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1 KLF family members are expressed in most if not all tiss
2 KLF-4 is abundantly present in normal breast epithelial
3 KLFs can bind to CACCC elements, which are important in
4 KLFs have diverse functions in stem cell biology, embryo
5 KLFs regulate axon growth in CNS neurons including retin
6 KLFs share a highly conserved zinc finger-based DNA bind
7 d KLF4 in the flow-activated LECs, and the 2 KLF proteins cooperate to regulate VEGF-A, VEGF-C, FGFR3
9 of anti-adipogenic proteins such as GATA-3, KLF-2, and transcriptional coactivator with PDZ binding
10 in/protein interaction domain disrupted in a KLF gene variant that associates to MODY7, contributing
11 n, expand our mechanistic understanding of a KLF associated to human disease, and outline cellular an
12 he existence of multiple biologically active KLF splice forms across the entire family of proteins.
14 al implications for mammalian vascular aging.KLF family transcription factors (KLFs) regulate many ce
16 ied deregulated proteins, including EBF1 and KLF transcription factors, that were not detected in pre
19 ess than 400 bp) containing potential GR and KLF binding sites were identified and examined for trans
22 sue- and organ-specific functions of SPs and KLFs in the digestive system including the oral cavity,
26 evidence supporting a relevant role for any KLF protein in doing both: transcriptionally inhibiting
27 )GPI antibodies reflects competition between KLFs and NF-kappaB for their common cofactor, CBP/p300.
29 ion of NF-kappaB transcriptional activity by KLFs reflects sequestration of the cotranscriptional act
32 hese results demonstrate that SID-containing KLF repressor proteins can inhibit cell growth and neopl
33 particularly of a CpG site within a critical KLF/Sp regulatory element required for butyrate inductio
34 Thus, coordinated activities of different KLFs regulate the regenerative capacity of CNS neurons.
43 4 and RNAi-mediated inhibition of endogenous KLF-4 supported the role of KLF-4 as a transcriptional r
44 vide cogent evidence implicating endothelial KLFs as essential in vivo regulators of vascular functio
49 he transcription factor Kruppel-like factor (KLF) 13 have comparable numbers of iNKT cells to C57BL/6
53 he transcription factor Kruppel-like factor (KLF) 4 in the development of IL-17-producing CD4(+) T ce
57 Several members of the Kruppel-like factor (KLF) family of transcription factors play important role
62 binding regions of the Kruppel-like factor (KLF) transcription factor in embryonic stem cells (ESCs)
63 induced upregulation of Kruppel-like factor (KLF)-2 and KLF4 in the flow-activated LECs, and the 2 KL
66 studies identified the Kruppel-like factor (KLF)2 as being inhibited by the inflammatory cytokine in
67 t studies reported that Kruppel-like factor (KLF)2 controls trafficking, development, and function of
70 ed vessels with reduced Kruppel-like factor (KLF)2, KLF4, endothelial nitric oxide synthase (eNOS), a
71 he transcription factor Kruppel-like factor (KLF)4 may have an important role in mediating the expres
72 ng as a coactivator for Kruppel-like factor (KLF)4-a driver of tissue-resident macrophage differentia
74 that the Kruppel-like transcription factor (KLF) 4 potently represses the expression of multiple SMC
77 acterized Kruppel-like transcription factor (KLF), in a sequence-specific manner, to mediate complex
79 identify the C. elegans Kruppel-like factor, KLF-1, as an essential and specific regulator of DR-indu
80 Several Kruppel-like transcription factors (KLF), including KLF15, are induced during reactivation f
88 ent insights implicate Kruppel-like factors (KLFs) as important regulators of vascular homeostasis, t
89 ity proteins (SPs) and Kruppel-like factors (KLFs) belong to the family of transcription factors that
91 tudies have implicated Kruppel-like factors (KLFs) including KLF5 in the renewal and maintenance of s
93 mbers of the Kruppel-like family of factors (KLFs) play essential roles in erythrocyte and T lymphocy
96 ruppel-like family of transcription factors (KLFs) constitute a subfamily of C2H2-type zinc finger pr
