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1 specifically enriched in genes regulated by Kruppel-like factors.
4 l-like factor (EKLF), which is also known as Kruppel-like factor 1 (KLF1), play a coordinating role i
6 ns in the key erythroid transcription factor Kruppel-like factor 1 in patients who presented with sev
8 aused by mutations in a trans-acting factor (Kruppel-like factor 1) and reveal an important pathway r
9 rs GATA1 (GATA1 binding protein 1) and KLF1 (Kruppel-like factor 1) cause benign and disease phenotyp
11 ssense mutation in the second zinc finger of Kruppel-like factor-1 (KLF1) leads to degenerate DNA-bin
13 t findings have supported a primary role for Kruppel-like factor 10 (KLF10) as an important transcrip
14 , NAB2 (Ngfi-A-binding protein-2) and KLF10 (Kruppel-like factor-10) that, when individually silenced
15 levels of a MAO A-transcriptional activator, Kruppel-like factor 11 (KLF11 , also recognized as trans
17 volutionarily conserved metabolic regulator, Kruppel-like factor 11 (KLF11), as a novel browning tran
18 s-induced MAO A and the transcription factor Kruppel-like factor 11 (KLF11, also called TIEG2, a memb
19 e (ImmGen) Consortium studies, we identified kruppel-like factor 12 (Klf12), encoding a novel transcr
20 viously showed that the transcription factor Kruppel-like factor 13 (KLF13) controls the late (3-5 da
21 Here we show that the transcription factor Kruppel-like factor 13 (KLF13) has a critical role in th
22 gene locus encoding the transcription factor Kruppel-like factor 14 (KLF14) are strongly associated w
29 y induced the ergogenic transcription factor Kruppel-like factor 15 (Klf15) while decreasing Fbxo32.
30 with known CREB target genes, we identified Kruppel-like factor 15 (KLF15), a kidney-enriched nuclea
33 ined that dual transcriptional regulation of Kruppel-like factor 15 (Klf15), by both the transforming
34 we established that PR-mediated induction of Kruppel-like factor 15 (KLF15), which can bind to GC-ric
36 rt and neural crest derivatives expressed 2, Kruppel-like factor 15, and cyclin G1 and the subsequent
37 dexamethasone-induced transcription factors, Kruppel-like factor 15, Slug, and SPDEF, stimulated the
42 cific deficiency of the transcription factor Kruppel-like factor 2 (KLF2) accelerates atherosclerosis
43 in expression of the atheroprotective factor Kruppel-like factor 2 (KLF2) and cytokines were also stu
45 The expression of the transcription factor Kruppel-like factor 2 (KLF2) and its vasoprotective targ
46 fects of flow-activated transcription factor Kruppel-like factor 2 (KLF2) are compromised in PAH.
48 icoagulant protein C system, is regulated by Kruppel-like factor 2 (KLF2) at the transcriptional leve
49 ndent upon the vascular transcription factor Kruppel-like factor 2 (KLF2) binding near the transcript
52 es are regulated by the transcription factor Kruppel-like factor 2 (KLF2) in conventional alphabeta T
53 eases expression of the transcription factor Kruppel-like factor 2 (KLF2) in multiple cell types.
55 flammatory role for the transcription factor Kruppel-like factor 2 (KLF2) in regulating activation of
57 l expansion and survival, we now report that Kruppel-like factor 2 (KLF2) is a key transcription fact
58 though mechanosensitive transcription factor Kruppel-like factor 2 (KLF2) is a major regulator of end
64 eroprotective flow, the transcription factor Kruppel-like factor 2 (KLF2) is crucial for maintaining
68 surface S1P-R1 expression, as well S1PR1 and Kruppel-like factor 2 (KLF2) transcripts, were significa
70 gulates other stress-sensitive genes such as Kruppel-like factor 2 (Klf2), endothelial nitric oxide s
71 l cell homeostasis as shown by activation of Kruppel-like factor 2 (KLF2), increased endothelial nitr
72 ons, which was associated with modulation of Kruppel-like factor 2 (KLF2), Kruppel-like factor 4 (KLF
73 shear stress-sensitive transcription factor, Kruppel-like Factor 2 (KLF2), mediates increased CBC sen
74 to facilitate a physical interaction between Kruppel-like factor 2 (KLF2), the major regulator of she
81 cell lung cancer through down-regulation of Kruppel-like factor 2 and p21, contrary to tumor suppres
82 This activation is instrumental in inducing Kruppel-like factor 2 and several immediate early genes
83 elial anti-inflammatory transcription factor Kruppel-like factor 2 as well as endothelial nitric oxid
92 065], P=1.73E-03) and had lower IRF2BP2 (and Kruppel-like factor 2) protein levels in peripheral bloo
93 Furthermore, we found that the expression of Kruppel-like factor 2, a key anti-inflammatory transcrip
94 f the sphingosine 1-phosphate 1 receptor and Kruppel-like factor 2, both of which regulate thymic and
98 PRCP(gt/gt) aortas express reduced levels of Kruppel-like factors 2 and 4, thrombomodulin, and eNOS m
99 onsequent detrimental overexpression of KLF (Kruppel-like factor) 2 and KLF4, recapitulating the hall
100 n of the zinc finger transcriptional factor, Kruppel-like factor-2 (KLF2) in tumor endothelial cells.
