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Article ; Online: What happens when the lights are left on? Transcriptomic and phenotypic habituation to light pollution.

Alaasam, Valentina J / Hui, Cassandra / Lomas, Johnathan / Ferguson, Stephen M / Zhang, Yong / Yim, Won Cheol / Ouyang, Jenny Q

iScience

2024 Volume 27, Issue 2, Page(s) 108864

Abstract: Artificial light at night (ALAN) is a ubiquitous pollutant worldwide. Exposure can induce immediate behavioral and physiological changes in animals, sometimes leading to severe health consequences. Nevertheless, many organisms persist in light-polluted ... ...

Abstract	Artificial light at night (ALAN) is a ubiquitous pollutant worldwide. Exposure can induce immediate behavioral and physiological changes in animals, sometimes leading to severe health consequences. Nevertheless, many organisms persist in light-polluted environments and may have mechanisms of habituating, reducing responses to repeated exposure over time, but this has yet to be tested experimentally. Here, we tested whether zebra finches (
Language	English
Publishing date	2024-01-12
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2024.108864
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: CmP Signaling Network Leads to Identification of Prognostic Biomarkers for Triple-Negative Breast Cancer in Caucasian Women.

Abou-Fadel, Johnathan / Bhalli, Muaz / Grajeda, Brian / Zhang, Jun

Genetic testing and molecular biomarkers

2022 Volume 26, Issue 4, Page(s) 198–219

Abstract: Objective: ...

Abstract	Objective:
MeSH term(s)	Biomarkers ; Carcinogenesis ; Female ; Humans ; Prognosis ; Proteomics ; Triple Negative Breast Neoplasms/genetics ; Triple Negative Breast Neoplasms/metabolism
Chemical Substances	Biomarkers
Language	English
Publishing date	2022-04-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	2486664-7
ISSN	1945-0257 ; 1945-0265
ISSN (online)	1945-0257
ISSN	1945-0265
DOI	10.1089/gtmb.2021.0221
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Article ; Online: Calm the raging hormone - A new therapeutic strategy involving progesterone-signaling for hemorrhagic CCMs.

Zhang, Jun / Abou-Fadel, Johnathan S

Vessel plus

2021 Volume 5

Abstract: Cerebral cavernous malformations (CCMs), one of the most common vascular malformations, are characterized by abnormally dilated intracranial microvascular capillaries resulting in increased susceptibility to hemorrhagic stroke. As an autosomal dominant ... ...

Abstract	Cerebral cavernous malformations (CCMs), one of the most common vascular malformations, are characterized by abnormally dilated intracranial microvascular capillaries resulting in increased susceptibility to hemorrhagic stroke. As an autosomal dominant disorder with incomplete penetrance, the majority of
Language	English
Publishing date	2021-07-05
Publishing country	United States
Document type	Journal Article
ISSN	2574-1209
ISSN (online)	2574-1209
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Key Members of the CmPn as Biomarkers Distinguish Histological and Immune Subtypes of Hepatic Cancers

Johnathan Abou-Fadel / Victoria Reid / Alexander Le / Jacob Croft / Jun Zhang

Diagnostics, Vol 13, Iss 1012, p

2023 Volume 1012

Abstract: Liver cancer, comprising hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA), is a leading cause of cancer-related deaths worldwide. The liver is a primary metabolic organ for progesterone (PRG) and PRG exerts its effects through classic nuclear ... ...

