ライフサイエンスコーパス: KLF

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 Here we identify Kruppel-like factor 1 (KLF-1) as a mediator of a cytoprotective response that d

8 d KLF4 in the flow-activated LECs, and the 2 KLF proteins cooperate to regulate VEGF-A, VEGF-C, FGFR3

9 essed transcription factors, such as group 2 KLFs, can play important roles in the specification of d

10 transcription factor, Kruppel-like factor 2 (KLF-2).

11 of anti-adipogenic proteins such as GATA-3, KLF-2, and transcriptional coactivator with PDZ binding

12 in/protein interaction domain disrupted in a KLF gene variant that associates to MODY7, contributing

13 n, expand our mechanistic understanding of a KLF associated to human disease, and outline cellular an

14 he existence of multiple biologically active KLF splice forms across the entire family of proteins.

15 In addition, KLF-4 and Elf-3, transcription factors involved in termi

16 al implications for mammalian vascular aging.KLF family transcription factors (KLFs) regulate many ce

17 In the human VEGF promoter, SAF-1- and KLF-4-binding elements are overlapping, whereas SAF-1 in

18 udies show that modulation of microRNA 7 and KLF recapitulates macrophage phenotypic changes.

19 ied deregulated proteins, including EBF1 and KLF transcription factors, that were not detected in pre

20 and pointing to interactions between Ets and KLF factors in promoting epithelial fate.

21 Since the ETS and KLF protein families have independently been recognized

22 ess than 400 bp) containing potential GR and KLF binding sites were identified and examined for trans

23 omoter, we tested the hypothesis that GR and KLF family members transactivate the bICP0 E promoter.

24 anscription factors including AP1, GRHL, and KLF family members.

25 s are overlapping, whereas SAF-1 induces and KLF-4 suppresses VEGF expression.

26 members of the SP (specificity protein) and KLF (Kruppel-like factor) families of transcription fact

27 eport, for the first time, that the SSRE and KLF elements are critical flow sensors necessary for a t

28 dual human beta-globin locus transgenic and KLF knockout mouse model was used.

29 sue- and organ-specific functions of SPs and KLFs in the digestive system including the oral cavity,

30 Studies have shown that SPs and KLFs regulate not only physiological processes such as g

31 KLF5 is another KLF member with an established link to embryonic stem ce

32 Here, we show that another KLF transcription factor, KLF10, also regulates myoblast

33 evidence supporting a relevant role for any KLF protein in doing both: transcriptionally inhibiting

34 ng human embryonic genome activation and are KLF-stimulated enhancers in naive human embryonic stem c

35 cooperatively hijack this complex to bind at KLFs gene loci and facilitate KLF14 gene expression in l

36 )GPI antibodies reflects competition between KLFs and NF-kappaB for their common cofactor, CBP/p300.

37 1-mediated induction of VEGF is repressed by KLF-4 transcription factor.

38 ion of NF-kappaB transcriptional activity by KLFs reflects sequestration of the cotranscriptional act

39 ial dynamics are modulated differentially by KLFs that promote or suppress growth.

40 an homologues than they are to other chicken KLFs.

41 hese results demonstrate that SID-containing KLF repressor proteins can inhibit cell growth and neopl

42 particularly of a CpG site within a critical KLF/Sp regulatory element required for butyrate inductio

43 Thus, coordinated activities of different KLFs regulate the regenerative capacity of CNS neurons.

44 Whereas beta7 is identified as direct KLF target, its repression by KLF3 is not connected to t

45 that KLF16 selectively binds three distinct KLF-binding sites (GC, CA, and BTE boxes).

46 EKLF/KLF-1 containing histidine to alanine mutations that dis

47 EKLF/KLF-1 is a 358-amino acid nuclear protein with an amino-

48 EKLF/KLF-1 is an erythroid-restricted transcription factor es

49 Erythroid Kruppel-like Factor (EKLF/KLF-1) is an erythroid-specific transcription factor tha

50 he nuclear localization signal (NLS) of EKLF/KLF-1 has not been empirically determined.

