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Article ; Online: Experimental Insights into the Interplay between Histone Modifiers and p53 in Regulating Gene Expression

Hyun-Min Kim / Xiaoyu Zheng / Ethan Lee

International Journal of Molecular Sciences, Vol 24, Iss 11032, p

2023 Volume 11032

Abstract: Chromatin structure plays a fundamental role in regulating gene expression, with histone modifiers shaping the structure of chromatin by adding or removing chemical changes to histone proteins. The p53 transcription factor controls gene expression, binds ...

Abstract	Chromatin structure plays a fundamental role in regulating gene expression, with histone modifiers shaping the structure of chromatin by adding or removing chemical changes to histone proteins. The p53 transcription factor controls gene expression, binds target genes, and regulates their activity. While p53 has been extensively studied in cancer research, specifically in relation to fundamental cellular processes, including gene transcription, apoptosis, and cell cycle progression, its association with histone modifiers has received limited attention. This review explores the interplay between histone modifiers and p53 in regulating gene expression. We discuss how histone modifications can influence how p53 binds to target genes and how this interplay can be disrupted in cancer cells. This review provides insights into the complex mechanisms underlying gene regulation and their implications for potential cancer therapy.
Keywords	histone modifications ; p53 ; cancer ; gene regulation ; chromatin structure ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	572
Language	English
Publishing date	2023-07-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Palaeoglaciation in the Low Latitude, Low Elevation Tropical Andes, Northern Peru

Ethan Lee / Neil Ross / Andrew C. G. Henderson / Andrew J. Russell / Stewart S. R. Jamieson / Derek Fabel

Frontiers in Earth Science, Vol

2022 Volume 10

Abstract: Characterising glaciological change within the tropical Andes is important because tropical glaciers are sensitive to climate change. Our understanding of glacier dynamics and how tropical glaciers respond to global climate perturbations is poorly ... ...

Abstract	Characterising glaciological change within the tropical Andes is important because tropical glaciers are sensitive to climate change. Our understanding of glacier dynamics and how tropical glaciers respond to global climate perturbations is poorly constrained. Studies of past glaciation in the tropical Andes have focused on locations where glaciers are still present or recently vacated cirques at high elevations. Few studies focused on lower elevation localities because it was assumed glaciers did not exist or were not as extensive. We present the first geomorphological evidence for past glaciations of the Lagunas de Las Huaringas, northern Peru, at elevations of 3,900–2,600 m a.s.l. Mapping was conducted using remotely-sensed optical imagery and a newly created high-resolution (∼2.5 m) digital elevation model (DEM). The area has abundant evidence for glaciation, including moraines, glacial cirques, hummocky terrain, glacial lineations and ice-sculpted bedrock. Two potential models for glaciation are hypothesised: 1) plateau-fed ice cap, or 2) valley glaciation. Assuming glaciers reached their maximum extent during the Local Last Glacial Maximum (LLGM), between 23.5 ± 0.5 and 21.2 ± 0.8 ka, the maximum reconstructed glacial area was 75.6 km2. A mean equilibrium line altitude (ELA) of 3,422 ± 30 m was calculated, indicating an ELA change of −1,178 ± 10 m compared to modern snowline elevation. There is an east to west ELA elevation gradient, lower in the east and higher in the west, in-line with modern day transfer of moisture. Applying lapse rates between 5.5 and 7.5°C/km provides a LLGM temperature cooling of between 6.5–8.8°C compared to present. These values are comparable to upper estimates from other studies within the northern tropical Andes and from ice-core reconstructions. The mapping of glacial geomorphology within the Lagunas de las Huaringas, evidences, for the first time, extensive glaciation in a low elevation region of northern Peru, with implications for our understanding of past climate in the ...
Keywords	Peru ; tropical Andes ; glacial geomorphology ; tropical glaciers ; ELA ; LGM ; Science ; Q
Subject code	550
Language	English
Publishing date	2022-04-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Accelerated mass loss of Himalayan glaciers since the Little Ice Age

Ethan Lee / Jonathan L. Carrivick / Duncan J. Quincey / Simon J. Cook / William H. M. James / Lee E. Brown

Scientific Reports, Vol 11, Iss 1, Pp 1-

2021 Volume 8

Abstract: Abstract Himalayan glaciers are undergoing rapid mass loss but rates of contemporary change lack long-term (centennial-scale) context. Here, we reconstruct the extent and surfaces of 14,798 Himalayan glaciers during the Little Ice Age (LIA), 400 to 700 ... ...

