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Article ; Online: Krüppel-like factors 4 and 5: unity in diversity.

Sur, Inderpreet

2009 Volume 10, Issue 8, Page(s) 594–603

Abstract: Krüppel-like factors (Klf) 4 and 5 belong to a family of zinc finger-containing transcription factors that share homology with the Drosophila gene Krüppel. They regulate proliferation and differentiation of a wide variety of cells and have been linked to ...

Abstract	Krüppel-like factors (Klf) 4 and 5 belong to a family of zinc finger-containing transcription factors that share homology with the Drosophila gene Krüppel. They regulate proliferation and differentiation of a wide variety of cells and have been linked to tumorigenesis. Their most striking role so far has turned out to be their ability to reprogram/ maintain embryonic stem cell fate. In this review, the data available in the field regarding their role in proliferation and differentiation and their coupling to carcinogenesis are summarized. The emphasis is on their context dependence and how they might be able to regulate diverse transcriptional outputs from the genome.
Language	English
Publishing date	2009-07-16
Publishing country	United Arab Emirates
Document type	Journal Article
ZDB-ID	2033677-9
ISSN	1875-5488 ; 1389-2029
ISSN (online)	1875-5488
ISSN	1389-2029
DOI	10.2174/138920209789503932
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Article ; Online: The role of enhancers in cancer.

Sur, Inderpreet / Taipale, Jussi

Nature reviews. Cancer

2016 Volume 16, Issue 8, Page(s) 483–493

Abstract: Enhancer elements function as the logic gates of the genetic regulatory circuitry. One of their most important functions is the integration of extracellular signals with intracellular cell fate information to generate cell type-specific transcriptional ... ...

Abstract	Enhancer elements function as the logic gates of the genetic regulatory circuitry. One of their most important functions is the integration of extracellular signals with intracellular cell fate information to generate cell type-specific transcriptional responses. Mutations occurring in cancer often misregulate enhancers that normally control the signal-dependent expression of growth-related genes. This misregulation can result from trans-acting mechanisms, such as activation of the transcription factors or epigenetic regulators that control enhancer activity, or can be caused in cis by direct mutations that alter the activity of the enhancer or its target gene specificity. These processes can generate tumour type-specific super-enhancers and establish a 'locked' gene regulatory state that drives the uncontrolled proliferation of cancer cells. Here, we review the role of enhancers in cancer, and their potential as therapeutic targets.
MeSH term(s)	Enhancer Elements, Genetic ; Epigenesis, Genetic ; Female ; Genetic Predisposition to Disease ; Humans ; Male ; Neoplasms/genetics ; Neoplasms/pathology
Language	English
Publishing date	2016
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2062767-1
ISSN	1474-1768 ; 1474-175X
ISSN (online)	1474-1768
ISSN	1474-175X
DOI	10.1038/nrc.2016.62
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Zs.A 5563: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 24: Show issues

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Article ; Online: Severe liver disease resembling PSC in mice with K5-Cre mediated deletion of Krüppel-like factor 5 (Klf5).

Bergström, Åsa / Gerling, Marco / Van Hul, Noémi / Fernández Moro, Carlos / Rozell, Björn / Toftgård, Rune / Sur, Inderpreet

Transgenic research

2021 Volume 30, Issue 5, Page(s) 701–707

Abstract: Chronic cholestatic liver diseases including primary sclerosing cholangitis (PSC) present a complex spectrum with regards to the cause, age of manifestation and histopathological features. Current treatment options are severely limited primarily due to a ...

Abstract	Chronic cholestatic liver diseases including primary sclerosing cholangitis (PSC) present a complex spectrum with regards to the cause, age of manifestation and histopathological features. Current treatment options are severely limited primarily due to a paucity of model systems mirroring the disease. Here, we describe the Keratin 5 (K5)-Cre; Klf5
MeSH term(s)	Animals ; Cholangitis, Sclerosing ; Integrases ; Keratin-5 ; Kruppel-Like Transcription Factors/genetics ; Liver ; Liver Diseases ; Mice
Chemical Substances	Keratin-5 ; Kruppel-Like Transcription Factors ; Cre recombinase (EC 2.7.7.-) ; Integrases (EC 2.7.7.-)
Language	English
Publishing date	2021-06-11
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	31620-9
ISSN	1573-9368 ; 0962-8819
ISSN (online)	1573-9368
ISSN	0962-8819
DOI	10.1007/s11248-021-00267-6
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Article: Severe liver disease resembling PSC in mice with K5-Cre mediated deletion of Krüppel-like factor 5 (Klf5)