51 The mutation in Caenorhabditis elegans KLF-3 leads to high TG accumulation in the worm's intest

52 4 and RNAi-mediated inhibition of endogenous KLF-4 supported the role of KLF-4 as a transcriptional r

53 vide cogent evidence implicating endothelial KLFs as essential in vivo regulators of vascular functio

54 ulated postnatally, whereas growth-enhancing KLFs were down-regulated.

55 For example, erythroid KLF (EKLF) regulates beta-globin expression during eryth

56 ed expression of the antiinflammatory factor KLF-2.

57 ased levels of cellular transcription factor KLF-4.

58 he transcription factor Kruppel-like factor (KLF) 13 have comparable numbers of iNKT cells to C57BL/6

59 Kruppel-like factor (KLF) 13 is a transcription factor that positively regula

60 Deficiency in Kruppel-like factor (KLF) 2 (also known as LKLF) leads to a massive loss of t

61 ion of antiinflammatory kruppel-like factor (KLF) 2 and KLF4.

62 he transcription factor Kruppel-like factor (KLF) 4 in the development of IL-17-producing CD4(+) T ce

63 e of myofibroblasts and Kruppel-like factor (KLF) 4 is upregulated in PDGFR-B(+) cells, inducing TGFB

64 owed that cardiomyocyte Kruppel-like factor (KLF) 5 regulates cardiac fatty acid oxidation.

65 Kruppel-like factor (KLF) 6 is a tumor-suppressor gene functionally inactivat

66 at sites influenced by Kruppel-like factor (KLF) and early growth response (EGR) transcription facto

67 ified conserved ETS and Kruppel-like factor (KLF) binding sites within the Flk1 enhancer.

68 in hematopoiesis is the Kruppel-like factor (KLF) family [1].

69 Several members of the Kruppel-like factor (KLF) family of transcription factors play important role

70 factor, a member of the Kruppel-like factor (KLF) family of transcriptional regulators.

71 Members of the Kruppel-like factor (KLF) family play wide-ranging and important roles in the

72 Kruppel-like factor (KLF) motifs were enriched in corneal epithelial enhancer

73 Kruppel-like factor (KLF) proteins are emerging as key regulators of lipid me

74 Kruppel-like factor (KLF) proteins have elicited significant attention due to

75 binding regions of the Kruppel-like factor (KLF) transcription factor in embryonic stem cells (ESCs)

76 olved in axonal growth, Kruppel-like factor (KLF) transcription factors-7 and -9, and that knockdown

77 Yang et al. found that Kruppel-like factor (KLF)-13 acts as a negative regulator of TGFbeta.

78 induced upregulation of Kruppel-like factor (KLF)-2 and KLF4 in the flow-activated LECs, and the 2 KL

79 es is the presence of a Kruppel-like factor (KLF)-containing Polycomb response element.

80 The importance of Kruppel-like factor (KLF)-mediated transcriptional pathways in the biochemist

81 studies identified the Kruppel-like factor (KLF)2 as being inhibited by the inflammatory cytokine in

82 t studies reported that Kruppel-like factor (KLF)2 controls trafficking, development, and function of

83 Kruppel-like factor (KLF)2 is a central regulator of endothelial and monocyte

84 press higher amounts of Kruppel-like factor (KLF)2, a regulator of S1P1 gene expression.

85 ed vessels with reduced Kruppel-like factor (KLF)2, KLF4, endothelial nitric oxide synthase (eNOS), a

86 he transcription factor Kruppel-like factor (KLF)4 may have an important role in mediating the expres

87 ng as a coactivator for Kruppel-like factor (KLF)4-a driver of tissue-resident macrophage differentia

88 red SMC is dependent on Krupple-like factor (KLF)4.

89 Here, we identify that Kruppel-like factor (KLF)6 promotes inflammation by restraining microRNA-223

90 that the Kruppel-like transcription factor (KLF) 4 potently represses the expression of multiple SMC

91 and three Kruppel-like transcription factor (KLF) family members, KLF4, KLF15, and promyelocytic leuk

92 The Kruppel-like transcription factor (KLF) family participates in diverse aspects of cellular

93 nc finger Kruppel-like transcription factor (KLF) family.