Abstract	Abstract Himalayan glaciers are undergoing rapid mass loss but rates of contemporary change lack long-term (centennial-scale) context. Here, we reconstruct the extent and surfaces of 14,798 Himalayan glaciers during the Little Ice Age (LIA), 400 to 700 years ago. We show that they have lost at least 40 % of their LIA area and between 390 and 586 km3 of ice; 0.92 to 1.38 mm Sea Level Equivalent. The long-term rate of ice mass loss since the LIA has been between − 0.011 and − 0.020 m w.e./year, which is an order of magnitude lower than contemporary rates reported in the literature. Rates of mass loss depend on monsoon influence and orographic effects, with the fastest losses measured in East Nepal and in Bhutan north of the main divide. Locally, rates of loss were enhanced with the presence of surface debris cover (by 2 times vs clean-ice) and/or a proglacial lake (by 2.5 times vs land-terminating). The ten-fold acceleration in ice loss we have observed across the Himalaya far exceeds any centennial-scale rates of change that have been recorded elsewhere in the world.
Keywords	Medicine ; R ; Science ; Q
Language	English
Publishing date	2021-12-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Casein Kinase 1α as a Regulator of Wnt-Driven Cancer

Chen Shen / Anmada Nayak / Ricardo A. Melendez / Daniel T. Wynn / Joshua Jackson / Ethan Lee / Yashi Ahmed / David J. Robbins

International Journal of Molecular Sciences, Vol 21, Iss 5940, p

2020 Volume 5940

Abstract: Wnt signaling regulates numerous cellular processes during embryonic development and adult tissue homeostasis. Underscoring this physiological importance, deregulation of the Wnt signaling pathway is associated with many disease states, including cancer. ...

Abstract	Wnt signaling regulates numerous cellular processes during embryonic development and adult tissue homeostasis. Underscoring this physiological importance, deregulation of the Wnt signaling pathway is associated with many disease states, including cancer. Here, we review pivotal regulatory events in the Wnt signaling pathway that drive cancer growth. We then discuss the roles of the established negative Wnt regulator, casein kinase 1α (CK1α), in Wnt signaling. Although the study of CK1α has been ongoing for several decades, the bulk of such research has focused on how it phosphorylates and regulates its various substrates. We focus here on what is known about the mechanisms controlling CK1α, including its putative regulatory proteins and alternative splicing variants. Finally, we describe the discovery and validation of a family of pharmacological CK1α activators capable of inhibiting Wnt pathway activity. One of the important advantages of CK1α activators, relative to other classes of Wnt inhibitors, is their reduced on-target toxicity, overcoming one of the major impediments to developing a clinically relevant Wnt inhibitor. Therefore, we also discuss mechanisms that regulate CK1α steady-state homeostasis, which may contribute to the deregulation of Wnt pathway activity in cancer and underlie the enhanced therapeutic index of CK1α activators.
Keywords	Wnt ; cancer ; targeted therapies ; CK1α ; kinase agonists ; review ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	570
Language	English
Publishing date	2020-08-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: High-throughput drug screening of fine-needle aspiration-derived cancer organoids

Kensey Bergdorf / Courtney Phifer / Vijaya Bharti / David Westover / Joshua Bauer / Anna Vilgelm / Ethan Lee / Vivian Weiss

STAR Protocols, Vol 1, Iss 3, Pp 100212- (2020)

2020

Abstract: Summary: Generation of fine-needle aspiration (FNA)-derived cancer organoids has allowed us to develop a number of downstream applications. In this protocol, we start with organoids cultured in a semi-solid format. We dissociate organoids into single ... ...