Bergström, Åsa / Gerling, Marco / Van Hul, Noémi / Fernández Moro, Carlos / Rozell, Björn / Toftgård, Rune / Sur, Inderpreet

Transgenic research. 2021 Oct., v. 30, no. 5

2021

Abstract	Chronic cholestatic liver diseases including primary sclerosing cholangitis (PSC) present a complex spectrum with regards to the cause, age of manifestation and histopathological features. Current treatment options are severely limited primarily due to a paucity of model systems mirroring the disease. Here, we describe the Keratin 5 (K5)-Cre; Klf5ᶠˡ/ᶠˡ mouse that spontaneously develops severe liver disease during the postnatal period with features resembling PSC including a prominent ductular reaction, fibrotic obliteration of the bile ducts and secondary degeneration/necrosis of liver parenchyma. Over time, there is an expansion of Sox9⁺ hepatocytes in the damaged livers suggestive of a hepatocyte-mediated regenerative response. We conclude that Klf5 is required for the normal function of the hepatobiliary system and that the K5-Cre; Klf5ᶠˡ/ᶠˡ mouse is an excellent model to probe the molecular events interlinking damage and regenerative response in the liver.
Keywords	bile ; genetic engineering ; hepatocytes ; histopathology ; keratin ; liver ; liver diseases ; mice ; models ; necrosis ; parenchyma (animal tissue) ; postpartum period
Language	English
Dates of publication	2021-10
Size	p. 701-707.
Publishing place	Springer International Publishing
Document type	Article
ZDB-ID	31620-9
ISSN	1573-9368 ; 0962-8819
ISSN (online)	1573-9368
ISSN	0962-8819
DOI	10.1007/s11248-021-00267-6
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Article ; Online: Single-Cell Transcriptomics of Traced Epidermal and Hair Follicle Stem Cells Reveals Rapid Adaptations during Wound Healing.

Joost, Simon / Jacob, Tina / Sun, Xiaoyan / Annusver, Karl / La Manno, Gioele / Sur, Inderpreet / Kasper, Maria

Cell reports

2018 Volume 25, Issue 3, Page(s) 585–597.e7

Abstract: Epithelial tissues, such as the skin, rely on cellular plasticity of stem cells (SCs) from different niches to restore tissue function after injury. How these molecularly and functionally diverse SC populations respond to injury remains elusive. Here, we ...

Abstract	Epithelial tissues, such as the skin, rely on cellular plasticity of stem cells (SCs) from different niches to restore tissue function after injury. How these molecularly and functionally diverse SC populations respond to injury remains elusive. Here, we genetically labeled Lgr5- or Lgr6-expressing cells from the hair follicle bulge and interfollicular epidermis (IFE), respectively, and monitored their individual transcriptional adaptations during wound healing using single-cell transcriptomics. Both Lgr5 and Lgr6 progeny rapidly induced a genetic wound signature that, for Lgr5 progeny, included the remodeling of receptors to permit interactions with the wound environment, a property that Lgr6 progeny possessed even before wounding. When contributing to re-epithelialization, Lgr5 progeny gradually replaced their bulge identity with an IFE identity, and this process started already before Lgr5 progeny left the bulge. Altogether, this study reveals how different SCs respond and adapt to a new environment, potentially explaining cellular plasticity of many epithelial tissues.
MeSH term(s)	Animals ; Cell Proliferation ; Cells, Cultured ; Epidermis/growth & development ; Epidermis/injuries ; Epidermis/metabolism ; Female ; Hair Follicle/cytology ; Hair Follicle/injuries ; Hair Follicle/metabolism ; Humans ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Re-Epithelialization ; Receptors, G-Protein-Coupled/physiology ; Single-Cell Analysis/methods ; Skin/cytology ; Skin/injuries ; Skin/metabolism ; Stem Cells/cytology ; Stem Cells/metabolism ; Transcriptome ; Wound Healing
Chemical Substances	Lgr5 protein, mouse ; Lgr6 protein, mouse ; Receptors, G-Protein-Coupled
Language	English
Publishing date	2018-10-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2018.09.059
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Article ; Online: Mice deficient of

Dave, Kashyap / Sur, Inderpreet / Yan, Jian / Zhang, Jilin / Kaasinen, Eevi / Zhong, Fan / Blaas, Leander / Li, Xiaoze / Kharazi, Shabnam / Gustafsson, Charlotte / De Paepe, Ayla / Månsson, Robert / Taipale, Jussi

eLife

2017 Volume 6

Abstract: The gene desert upstream of ... ...