94 acterized Kruppel-like transcription factor (KLF), in a sequence-specific manner, to mediate complex

95 Kruppel-like transcription factor (KLF)13, previously shown to regulate RANTES expression i

96 identify the C. elegans Kruppel-like factor, KLF-1, as an essential and specific regulator of DR-indu

97 tudies revealed GR and Kruppel-like factors (KLF), KLF4 or KLF15 for example, cooperatively transacti

98 of four Kruppel-like transcription factors (KLF), i.e., KLF4, KLF6, PLZF (promyelocytic leukemia zin

99 Several Kruppel-like transcription factors (KLF), including KLF15, are induced during reactivation f

100 Kruppel-like factors (KLFs) are a family of 17 transcription factors character

101 The Kruppel-like factors (KLFs) are a family of C2/H2 zinc finger DNA-binding prot

102 The Kruppel-like factors (KLFs) are a family of Cys2His2 zinc-finger DNA binding p

103 Kruppel-like factors (KLFs) are a family of zinc-finger transcription factors

104 Kruppel-like factors (KLFs) are a group of transcription factors that appear t

105 Kruppel-like factors (KLFs) are transcription factors that govern metabolic ho

106 Kruppel-like factors (KLFs) are transcription factors that have recently emerg

107 Kruppel-like factors (KLFs) are zinc finger transcription factors that share h

108 ent insights implicate Kruppel-like factors (KLFs) as important regulators of vascular homeostasis, t

109 ity proteins (SPs) and Kruppel-like factors (KLFs) belong to the family of transcription factors that

110 Kruppel-like factors (KLFs) control cell differentiation and embryonic develop

111 tudies have implicated Kruppel-like factors (KLFs) including KLF5 in the renewal and maintenance of s

112 Kruppel-like factors (KLFs) play a critical role in regulating the endothelial

113 egulatory elements and Kruppel-like factors (KLFs) transcription factors.

114 mbers of the Kruppel-like family of factors (KLFs) play essential roles in erythrocyte and T lymphocy

115 The Kruppel-like transcription factors (KLFs) are important regulators of cell proliferation and

116 ruppel-like family of transcription factors (KLFs) are important regulators of inflammation.

117 ruppel-like family of transcription factors (KLFs) constitute a subfamily of C2H2-type zinc finger pr

118 ike C2/H2 zinc finger transcription factors (KLFs) control development and differentiation.

119 species, Kruppel-like transcription factors (KLFs) have been identified as key components of adipogen

120 ular aging.KLF family transcription factors (KLFs) regulate many cellular processes, including prolif

121 ruppel-like family of transcription factors (KLFs) regulate the expression of genes involved in cell

122 anges in Kruppel-like transcription factors (KLFs).

123 at Kruppel-like transcription (KLF) factors, KLF 4 and 15, are inversely expressed; most importantly,

124 -related family members Kruppel-like family (KLF) 13/FKLF2/BTEB3 and Sp1 on PR-B transactivity.

125 lated by overexpressing Kruppel-like family (KLF) transcription factors, or mitochondrial dynamics we

126 factors in distinct families, including FOX, KLF, SOX, and MITF/Myc.

127 of these cells, the zinc finger protein GKLF/KLF-4 was recently identified as a novel oncogene.

128 ggest this study provides a paradigm for how KLFs work in incoherent feed-forward loops or networks t

129 We also highlight how KLFs have been implicated in human diseases and outline

130 ic, longevity assurance pathway and identify KLF-1 as a central factor in orchestrating this response

131 We identify KLF-family transcription factors as direct target genes

132 analyses and transcriptomic data implicated KLFs as regulators of attachment cells.

133 eral putative cis-regulatory sites including KLFs, AP-2, EGRF and Sp-1.

134 Indeed, KLFs have been implicated in subtypes of leukemia, lymph

135 Gene targeting of individual KLFs in mice has uncovered novel and unexpected physiolo

136 g ETS TFs and loss of interactions involving KLF TFs to different mutations in the TERT promoter, and

137 Many KLFs show a circadian expression in the liver.

138 ion as key biochemical mechanisms modulating KLF-mediated neurotransmitter gene transcription.

139 ythroid cells (the TR2/TR4 heterodimer, MYB, KLFs, BCL11A, and SOX6).