Abstract	Summary: Generation of fine-needle aspiration (FNA)-derived cancer organoids has allowed us to develop a number of downstream applications. In this protocol, we start with organoids cultured in a semi-solid format. We dissociate organoids into single cells and then plate in a 384-well format for high-throughput drug screening. While this method must be fine-tuned for each individual organoid culture, it offers a format well suited for rapidly screening medium-sized drug/compound libraries (500–5,000 molecules) and generating dose-response curves to measure relative efficacy.For complete details on the use and execution of this protocol, please refer to Lee et al. (2020) and Vilgelm et al. (2020).
Keywords	Cell culture ; Cell-based Assays ; Cancer ; High Throughput Screening ; Organoids ; Science (General) ; Q1-390
Language	English
Publishing date	2020-12-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: DDR1 contributes to kidney inflammation and fibrosis by promoting the phosphorylation of BCR and STAT3

Corina M. Borza / Gema Bolas / Fabian Bock / Xiuqi Zhang / Favour C. Akabogu / Ming-Zhi Zhang / Mark de Caestecker / Min Yang / Haichun Yang / Ethan Lee / Leslie Gewin / Agnes B. Fogo / W. Hayes McDonald / Roy Zent / Ambra Pozzi

JCI Insight, Vol 7, Iss

2022 Volume 3

Abstract: Discoidin domain receptor 1 (DDR1), a receptor tyrosine kinase activated by collagen, contributes to chronic kidney disease. However, its role in acute kidney injury and subsequent development of kidney fibrosis is not clear. Thus, we performed a model ... ...

Abstract	Discoidin domain receptor 1 (DDR1), a receptor tyrosine kinase activated by collagen, contributes to chronic kidney disease. However, its role in acute kidney injury and subsequent development of kidney fibrosis is not clear. Thus, we performed a model of severe ischemia/reperfusion-induced acute kidney injury that progressed to kidney fibrosis in WT and Ddr1-null mice. We showed that Ddr1-null mice had reduced acute tubular injury, inflammation, and tubulointerstitial fibrosis with overall decreased renal monocyte chemoattractant protein (MCP-1) levels and STAT3 activation. We identified breakpoint cluster region (BCR) protein as a phosphorylated target of DDR1 that controls MCP-1 production in renal proximal tubule epithelial cells. DDR1-induced BCR phosphorylation or BCR downregulation increased MCP-1 secretion, suggesting that BCR negatively regulates the levels of MCP-1. Mechanistically, phosphorylation or downregulation of BCR increased β-catenin activity and in turn MCP-1 production. Finally, we showed that DDR1-mediated STAT3 activation was required to stimulate the secretion of TGF-β. Thus, DDR1 contributes to acute and chronic kidney injury by regulating BCR and STAT3 phosphorylation and in turn the production of MCP-1 and TGF-β. These findings identify DDR1 an attractive therapeutic target for ameliorating both proinflammatory and profibrotic signaling in kidney disease.
Keywords	Cell biology ; Nephrology ; Medicine ; R
Subject code	616
Language	English
Publishing date	2022-02-01T00:00:00Z
Publisher	American Society for Clinical investigation
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: SELENOP modifies sporadic colorectal carcinogenesis and WNT signaling activity through LRP5/6 interactions

Jennifer M. Pilat / Rachel E. Brown / Zhengyi Chen / Nathaniel J. Berle / Adrian P. Othon / M. Kay Washington / Shruti A. Anant / Suguru Kurokawa / Victoria H. Ng / Joshua J. Thompson / Justin Jacobse / Jeremy A. Goettel / Ethan Lee / Yash A. Choksi / Ken S. Lau / Sarah P. Short / Christopher S. Williams

The Journal of Clinical Investigation, Vol 133, Iss

2023 Volume 13

Abstract: Although selenium deficiency correlates with colorectal cancer (CRC) risk, the roles of the selenium-rich antioxidant selenoprotein P (SELENOP) in CRC remain unclear. In this study, we defined SELENOP’s contributions to sporadic CRC. In human single-cell ...