Abstract	Liver cancer, comprising hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA), is a leading cause of cancer-related deaths worldwide. The liver is a primary metabolic organ for progesterone (PRG) and PRG exerts its effects through classic nuclear PRG receptors (nPRs) and non-classic membrane PRG receptors (mPRs) or a combination of both. Previous studies have shown that the CCM signaling complex (CSC) couples both nPRs and mPRs to form the CmPn (CSC-mPR-PRG-nPR) signaling network, which is involved in multiple cellular signaling pathways, including tumorigenesis of various cancers. Despite advances in treatment, 5-year survival rates for liver cancer patients remain low, largely due to the chemoresistant nature of HCCs. The lack of sensitive and specific biomarkers for liver cancer diagnosis and prognosis emphasizes the need for identifying new potential biomarkers. We propose the potential use of CmPn members’ expression data as prognostic biomarkers or biomarker signatures for the major types of hepatic cancer, including HCCs and CCAs, as well as rare subtypes such as undifferentiated pleomorphic sarcoma (UPS) and hepatic angiosarcoma (HAS). In this study, we investigated the CmPn network through RNAseq data and immunofluorescence techniques to measure alterations to key cancer pathways during liver tumorigenesis. Our findings reveal significant differential expression of multiple CmPn members, including CCM1, PAQR7, PGRMC1, and nPRs, in both HCCs and CCAs, highlighting the crucial roles of mPRs, nPRs, and CSC signaling during liver tumorigenesis. These key members of the CmPn network may serve as potential biomarkers for the diagnosis and prognosis of liver cancer subtypes, including rare subtypes.
Keywords	liver cancer ; liver cancer subtypes ; immunological subtypes ; classic nuclear progesterone receptors ; non-classic membrane progesterone receptors ; biomarkers ; Medicine (General) ; R5-920
Subject code	610
Language	English
Publishing date	2023-03-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Microscopy Techniques to Investigate CCM Pathogenesis.

Abou-Fadel, Johnathan / Zhang, Jun

Methods in molecular biology (Clifton, N.J.)

2020 Volume 2152, Page(s) 303–310

Abstract: Cellular techniques allow researchers to discover underlying mechanisms of pathogenesis of CCMs in vitro before carrying over into in vivo models; optimization of these techniques facilitates the rapid discovery of CCM-associated gene and protein targets. ...

Abstract	Cellular techniques allow researchers to discover underlying mechanisms of pathogenesis of CCMs in vitro before carrying over into in vivo models; optimization of these techniques facilitates the rapid discovery of CCM-associated gene and protein targets. Here, we describe optimized cell culture applications which are essential for successful molecular techniques and will offer researchers effective methods for plasmid transfections, facilitating mammalian cell expression, subcellular localization, and fluorescence microscopy. RNA interference (RNAi) treatment of cells allows for various in vitro cellular assays as well as confocal microscopy experiments. Together, all these methods allow for an in-depth analysis of the cellular mechanisms underlying CCM pathogenesis to be explored and further dissected.
MeSH term(s)	Biomarkers ; Cell Line ; Disease Susceptibility ; Endothelial Cells/metabolism ; Gene Expression ; Hemangioma, Cavernous, Central Nervous System/etiology ; Hemangioma, Cavernous, Central Nervous System/pathology ; Humans ; Microscopy/instrumentation ; Microscopy/methods ; Microscopy, Confocal ; Microscopy, Fluorescence ; Plasmids/genetics ; Protein Transport ; RNA, Small Interfering/genetics ; Transfection
Chemical Substances	Biomarkers ; RNA, Small Interfering
Language	English
Publishing date	2020-06-10
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-0640-7_22
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Article ; Online: Preparation and Analysis of Protein Extracts to Investigate CCM Pathogenesis.

Abou-Fadel, Johnathan / Zhang, Jun

Methods in molecular biology (Clifton, N.J.)

2020 Volume 2152, Page(s) 311–324

Abstract: Molecular techniques allow for the rapid discovery of CCM-associated protein targets, crucial to understanding CCM pathogenesis. Here, we describe optimized protein extraction methods that allow for extraction from whole cell, and/or cellular sub- ... ...