101 regulating NF-E2-related factor-2 (Nrf2) and Kruppel-like factor-2 (KLF2), two transcription factors
103 ow that the zinc finger transcription factor Kruppel-like factor 3 (KLF3) directly represses galectin
105 well-characterized transcriptional repressor Kruppel-like factor 3 (KLF3), which, in turn, directly r
107 tracellular domain) transactivated the mouse Kruppel-like factor 4 (Klf) promoter and that Klf4 direc
109 istically, we found that miR-135b-5p targets Kruppel-like factor 4 (KLF4) and binds to its 3' UTR, le
110 Here we report our studies that identify Kruppel-like factor 4 (KLF4) as a critical regulator of
111 in and TF footprint analysis which unearthed Kruppel-like Factor 4 (KLF4) as a potential key regulato
112 ed that the zinc finger transcription factor Kruppel-like factor 4 (KLF4) can promote RAS-ERK signali
113 thickness and PU mouse models, we found that Kruppel-like factor 4 (KLF4) deficiency resulted in decr
114 Here, we explore the mechanisms that loss of Kruppel-like factor 4 (KLF4) exacerbates oncogenic TGF-b
116 omplex long-range enhancer cluster governing Kruppel-like factor 4 (Klf4) expression in naive pluripo
117 we have shown that the transcription factor Kruppel-like factor 4 (KLF4) governs mitochondrial bioge
119 s death-associated protein kinase (DAPK) and Kruppel-like factor 4 (KLF4) in CRC cells, resulting in
120 to overexpress the transcriptional regulator Kruppel-like factor 4 (Klf4) in esophageal epithelia of
121 ole for the zinc finger transcription factor Kruppel-like factor 4 (KLF4) in the modulation of the in
140 ophage lineage identity transcription factor Kruppel-like factor 4 (KLF4) to be inhibited during LC d
142 d that gemfibrozil induced the activation of Kruppel-like factor 4 (KLF4) via the PI 3-kinase-AKT pat
143 ng cascade involving sustained expression of Kruppel-like factor 4 (KLF4), a regulator of stem cell m
144 We demonstrate that miR-29 directly targets Kruppel-like factor 4 (KLF4), a transcription factor req
149 date the underlying mechanism, we focused on Kruppel-like factor 4 (KLF4), and decoupled its mCpG- an
150 modulation of Kruppel-like factor 2 (KLF2), Kruppel-like factor 4 (KLF4), and suppressor of cytokine
151 many human transcription factors, including Kruppel-like factor 4 (KLF4), as sequence-specific DNA m
156 polarization involves induction of STAT6 and Kruppel-like factor 4 (KLF4), which induce each other an
160 man gastric tumors had reduced expression of Kruppel-like factor 4 and increased expression of FoxM1
161 in keratinocytes via the combined actions of Kruppel-like factor 4 and NF-kappaB transcription factor
162 arget of rapamycin pathway inhibits ELF4 and Kruppel-like factor 4 expression downstream of ERK and P
163 xpression of the E74-like factor (ELF) 4 and Kruppel-like factor 4 genes to release naive CD8(+) T ce
165 of key VSMC differentiation genes; notably, Kruppel-like factor 4 was found to be a direct target of
166 ssion of transcription factors such as KLF4 (Kruppel-like factor 4) and EGR1 (early-growth-response 1
167 CIN (fascin actin-bundling protein 1), KLF4 (Kruppel-like factor 4), Yes1 (YES proto-oncogene 1), and
169 ophage polarization, including STAT3, STAT6, Kruppel-like factor 4, and peroxisome proliferator-activ
171 ntrol of expression of transcription factors Kruppel-like factors 4 or 5 (Klf4 or Klf5) which in turn
179 tigated the role of the transcription factor Kruppel-like factor 5 (KLF5) in ADM and KRAS-mediated fo
188 ow that the zinc finger transcription factor Kruppel-like factor 5 (KLF5) transactivates NOTCH1 in th
189 are primarily regulated by ovarian hormones, Kruppel-like factor 5 (KLF5), a zinc finger-containing t
190 ced age-related disorders, it is unclear how Kruppel-like factor 5 (Klf5), an essential transcription
198 d with increased cardiac expression of KLF5 (Kruppel-like factor-5) and PPARalpha (peroxisome prolife
200 onal network involving the tumor suppressors Kruppel-like factor 6 (KLF6) and forkhead box O1 (FOXO1)
202 programmed cell death protein 4 (PDCD4) and Kruppel-like factor 6 (KLF6) as critical regulators and
205 of the transcription factor/tumor suppressor Kruppel-like factor 6 (KLF6) has been described in prost