Abstract	Although selenium deficiency correlates with colorectal cancer (CRC) risk, the roles of the selenium-rich antioxidant selenoprotein P (SELENOP) in CRC remain unclear. In this study, we defined SELENOP’s contributions to sporadic CRC. In human single-cell cRNA-Seq (scRNA-Seq) data sets, we discovered that SELENOP expression rose as normal colon stem cells transformed into adenomas that progressed into carcinomas. We next examined the effects of Selenop KO in a mouse adenoma model that involved conditional, intestinal epithelium-specific deletion of the tumor suppressor adenomatous polyposis coli (Apc) and found that Selenop KO decreased colon tumor incidence and size. We mechanistically interrogated SELENOP-driven phenotypes in tumor organoids as well as in CRC and noncancer cell lines. Selenop-KO tumor organoids demonstrated defects in organoid formation and decreases in WNT target gene expression, which could be reversed by SELENOP restoration. Moreover, SELENOP increased canonical WNT signaling activity in noncancer and CRC cell lines. In defining the mechanism of action of SELENOP, we mapped protein-protein interactions between SELENOP and the WNT coreceptors low-density lipoprotein receptor–related proteins 5 and 6 (LRP5/6). Last, we confirmed that SELENOP-LRP5/6 interactions contributed to the effects of SELENOP on WNT activity. Overall, our results position SELENOP as a modulator of the WNT signaling pathway in sporadic CRC.
Keywords	Gastroenterology ; Medicine ; R
Subject code	570
Language	English
Publishing date	2023-07-01T00:00:00Z
Publisher	American Society for Clinical Investigation
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Immunofluorescent staining of cancer spheroids and fine-needle aspiration-derived organoids

Kensey N. Bergdorf / Courtney J. Phifer / Matthew E. Bechard / Mason A. Lee / Oliver G. McDonald / Ethan Lee / Vivian L. Weiss

STAR Protocols, Vol 2, Iss 2, Pp 100578- (2021)

2021

Abstract: Summary: Our organoid generation technique has allowed for the development of downstream organoid applications. Here, we detail an accessible, straightforward protocol for immunofluorescent staining and imaging of thyroid cancer organoids, particularly ... ...

Abstract	Summary: Our organoid generation technique has allowed for the development of downstream organoid applications. Here, we detail an accessible, straightforward protocol for immunofluorescent staining and imaging of thyroid cancer organoids, particularly those with tumor de-differentiation. Immunofluorescence is a powerful tool to help understand the localization of cell types within organoids and determine the interactions between those cells. As organoids have been shown to recapitulate patient tumor morphology, immunofluorescent staining and imaging of organoids allows for enhanced understanding of near in vivo structures.For complete details on the use and execution of this protocol, please refer to Lee et al. (2020) and Vilgelm et al. (2020).
Keywords	Cell culture ; Cancer ; Microscopy ; Organoids ; Science (General) ; Q1-390
Language	English
Publishing date	2021-06-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Socioeconomic deprivation and prognostic outcomes in acute coronary syndrome: A meta-analysis using multidimensional socioeconomic status indices.

International journal of cardiology

2023 Volume 383, Page(s) 140–150

Abstract: Background: Low socioeconomic status (SES) is an important prognosticator amongst patients with acute coronary syndrome (ACS). This paper analysed the effects of SES on ACS outcomes.: Methods: Medline and Embase were searched for articles reporting ... ...

