Human KLF17 is a new member of the Sp/KLF family of transcription factors

Vliet, Jane van; Crofts, Linda; Quinlan, Kate; Czolij, R.; Perkins, Andrew C.; Crossley, Merlin

doi:10.1016/j.ygeno.2005.12.011

Cited by 103 publications

(86 citation statements)

References 34 publications

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“…1A) (1,11). As well as structural homology, members of each group also show functional similarities.…”

Section: The Klf Familymentioning

confidence: 99%

“…Analysis was done using Phylogeny Analysis software developed by the Australian National Genome Information Service [figure adapted from Ref. (1)]. B: The amino acid sequence of human KLF3.…”

Section: The Structure and Molecular Interactions Of Klf3mentioning

confidence: 99%

“…To date, 17 family members have been described (1) and all share homology with the zinc finger DNA-binding domain of the Drosophila segmentation factor Krüppel (2). KLFs have a highly conserved C-terminal DNA-binding domain consisting of three classical C2H2 zinc fingers that contact CACCC box motifs and GC-rich sequences in the promoters and enhancers of target genes (3).…”

Section: Introductionmentioning

confidence: 99%

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The mammalian zinc finger transcription factor Krüppel‐like factor 3 (KLF3/BKLF)

2011

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KLF3 is a member of the Krüppel‐like factor (KLF) family of transcription factors. These proteins are classified by the presence of three C‐terminal C2H2 zinc fingers that allow sequence‐specific binding to CACCC boxes and GC‐rich motifs found in the promoters, enhancers, and other control regions of target genes. KLFs have diverse biological roles, regulating proliferation, differentiation, and apoptosis in many tissues throughout development. KLF3 is a transcriptional repressor that binds the cofactor C‐terminal binding protein, which in turn recruits a large repressor complex to mediate transcriptional silencing. In addition to an understanding of the molecular mechanisms that allow KLF3 to regulate the expression of its target genes, the biological roles of this transcription factor are now being defined. In agreement with the widespread expression pattern of this transcription factor, it is becoming clear that KLF3 is an important regulator of several biological processes, including adipogenesis, erythropoiesis, and B cell development. © 2011 IUBMB IUBMB Life, 63(2): 86–93, 2011

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“…1A) (1,11). As well as structural homology, members of each group also show functional similarities.…”

Section: The Klf Familymentioning

confidence: 99%

Section: The Structure and Molecular Interactions Of Klf3mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The mammalian zinc finger transcription factor Krüppel‐like factor 3 (KLF3/BKLF)

2011

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“…The DNA binding domain of Drosophila Krüppel is constituted by five Cys 2 -His 2 type zinc finger structures, which are interconnected by linker sequences relatively conserved in a group of human transcription factors constituting the family of Krüppel-like Factors (KLF) (1). Most significantly, KLFs represent one of the most diverse set of regulators in vertebrate organisms, composed of 17 members in humans (Table 1), in addition to nine specificity protein (Sp) factors that share a similar DNA binding domain (also called Sp/KLF family) (2,3). Hence, all proteins of KLF family are characterized by a high conserved DNA binding domain composed of three zinc fingers (4), invariably located in their C-terminal region, except for KLFs 9-11.…”

Section: Krüppel-like Transcription Factorsmentioning

confidence: 99%

Biology of Krüppel‐like factor 6 transcriptional regulator in cell life and death

2010

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SummaryAn essential role for the Krü ppel-like transcription factor family has been determined in the regulation of remarkable processes including cell proliferation, differentiation, signal transduction, oncogenesis, and cell death. A member of this group, Krü ppel-like factor 6 (KLF6), identified on the basis of its ability to regulate a group of genes belonging to the carcinoembryonic antigen gene family, has been involved in human carcinogenesis. Early studies proposed a tumor suppressor function for KLF6 because of its ability to reduce cell proliferation through several biochemical mechanisms including regulation of cell cycle components, oncogene products, and apoptosis. Mutations within the klf6 gene, decreased expression and/or loss-of-heterozygosity were associated with the development of different human malignancies, and, hence, further supporting the tumor suppressor function of KLF6. This view has been challenged by other studies in distinct types of human cancers describing infrequent genetic alterations of klf6 gene or even enhanced expression in some tumors. The scenario about KLF6 function became still more complex as the description of oncogenic KLF6 splice variant 1 (SV1) with dominant negative activity against the wild type KLF6 (wtKLF6) protein. Additionally, increased evidence is suggesting that KLF6 is a bonafide target of several signaling cascades, which ultimate regulatory effect on this protein could drive decisions of cell life and death, facing the dilemma about how wtKLF6 could be involved in both processes. These apparently conflicting situations, emerged by apparently opposite effects mediated by wtKLF6, may be related, at least in part, to the biological cross-talk with the c-Jun oncoprotein. Depending on the stimulus received by the cell, wtKLF6 interaction with c-Jun determines different cell outcomes such as proliferation control or apoptosis. Thus, KLF6 responsiveness represents a kind of cell warning signal on receiving different stimuli, including oncogenic activation and microbial infections, orchestrating the implementation of proliferation and apoptotic programs.

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“…KLF1 is the founding member of a family of 17 transcription factors in mammals, which is defined by the presence of three highly similar C 2 H 2 type zinc fingers at the C terminus (Miller and Bieker 1993;van Vliet et al 2006). Expression of Klf1 is remarkably restricted to erythroid cells and their precursors (Miller and Bieker 1993) and is critical in erythroid versus megakaryocyte lineage choice (Starck et al 2003;Siatecka et al 2007;Tallack and Perkins 2010).…”

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confidence: 99%

A global role for KLF1 in erythropoiesis revealed by ChIP-seq in primary erythroid cells

et al. 2010

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KLF1 regulates a diverse suite of genes to direct erythroid cell differentiation from bipotent progenitors. To determine the local cis-regulatory contexts and transcription factor networks in which KLF1 operates, we performed KLF1 ChIP-seq in the mouse. We found at least 945 sites in the genome of E14.5 fetal liver erythroid cells which are occupied by endogenous KLF1. Many of these recovered sites reside in erythroid gene promoters such as Hbb-b1, but the majority are distant to any known gene. Our data suggests KLF1 directly regulates most aspects of terminal erythroid differentiation including production of alpha-and beta-globin protein chains, heme biosynthesis, coordination of proliferation and anti-apoptotic pathways, and construction of the red cell membrane and cytoskeleton by functioning primarily as a transcriptional activator. Additionally, we suggest new mechanisms for KLF1 cooperation with other transcription factors, in particular the erythroid transcription factor GATA1, to maintain homeostasis in the erythroid compartment.

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Human KLF17 is a new member of the Sp/KLF family of transcription factors

Cited by 103 publications

References 34 publications

The mammalian zinc finger transcription factor Krüppel‐like factor 3 (KLF3/BKLF)

The mammalian zinc finger transcription factor Krüppel‐like factor 3 (KLF3/BKLF)

Biology of Krüppel‐like factor 6 transcriptional regulator in cell life and death

A global role for KLF1 in erythropoiesis revealed by ChIP-seq in primary erythroid cells

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