207 etic activation of the tumor suppressor gene Kruppel-like factor 6 (KLF6) plays a role in ERMA-induce
208 The polymorphism, KLF6-IVS1-27A, in the Kruppel-like factor 6 (KLF6) transcription factor gene e
209 estingly, a key factor in tissue remodeling, Kruppel-like factor 6 (KLF6) translocates to the cell nu
212 domain of LCoR and the transcription factor Kruppel-like factor 6 (KLF6), a putative tumor suppresso
217 manner dependent on the transcription factor Kruppel-like factor 6 , suggesting that this pathway und
219 onjunction with the tumor suppressor protein Kruppel-like factor 6 functioning as an AhR binding part
223 Here we show that the transcription factor Kruppel-like factor 7 (KLF7) is overexpressed in PDACs,
224 nown coactivator of the transcription factor Kruppel-like factor 7 (KLF7), which regulates genes requ
230 -Myc, Cyclin D1, Bcl-xL, Survivin, VEGF, and Kruppel-like factor 8, which is identified as a Stat3 ta
231 eogenesis utilizing the transcription factor Kruppel-like factor 9 (KLF9) in physiology and disease s
233 41 transcription factors including circadian Kruppel-like factor 9 (KLF9), and ~260 of their target g
234 of a negative regulator of dendritic spines, Kruppel-like factor 9 (Klf9), in mature DGCs enhanced in
235 GR1), forkhead box protein A3 (FOXA3), JUNB, Kruppel-like factor 9 (KLF9), KLF10, and REV-ERBalpha-we
236 Nrf2 stimulates expression of transcription Kruppel-like factor 9 (Klf9), resulting in further Klf9-
237 o3), thyroid receptors (tralpha, trbeta) and Kruppel-like factor 9 (klf9), suggesting regulation by t
238 identified a circadian transcription factor, Kruppel-like factor 9 (Klf9), that is substantially up-r
240 -of-function approaches, we also showed that Kruppel-like factor 9 was a key mediator of this effect
246 man erythroid cells, expression of erythroid Kruppel-like factor (EKLF) precedes PlGF, and its enforc
247 thin the second zinc finger of the erythroid Kruppel-like factor (EKLF), a critical erythroid regulat
248 here transcription factors such as erythroid Kruppel-like factor (EKLF), which is also known as Krupp
254 tic leukemia 1 protein (Tal1), and Erythroid Kruppel-like factor (EKLF; henceforth referred to as Klf
257 Our group and others have implicated the Kruppel-like factor family of transcription factors as c
261 signals implicate lower-frequency variants, Kruppel-like factors, Hedgehog signaling, Hippo-YAP sign
262 review focuses on the relevant literature of Kruppel-like factors in leukocyte biology and their impl
263 OXO may represent a broad mechanism by which Kruppel-like factors integrate with insulin signaling to
264 ctor 4 (Klf; previously known a gut-enriched Kruppel-like factor) is a DNA-binding transcriptional re
265 c mice deficient in the transcription factor Kruppel-like factor (KLF) 13 have comparable numbers of
268 entified a role for the transcription factor Kruppel-like factor (KLF) 4 in the development of IL-17-
269 nomics, we have identified conserved ETS and Kruppel-like factor (KLF) binding sites within the Flk1
270 he Sp1 transcription factor, a member of the Kruppel-like factor (KLF) family of transcriptional regu
274 scription factors involved in axonal growth, Kruppel-like factor (KLF) transcription factors-7 and -9
275 chanistically, ORAI1 induced upregulation of Kruppel-like factor (KLF)-2 and KLF4 in the flow-activat
276 Regulating these states is the presence of a Kruppel-like factor (KLF)-containing Polycomb response e
279 leted mice have injured vessels with reduced Kruppel-like factor (KLF)2, KLF4, endothelial nitric oxi
280 duced activation of the transcription factor Kruppel-like factor (KLF)4 may have an important role in
281 dent pathway by serving as a coactivator for Kruppel-like factor (KLF)4-a driver of tissue-resident m
282 croarray and experimental data revealed that Kruppel-like factor (Klf)5 was the most up-regulated tra
285 erein, we report that a TGF-beta1-responsive Kruppel- like factor, KLF10, is strongly expressed in PA
286 expression of FABP5 is down-regulated by the Kruppel-like factor KLF2, suggesting a tumor suppressor
288 titution of the sole sumoylation site of the Kruppel-like factor (KLF4), a well known reprogramming f
298 of enhancer RNAs pointed a central role for Kruppel-like factor, MEF2C, ETS, NFY, ATF, E2F2, and NRF