Abstract	Background: Low socioeconomic status (SES) is an important prognosticator amongst patients with acute coronary syndrome (ACS). This paper analysed the effects of SES on ACS outcomes. Methods: Medline and Embase were searched for articles reporting outcomes of ACS patients stratified by SES using a multidimensional index, comprising at least 2 of the following components: Income, Education and Employment. A comparative meta-analysis was conducted using random-effects models to estimate the risk ratio of all-cause mortality in low SES vs high SES populations, stratified according to geographical region, study year, follow-up duration and SES index. Results: A total of 29 studies comprising of 301,340 individuals were included, of whom 43.7% were classified as low SES. While patients of both SES groups had similar cardiovascular risk profiles, ACS patients of low SES had significantly higher risk of all-cause mortality (adjusted HR:1.19, 95%CI: 1.10-1.1.29, p < 0.001) compared to patients of high SES, with higher 1-year mortality (RR:1.08, 95%CI:1.03-1.13, p = 0.0057) but not 30-day mortality (RR:1.07, 95%CI:0.98-1.16, p = 0.1003). Despite having similar rates of ST-elevation myocardial infarction and non-ST-elevation ACS, individuals with low SES had lower rates of coronary revascularisation (RR:0.95, 95%CI:0.91-0.99, p = 0.0115) and had higher cerebrovascular accident risk (RR:1.25, 95%CI:1.01-1.55, p = 0.0469). Excess mortality risk was independent of region (p = 0.2636), study year (p = 0.7271) and duration of follow-up (p = 0.0604) but was dependent on the SES index used (p < 0.0001). Conclusion: Low SES is associated with increased mortality post-ACS, with suboptimal coronary revascularisation rates compared to those of high SES. Concerted efforts are needed to address the global ACS-related socioeconomic inequity. Registration and protocol: The current study was registered with PROSPERO, ID: CRD42022347987.
MeSH term(s)	Humans ; Acute Coronary Syndrome/diagnosis ; Acute Coronary Syndrome/surgery ; Prognosis ; Social Class ; ST Elevation Myocardial Infarction ; Low Socioeconomic Status
Language	English
Publishing date	2023-04-26
Publishing country	Netherlands
Document type	Meta-Analysis ; Journal Article
ZDB-ID	779519-1
ISSN	1874-1754 ; 0167-5273
ISSN (online)	1874-1754
ISSN	0167-5273
DOI	10.1016/j.ijcard.2023.04.042
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: The Drosophila MCPH1-B isoform is a substrate of the APCCdh1 E3 ubiquitin ligase complex

Sarah G. Hainline / Jamie L. Rickmyre / Leif R. Neitzel / Laura A. Lee / Ethan Lee

Biology Open, Vol 3, Iss 7, Pp 669-

2014 Volume 676

Abstract: The Anaphase-Promoting Complex (APC) is a multi-subunit E3 ubiquitin ligase that coordinates progression through the cell cycle by temporally and spatially promoting the degradation of key proteins. Many of these targeted proteins have been shown to play ...

Abstract	The Anaphase-Promoting Complex (APC) is a multi-subunit E3 ubiquitin ligase that coordinates progression through the cell cycle by temporally and spatially promoting the degradation of key proteins. Many of these targeted proteins have been shown to play important roles in regulating orderly progression through the cell cycle. Using a previously described Drosophila in vitro expression cloning approach, we screened for new substrates of the APC in Xenopus egg extract and identified Drosophila MCPH1 (dMCPH1), a protein encoded by the homolog of a causative gene for autosomal recessive primary microcephaly in humans. The dMCPH1-B splice form, but not the dMCPH1-C splice form, undergoes robust degradation in Xenopus interphase egg extract in a Cdh1-dependent manner. Degradation of dMCPH1-B is controlled by an N-terminal destruction box (D-box) motif as its deletion or mutation blocks dMCPH1-B degradation. dMCPH1 levels are increased in Drosophila morula (APC2) mutant embryos, consistent with dMCPH1 being an APC substrate in vivo. Using a purified, reconstituted system, we show that dMCPH1-B is ubiquitinated by APCCdh1, indicating that the effect of APC on dMCPH1-B ubiquitination and degradation is direct. Full-length human MCPH1 (hMCPH1) has been predicted to be an APC substrate based on its interaction with the APC subunit Cdc27. We were not able to detect changes in hMCPH1 levels during the cell cycle in cultured human cells. Overexpression of hMCPH1 (or dMCPH1-B) in developing Xenopus embryos, however, disrupts cell division, suggesting that proper regulation of hMCPH1 and dMCPH1-B activity plays a critical role in proper cell-cycle progression.
Keywords	Anaphase-Promoting Complex ; Drosophila ; MCPH1 ; Ubiquitination ; Xenopus egg extract ; Science ; Q ; Biology (General) ; QH301-705.5
Subject code	572
Language	English
Publishing date	2014-06-01T00:00:00Z
Publisher	The Company of Biologists
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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