140 was also required for GR- and SLUG-, but not KLF family member-, mediated transactivation of the ICP4

141 tif is transactivated by GR and Slug but not KLF family members.

142 iated with ARC through increasing binding of KLF-10 and thus decreasing CRYAA transcription.

143 Inducible depletion of KLF factors in PSCs caused a genome-wide decrease in enh

144 factor 8 (KLF8) is a member of the family of KLF transcription factors.

145 in cancer that involves concomitant loss of KLF-4-HDAC-mediated transcriptional repression and activ

146 data support a model in which modulation of KLF-1 by WWP-1 regulates diet-restriction-induced longev

147 and mediates multiple monoubiquitylation of KLF-1 in vitro and in cellulo.

148 al ChIP assays demonstrated the occupancy of KLF-4, HDAC2, and HDAC3 in the VEGF promoter in normal M

149 and consequent detrimental overexpression of KLF (Kruppel-like factor) 2 and KLF4, recapitulating the

150 Ectopic overexpression of KLF-4 and RNAi-mediated inhibition of endogenous KLF-4 s

151 analysis revealed an over-representation of KLF transcription factor (TF) binding sites in gained en

152 on of endogenous KLF-4 supported the role of KLF-4 as a transcriptional repressor of VEGF and an inhi

153 Co-transfection of KLF-4 and HDAC expression plasmids in breast cancer cell

154 t be associated with decreased expression of KLFs, which in turn might facilitate cellular activation

155 Here, we review the crucial functions of KLFs in mammalian embryogenesis, stem cell biology and r

156 stematic study of the expression patterns of KLFs during erythroid development.

157 RGC connectivity, understanding the role of KLFs in regulating neurite outgrowth and Eph receptor ex

158 function, and possible redundancy with other KLF paralogues.

159 Here, the authors position KLFs as important regulators of autophagy and lifespan i

160 tif that differs from a previously published KLF motif identified by a SELEX experiment, but the new

161 han 400 bp) containing two GREs and putative KLF binding sites present within genes encoding unique l

162 led a direct binding of KLF9 to the putative KLF binding motif.

163 A redox-regulated KLF-1 activation and transfer to the nucleus coincides w

164 on key biochemical mechanisms for regulating KLF sites involved in reproductive biology.

165 s S1PR1 and CCR7, and their master regulator KLF-2, and reduced chemotaxis toward S1P and CCL21.

166 Related KLF family members suppressed or enhanced axon growth to

167 understanding KLF16 and other highly related KLF proteins.

168 5 promoter contains multiple GC- and GT-rich KLF-binding sites, which, as shown by ChIP-assays, bind

169 transcription in the uterus involving select KLF members.

170 Several KLF members have been shown to play a role in oncogenesi

171 In addition, several KLF family members are downstream targets of stimuli and

172 Of note, several KLFs are also crucial for maintaining pluripotency and,

173 assays, KLF16 binds specifically to a single KLF site near the EphA5 transcription start site that is

174 sal stripe factors (USFs), comprises ~30 SP, KLF, EGR, and ZBTB family members that recognize overlap

175 es transcription by binding to a distinct Sp-KLF site within the Drd2 promoter (-98 to -94) and recru

176 Sp/KLF family of factors regulates gene expression by bindi

177 ies identify a mechanism for antagonizing Sp/KLF protein repression function via SHP, with this proce

178 , we show that KLF11, an SP/Kruppel-like (SP/KLF) transcription factor, mutated in French maturity on

179 ase genes, with notable representation of SP/KLF and AP-1/2 TFs.

180 easured the expression levels of selected Sp/KLF factors in primary cells of fetal and adult stages o

181 fetal and adult erythroid cells for some Sp/KLF factors.

182 comprehensive screen of 24 members of the Sp/KLF family due to its TGFbeta inducibility, its ability

183 The Sp/KLF transcription factor basic transcription element-bin

184 this study, we evaluated the role of the Sp/KLF transcription factor KLF11/Klf11 in the pathogenesis

185 tional regulatory mechanism involving the SP/KLF transcription factors, SP2 and KLF6.

