbonic anhydrase III. (Q38347948) (← links)
- Functional features of EVI1 and EVI1Δ324 isoforms of MECOM gene in genome-wide transcription regulation and oncogenicity (Q38459749) (← links)
- Review: Aberrant EVI1 expression in acute myeloid leukaemia (Q38686515) (← links)
- Functions of Prdm16 in thermogenic fat cells (Q38844693) (← links)
- EVI1 induces myelodysplastic syndrome in mice (Q39951095) (← links)
- Stereochemical basis of DNA recognition by Zn fingers (Q40230658) (← links)
- Oncogenic role of "master" transcription factors in human leukemias and sarcomas: a developmental model (Q40951680) (← links)
- Evi1 regulates Notch activation to induce zebrafish hematopoietic stem cell emergence. (Q42727640) (← links)
- EVI-1 modulates leukemogenic potential and apoptosis sensitivity in human acute lymphoblastic leukemia. (Q43486412) (← links)
- The Evi1 proto-oncogene is required at midgestation for neural, heart, and paraxial mesenchyme development (Q44536836) (← links)
- X-MyT1, a Xenopus C2HC-type zinc finger protein with a regulatory function in neuronal differentiation (Q48056539) (← links)
- Evi1 is specifically expressed in the distal tubule and duct of the Xenopus pronephros and plays a role in its formation. (Q52021980) (← links)
- Direct interaction between the PRDM3 and PRDM16 tumor suppressors and the NuRD chromatin remodeling complex (Q63379240) (← links)
- EVI1 carboxy-terminal phosphorylation is ATM-mediated and sustains transcriptional modulation and self-renewal via enhanced CtBP1 association (Q64147072) (← links)