Abstract	The gene desert upstream of the
MeSH term(s)	Animals ; Carcinogenesis ; Enhancer Elements, Genetic ; Gene Expression ; Mice ; Mice, Knockout ; Proto-Oncogene Proteins c-myc/biosynthesis ; Proto-Oncogene Proteins c-myc/genetics ; Sequence Deletion
Chemical Substances	Myc protein, mouse ; Proto-Oncogene Proteins c-myc
Language	English
Publishing date	2017-06-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.23382
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Article ; Online: A protein activity assay to measure global transcription factor activity reveals determinants of chromatin accessibility.

Wei, Bei / Jolma, Arttu / Sahu, Biswajyoti / Orre, Lukas M / Zhong, Fan / Zhu, Fangjie / Kivioja, Teemu / Sur, Inderpreet / Lehtiö, Janne / Taipale, Minna / Taipale, Jussi

Nature biotechnology

2018 Volume 36, Issue 6, Page(s) 521–529

Abstract: No existing method to characterize transcription factor (TF) binding to DNA allows genome-wide measurement of all TF-binding activity in cells. Here we present a massively parallel protein activity assay, active TF identification (ATI), that measures the ...

Abstract	No existing method to characterize transcription factor (TF) binding to DNA allows genome-wide measurement of all TF-binding activity in cells. Here we present a massively parallel protein activity assay, active TF identification (ATI), that measures the DNA-binding activity of all TFs in cell or tissue extracts. ATI is based on electrophoretic separation of protein-bound DNA sequences from a highly complex DNA library and subsequent mass-spectrometric identification of the DNA-bound proteins. We applied ATI to four mouse tissues and mouse embryonic stem cells and found that, in a given tissue or cell type, a small set of TFs, which bound to only ∼10 distinct motifs, displayed strong DNA-binding activity. Some of these TFs were found in all cell types, whereas others were specific TFs known to determine cell fate in the analyzed tissue or cell type. We also show that a small number of TFs determined the accessible chromatin landscape of a cell, suggesting that gene regulatory logic may be simpler than previously appreciated.
MeSH term(s)	Animals ; Base Sequence ; Binding Sites/genetics ; Biotechnology ; Cell Differentiation ; Chromatin/genetics ; Chromatin/metabolism ; DNA/genetics ; DNA/metabolism ; Drosophila melanogaster/genetics ; Drosophila melanogaster/metabolism ; Mice ; Mouse Embryonic Stem Cells/cytology ; Mouse Embryonic Stem Cells/metabolism ; Protein Binding ; Saccharomyces cerevisiae/genetics ; Saccharomyces cerevisiae/metabolism ; Schizosaccharomyces/genetics ; Schizosaccharomyces/metabolism ; Species Specificity ; Tissue Distribution ; Transcription Factors/metabolism
Chemical Substances	Chromatin ; Transcription Factors ; DNA (9007-49-2)
Language	English
Publishing date	2018-05-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1311932-1
ISSN	1546-1696 ; 1087-0156
ISSN (online)	1546-1696
ISSN	1087-0156
DOI	10.1038/nbt.4138
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Zs.A 2167: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 137: Show issues
Zs.MG 43: Show issues

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Article ; Online: Lessons from functional analysis of genome-wide association studies.

Sur, Inderpreet / Tuupanen, Sari / Whitington, Thomas / Aaltonen, Lauri A / Taipale, Jussi

Cancer research

2013 Volume 73, Issue 14, Page(s) 4180–4184

Abstract: Most cancer-associated single-nucleotide polymorphisms (SNP) identified using genome-wide association studies are located outside of protein-coding regions, and their significance and mode of action have been a source of continuing debate. One proposed ... ...

Abstract	Most cancer-associated single-nucleotide polymorphisms (SNP) identified using genome-wide association studies are located outside of protein-coding regions, and their significance and mode of action have been a source of continuing debate. One proposed mechanism of action of the SNPs is that they would affect the activity of enhancer elements regulating critical target genes. In this review, we summarize recent results that substantiate this model. These studies have identified a cancer-specific enhancer element at the 8q24 gene desert that controls the expression of the MYC oncogene. We further discuss implications of the observed difference between normal growth control and cancer for drug development, and the inherent features of genome-wide association studies that may specifically lead to identification of disease-specific regulatory elements.
MeSH term(s)	Animals ; Enhancer Elements, Genetic ; Genes, myc ; Genome-Wide Association Study/methods ; Humans ; Polymorphism, Single Nucleotide
Language	English
Publishing date	2013-07-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-13-0789
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Article ; Online: Inhibition of NF-kappaB signaling interferes with phorbol ester-induced growth arrest of keratinocytes in a TNFR1-independent manner.

