Synergistic transcription activation by Maf and Sox and their subnuclear localization are disrupted by a mutation in Maf that causes cataract.
about
Design and implementation of bimolecular fluorescence complementation (BiFC) assays for the visualization of protein interactions in living cells.Bimolecular fluorescence complementation (BiFC) analysis as a probe of protein interactions in living cells.Lens fiber cell differentiation and denucleation are disrupted through expression of the N-terminal nuclear receptor box of NCOA6 and result in p53-dependent and p53-independent apoptosis.Sox5 and c-Maf cooperatively induce Th17 cell differentiation via RORγt induction as downstream targets of Stat3.Visualization of molecular interactions using bimolecular fluorescence complementation analysis: characteristics of protein fragment complementation.Differential gene regulation by selective association of transcriptional coactivators and bZIP DNA-binding domainsTissue-specific regulation of the mouse alphaA-crystallin gene in lens via recruitment of Pax6 and c-Maf to its promoter.Subnuclear compartmentalization of sequence-specific transcription factors and regulation of eukaryotic gene expression.Genetic and epigenetic mechanisms of gene regulation during lens development.Large Maf Transcription Factors: Cousins of AP-1 Proteins and Important Regulators of Cellular Differentiation.Visualization of molecular interactions by fluorescence complementation.Pax6 is misexpressed in Sox1 null lens fiber cells.Advanced fluorescence microscopy techniques--FRAP, FLIP, FLAP, FRET and FLIM.Role of c-Maf in Chondrocyte Differentiation: A Review.Subnuclear re-localization of SOX10 and p54NRB correlates with a unique neurological phenotype associated with SOX10 missense mutations.Bimolecular fluorescence complementation: visualization of molecular interactions in living cells.Identification and functional analysis of SOX10 missense mutations in different subtypes of Waardenburg syndrome.CD13/APN transcription is regulated by the proto-oncogene c-Maf via an atypical response element.A heterozygous c-Maf transactivation domain mutation causes congenital cataract and enhances target gene activation.Sequential and combinatorial roles of maf family genes define proper lens development.Design of fusion proteins for bimolecular fluorescence complementation (BiFC).Visualization of protein interactions in living cells using bimolecular fluorescence complementation (BiFC) analysis.Signaling and Gene Regulatory Networks in Mammalian Lens Development.Mutation update of transcription factor genes FOXE3, HSF4, MAF, and PITX3 causing cataracts and other developmental ocular defects.The transcription factor c-Maf controls touch receptor development and function.
P2860
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P2860
Synergistic transcription activation by Maf and Sox and their subnuclear localization are disrupted by a mutation in Maf that causes cataract.
description
2004 nî lūn-bûn
@nan
2004年の論文
@ja
2004年論文
@yue
2004年論文
@zh-hant
2004年論文
@zh-hk
2004年論文
@zh-mo
2004年論文
@zh-tw
2004年论文
@wuu
2004年论文
@zh
2004年论文
@zh-cn
name
Synergistic transcription acti ...... n in Maf that causes cataract.
@en
type
label
Synergistic transcription acti ...... n in Maf that causes cataract.
@en
prefLabel
Synergistic transcription acti ...... n in Maf that causes cataract.
@en
P2860
P1476
Synergistic transcription acti ...... n in Maf that causes cataract.
@en
P2093
Nirmala Rajaram
P2860
P304
P356
10.1128/MCB.24.13.5694-5709.2004
P407
P577
2004-07-01T00:00:00Z