98 species, Kruppel-like transcription factors (KLFs) have been identified as key components of adipogen
99 ular aging.KLF family transcription factors (KLFs) regulate many cellular processes, including prolif
100 ruppel-like family of transcription factors (KLFs) regulate the expression of genes involved in cell
102 at Kruppel-like transcription (KLF) factors, KLF 4 and 15, are inversely expressed; most importantly,
104 lated by overexpressing Kruppel-like family (KLF) transcription factors, or mitochondrial dynamics we
106 ggest this study provides a paradigm for how KLFs work in incoherent feed-forward loops or networks t
115 in cancer that involves concomitant loss of KLF-4-HDAC-mediated transcriptional repression and activ
116 data support a model in which modulation of KLF-1 by WWP-1 regulates diet-restriction-induced longev
118 al ChIP assays demonstrated the occupancy of KLF-4, HDAC2, and HDAC3 in the VEGF promoter in normal M
120 on of endogenous KLF-4 supported the role of KLF-4 as a transcriptional repressor of VEGF and an inhi
122 t be associated with decreased expression of KLFs, which in turn might facilitate cellular activation
123 Here, we review the crucial functions of KLFs in mammalian embryogenesis, stem cell biology and r
125 RGC connectivity, understanding the role of KLFs in regulating neurite outgrowth and Eph receptor ex
127 tif that differs from a previously published KLF motif identified by a SELEX experiment, but the new
132 5 promoter contains multiple GC- and GT-rich KLF-binding sites, which, as shown by ChIP-assays, bind
137 assays, KLF16 binds specifically to a single KLF site near the EphA5 transcription start site that is
138 es transcription by binding to a distinct Sp-KLF site within the Drd2 promoter (-98 to -94) and recru
140 ies identify a mechanism for antagonizing Sp/KLF protein repression function via SHP, with this proce
141 , we show that KLF11, an SP/Kruppel-like (SP/KLF) transcription factor, mutated in French maturity on
142 easured the expression levels of selected Sp/KLF factors in primary cells of fetal and adult stages o
144 comprehensive screen of 24 members of the Sp/KLF family due to its TGFbeta inducibility, its ability
146 this study, we evaluated the role of the Sp/KLF transcription factor KLF11/Klf11 in the pathogenesis
149 rect activation of the MAO A promoter via Sp/KLF-binding sites; 4) KLF11 knockout mice show reduced M
150 r families (including CREB, ETS, EGR-1, SP1, KLF, MAZ, HIF-1, and STATs) that play important roles in
152 These data suggest that one or more Sp1/KLF family members play a role in PRE function in Drosop
153 derive a consensus binding site for the Sp1/KLF Drosophila family members and show that this consens
157 ously showed that a binding site for the Sp1/KLF family of zinc-finger proteins is required for PRE a
161 ring extents, and several growth-suppressive KLFs were up-regulated postnatally, whereas growth-enhan
167 y inflammation, raising the possibility that KLFs and their upstream signals are of therapeutic inter
171 c cardiac hypertrophy, a direct role for the KLF family in cardiac metabolism has not been previously
172 tilization and is the first to implicate the KLF transcription factor family in cardiac metabolism.
174 zed KLF2, a KLF4 homolog and a member of the KLF family of transcription factors with a known role in
175 ppel-like factor 2 (KLF2) is a member of the KLF family of zinc-finger transcription factors and is i
177 y small molecules that target members of the KLF subfamily of transcription factors to regulate biolo
178 and proteomic breadth and complexity of the KLF transcription factor family, revealing the existence
179 ptional activation by KLF13, a member of the KLF/Sp1 family, either individually or cooperatively.
181 observations are the first to implicate the KLFs as novel participants in the endothelial proinflamm
185 epithelium that Kruppel-like transcription (KLF) factors, KLF 4 and 15, are inversely expressed; mos
186 tion of the iNOS promoter is mediated by two KLF DNA-binding sites at -95 and -212 bp, and mutation o
188 monstrate that WWP-1 directly interacts with KLF-1 and mediates multiple monoubiquitylation of KLF-1
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