A functional screen for Krüppel-like factors that regulate the human γ-globin gene through the CACCC promoter element

Zhang, Ping; Basu, P.; Redmond, Latasha C.; Morris, Pamela E.; Rupon, Jeremy; Ginder, Gordon D.; Lloyd, Joyce A.

doi:10.1016/j.bcmd.2005.04.009

Cited by 59 publications

(54 citation statements)

References 30 publications

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“…In the mouse embryo, there is robust developmental expression of KLF13 in the heart, cephalic mesenchyme, dermis, and epithelial layers of the gut and urinary bladder [50]. There are a number of reports describing the important role of KLF13 in the transcriptional regulation of erythroid gene expression [51,52] and its critical role in the induction of RANTES expression in activated T-lymphocytes [48,53].…”

Section: Klf13mentioning

confidence: 99%

Kruppel-like Factors (KLFs) in muscle biology

Haldar¹,

Ibrahim²,

Jain³

2007

Journal of Molecular and Cellular Cardiology

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The Kruppel-like Factor (KLF) family of zinc-finger transcription factors are critical regulators of cell differentiation, phenotypic modulation and physiologic function. An emerging body of evidence implicates an important role for these factors in cardiovascular biology, however, the role of KLFs in muscle biology is only beginning to be understood. This article reviews the published data describing the role of KLFs in cardiomyocytes, smooth muscle cells, and skeletal muscle and highlights the importance of these factors in cardiovascular development, physiology and disease pathobiology.

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Section: Klf13mentioning

confidence: 99%

Kruppel-like Factors (KLFs) in muscle biology

Haldar¹,

Ibrahim²,

Jain³

2007

Journal of Molecular and Cellular Cardiology

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“…Klf8 also acts as a transcriptional repressor and interacts with the co-repressor CtBP through a PVDLS motif (7). There are two reports implicating Klf8 in ␥-globin gene repression (25,26). Klf8 has also been implicated in cell cycle progression and has been shown to be a downstream target of the cell cycle regulator focal adhesion kinase (27).…”

mentioning

confidence: 99%

A Network of Krüppel-like Factors (Klfs)

Eaton¹,

Funnell²,

Sue³

et al. 2008

Journal of Biological Chemistry

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“…The CACCC sequence was initially reported to be required for KLF11-mediated activation of +-globin gene promoter [8], whereas a later study failed to induce significant alterations of +-globin gene promoter activity by cotransfected KLF11 [17]. However, KLF11 seems to be expendable for globin gene expression since KLF11 −/− mice display normal haematopoiesis at all stages of development [18].…”

Section: Discussionmentioning

confidence: 98%

Human Krüppel-like factor 11 inhibits human proinsulin promoter activity in pancreatic beta cells

et al. 2007

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Aims/hypothesis The Krüppel-like factor 11 (KLF11; TIEG2), a pancreas-enriched Sp1-like transcription factor, is a known negative regulator of pancreatic exocrine cell growth. A recent study indicated KLF11-induced activation of the human proinsulin promoter (hInsP). Materials and methods We investigated the functional role of KLF11 in pancreatic beta cells. Results Endogenous KLF11 mRNA expression was found in whole rat pancreas, human pancreatic islets and INS-1E beta cells and was profoundly reduced by high glucose in INS-1E. Cotransfections of INS-1E and beta-TC3 beta cells with a human (h)KLF11 expression plasmid and an hInsP-driven reporter plasmid resulted in a substantial dose-dependent and glucose-independent inhibition of proinsulin promoter activity. 5′-deletion of hInsP demonstrated that hKLF11 acts via DNA sequences upstream of −173 and requires the beta cellspecific transcription machinery, since hKLF11-mediated inhibition of promoter activity was abolished in HEK293

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A functional screen for Krüppel-like factors that regulate the human γ-globin gene through the CACCC promoter element

Cited by 59 publications

References 30 publications

Kruppel-like Factors (KLFs) in muscle biology

Kruppel-like Factors (KLFs) in muscle biology

A Network of Krüppel-like Factors (Klfs)

Human Krüppel-like factor 11 inhibits human proinsulin promoter activity in pancreatic beta cells

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