Sur, Inderpreet / Ulvmar, Maria / Jungedal, Roger / Toftgård, Rune

Journal of receptor and signal transduction research

2009 Volume 29, Issue 1, Page(s) 44–51

Abstract: A skin-specific block in NF-kappaB signaling leads to hyperproliferation of the keratinocytes, inflammation, and spontaneous development of squamous cell carcinoma (SCC). Here we show that an inhibition of NF-kappaB signaling in keratinocytes, via the ... ...

Abstract	A skin-specific block in NF-kappaB signaling leads to hyperproliferation of the keratinocytes, inflammation, and spontaneous development of squamous cell carcinoma (SCC). Here we show that an inhibition of NF-kappaB signaling in keratinocytes, via the expression of the super-repressor/ degradation-resistant form of the IkappaBalpha protein (IkappaBalphaDN), interferes with the growth arrest induced by the tumor promoter 12-O-tetradecanoylphorbol 13-acetate (TPA). The IkappaBalphaDN cells are able to overcome the TPA-induced cell cycle block. Although SCC development as well as hyperproliferation due to IkappaBalphaDN expression in keratinocytes is known to require TNFR1 signaling, the effect of IkappaBalphaDN on phorbol ester signaling is downstream/independent of TNFR1. These data thus identify an interaction between IkappaBalphaDN and the tumor promoter TPA in the growth regulation of keratinocytes. The proposed mechanism is also likely to be significant in the process of cancer development due to NF-kappaB inhibition.
MeSH term(s)	Animals ; Carcinogens/pharmacology ; Cell Cycle/physiology ; Cell Line ; Cell Proliferation ; Female ; Humans ; I-kappa B Proteins/metabolism ; Keratinocytes/cytology ; Keratinocytes/drug effects ; Keratinocytes/physiology ; Male ; Mice ; Mice, Knockout ; NF-KappaB Inhibitor alpha ; NF-kappa B/antagonists & inhibitors ; NF-kappa B/metabolism ; Protein Kinase C/antagonists & inhibitors ; Protein Kinase C/metabolism ; Rats ; Receptors, Tumor Necrosis Factor, Type I/genetics ; Receptors, Tumor Necrosis Factor, Type I/metabolism ; Signal Transduction/physiology ; Tetradecanoylphorbol Acetate/pharmacology
Chemical Substances	Carcinogens ; I-kappa B Proteins ; NF-kappa B ; NFKBIA protein, human ; Nfkbia protein, mouse ; Nfkbia protein, rat ; Receptors, Tumor Necrosis Factor, Type I ; NF-KappaB Inhibitor alpha (139874-52-5) ; Protein Kinase C (EC 2.7.11.13) ; Tetradecanoylphorbol Acetate (NI40JAQ945)
Language	English
Publishing date	2009
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1230969-2
ISSN	1532-4281 ; 1079-9893
ISSN (online)	1532-4281
ISSN	1079-9893
DOI	10.1080/10799890802679876
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Article ; Online: The two-faced NF-kappaB in the skin.

Sur, Inderpreet / Ulvmar, Maria / Toftgård, Rune

International reviews of immunology

2008 Volume 27, Issue 4, Page(s) 205–223

Abstract: The role of the transcription factor NF-kappa B, particularly its coupling to inflammation and cancer, has generated considerable interest in recent years. NF-kappa B in the skin is crucial for morphogenesis and homeostasis. Perturbations in its activity ...

Abstract	The role of the transcription factor NF-kappa B, particularly its coupling to inflammation and cancer, has generated considerable interest in recent years. NF-kappa B in the skin is crucial for morphogenesis and homeostasis. Perturbations in its activity are linked to developmental skin defects, inflammatory skin disease, and skin cancer. However, the most striking aspect of NF-kappa B function in the skin is its two-faced behavior--both activation and inhibition of the pathway causes inflammation. In this review, we focus on the role of NF-kappa B in the skin and summarize the current knowledge in the field arising from animal models as well as human disease studies.
MeSH term(s)	Animals ; Cell Proliferation ; Humans ; Inflammation ; Mice ; Morphogenesis/physiology ; NF-kappa B/physiology ; Signal Transduction ; Skin/growth & development ; Skin/immunology ; Skin/metabolism ; Skin/pathology ; Skin Diseases/etiology ; Skin Diseases/immunology ; Skin Diseases/metabolism ; Skin Neoplasms/etiology ; Skin Neoplasms/immunology ; Skin Neoplasms/metabolism
Chemical Substances	NF-kappa B
Language	English
Publishing date	2008
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	632825-8
ISSN	1563-5244 ; 1545-5858 ; 0883-0185
ISSN (online)	1563-5244 ; 1545-5858
ISSN	0883-0185
DOI	10.1080/08830180802130319
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