186 KLF11, also called TIEG2, a member of the Sp/KLF- family), which inhibits cell growth.

187 rect activation of the MAO A promoter via Sp/KLF-binding sites; 4) KLF11 knockout mice show reduced M

188 r families (including CREB, ETS, EGR-1, SP1, KLF, MAZ, HIF-1, and STATs) that play important roles in

189 There are 10 Sp1/KLF family members in Drosophila, and nine of them bind

190 These data suggest that one or more Sp1/KLF family members play a role in PRE function in Drosop

191 derive a consensus binding site for the Sp1/KLF Drosophila family members and show that this consens

192 Here, we report that the Sp1/KLF family member Spps binds specifically to Ubx and eng

193 The Sp1/KLF family of factors regulates diverse cellular process

194 , Site 2, can be bound by members of the Sp1/KLF family of zinc finger proteins.

195 ously showed that a binding site for the Sp1/KLF family of zinc-finger proteins is required for PRE a

196 ) as a model, we uncover the role of the SP1/KLF transcription factor Huckebein (Hkb) in coordinating

197 Indeed, specific KLFs represent key components of a cross-regulating plur

198 In summary, KLFs use regulatory circuits to steer lymphocyte maturat

199 We review literature supporting KLFs as shared mechanisms in stress adaptation and cellu

200 ring extents, and several growth-suppressive KLFs were up-regulated postnatally, whereas growth-enhan

201 wp-1-overexpressing animals, indicating that KLF-1 functions within the same pathway as WWP-1.

202 Elegant studies have revealed that KLF proteins are important regulators of two major molec

203 We show that KLF family DNA binding sites are necessary for miR-150 p

204 We further show that KLF-1 activates genes involved in the xenobiotic detoxif

205 We show that KLF-4 recruits histone deacetylases (HDACs) -2 and -3 at

206 Our results suggest that KLF homologs make unique contributions to regulation by

207 y inflammation, raising the possibility that KLFs and their upstream signals are of therapeutic inter

208 Recent studies have shown that KLFs play a fundamental role in regulating diverse biolo

209 The KLF family of genes consists of >/=17 members, which are

210 The KLF mutation demonstrated an integration site-specific d

211 This allows the KLF-3 transcription factor to facilitate expression of t

212 shear stress response element (SSRE) and the KLF (Kruppel-like factor) element.

213 data supported the importance of ERG and the KLF family of transcription factors in AAA disease.

214 in the IL-2 promoter is a CACCC element, the KLF consensus binding motif.

215 c cardiac hypertrophy, a direct role for the KLF family in cardiac metabolism has not been previously

216 tilization and is the first to implicate the KLF transcription factor family in cardiac metabolism.

217 Members of the KLF family of transcription factors regulate regenerativ

218 zed KLF2, a KLF4 homolog and a member of the KLF family of transcription factors with a known role in

219 ppel-like factor 2 (KLF2) is a member of the KLF family of zinc-finger transcription factors and is i

220 gene expression by different members of the KLF gene family.

221 y small molecules that target members of the KLF subfamily of transcription factors to regulate biolo

222 and proteomic breadth and complexity of the KLF transcription factor family, revealing the existence

223 ptional activation by KLF13, a member of the KLF/Sp1 family, either individually or cooperatively.

224 and identified cytochrome P450 oxidases, the KLF-1 main effectors, as longevity-assurance factors of

225 was found to be a collaborating motif to the KLF motif in ESCs.

226 Within the KLF family, we identified KLF10 upregulation in a multit

227 observations are the first to implicate the KLFs as novel participants in the endothelial proinflamm

228 In essence, knowing that these KLF isoforms exist provides the first step toward unders

229 the metastatic behavior of the tumor; thus, KLF-SV1 may represent a novel therapeutic target.

230 nal regulation by SRF via its recruitment to KLF binding sites.

231 epithelium that Kruppel-like transcription (KLF) factors, KLF 4 and 15, are inversely expressed; mos

232 tion of the iNOS promoter is mediated by two KLF DNA-binding sites at -95 and -212 bp, and mutation o

233 However, whether KLF proteins mediate these key processes in a separate o

234 monstrate that WWP-1 directly interacts with KLF-1 and mediates multiple monoubiquitylation of KLF-1

235 Here, we identified a novel Xenopus KLF gene, neptune, which is highly expressed in the vent