Abstract	Molecular techniques allow for the rapid discovery of CCM-associated protein targets, crucial to understanding CCM pathogenesis. Here, we describe optimized protein extraction methods that allow for extraction from whole cell, and/or cellular sub-compartments, including nuclear, mitochondria, cytoplasmic, and membrane-bound proteins, from lysates. This allows for the analysis of in vitro co-immunoprecipitation (Co-IP), label-free measurement of protein-protein interactions, multiplex protein-lipid binding assays, and western blots. Together, all these methods allow for a global analysis of the molecular mechanisms underlying CCM pathogenesis.
MeSH term(s)	Carrier Proteins ; Chromatography, Affinity ; Hemangioma, Cavernous, Central Nervous System/etiology ; Hemangioma, Cavernous, Central Nervous System/metabolism ; Humans ; Immunoprecipitation ; Lipids ; Protein Binding ; Protein Interaction Mapping ; Proteome ; Proteomics/instrumentation ; Proteomics/methods
Chemical Substances	Carrier Proteins ; Lipids ; Proteome
Language	English
Publishing date	2020-06-10
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-0640-7_23
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: In-silico analysis of nonsynonymous genomic variants within CCM2 gene reaffirm the existence of dual cores within typical PTB domain

Akhil Padarti / Ofek Belkin / Johnathan Abou-Fadel / Jun Zhang

Biochemistry and Biophysics Reports, Vol 29, Iss , Pp 101218- (2022)

2022

Abstract: Purpose: The objective of this study is to validate the existence of dual cores within the typical phosphotyrosine binding (PTB) domain and to identify potentially damaging and pathogenic nonsynonymous coding single nuclear polymorphisms (nsSNPs) in the ... ...

Abstract	Purpose: The objective of this study is to validate the existence of dual cores within the typical phosphotyrosine binding (PTB) domain and to identify potentially damaging and pathogenic nonsynonymous coding single nuclear polymorphisms (nsSNPs) in the canonical PTB domain of the CCM2 gene that causes cerebral cavernous malformations (CCMs). Methods: The nsSNPs within the coding sequence for PTB domain of human CCM2 gene, retrieved from exclusive database searches, were analyzed for their functional and structural impact using a series of bioinformatic tools. The effects of mutations on the tertiary structure of the PTB domain in human CCM2 protein were predicted to examine the effect of nsSNPs on the tertiary structure of PTB Cores. Results: Our mutation analysis, through alignment of protein structures between wildtype CCM2 and mutant, predicted that the structural impacts of pathogenic nsSNPs is biophysically limited to only the spatially adjacent substituted amino acid site with minimal structural influence on the adjacent core of the PTB domain, suggesting both cores are independently functional and essential for proper CCM2 PTB function. Conclusion: Utilizing a combination of protein conservation and structure-based analysis, we analyzed the structural effects of inherited pathogenic mutations within the CCM2 PTB domain. Our results predicted that the pathogenic amino acid substitutions lead to only subtle changes locally, confined to the surrounding tertiary structure of the PTB core within which it resides, while no structural disturbance to the neighboring PTB core was observed, reaffirming the presence of independently functional dual cores in the CCM2 typical PTB domain.
Keywords	In-silico analysis ; Tertiary structure ; Superimposition of protein structures ; Amino acid substitution ; Single nucleotide polymorphisms (SNPs) ; Nonsynonymous single nucleotide polymorphisms (nsSNPs) ; Biology (General) ; QH301-705.5 ; Biochemistry ; QD415-436
Subject code	500
Language	English
Publishing date	2022-03-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Circulating Blood Prognostic Biomarker Signatures for Hemorrhagic Cerebral Cavernous Malformations (CCMs).

Croft, Jacob / Grajeda, Brian / Aguirre, Luis A / Abou-Fadel, Johnathan S / Ellis, Cameron C / Estevao, Igor / Almeida, Igor C / Zhang, Jun

International journal of molecular sciences

2024 Volume 25, Issue 9

Abstract: Cerebral cavernous malformations (CCMs) are a neurological disorder characterized by enlarged intracranial capillaries in the brain, increasing the susceptibility to hemorrhagic strokes, a major cause of death and disability worldwide. The limited ... ...

Abstract	Cerebral cavernous malformations (CCMs) are a neurological disorder characterized by enlarged intracranial capillaries in the brain, increasing the susceptibility to hemorrhagic strokes, a major cause of death and disability worldwide. The limited treatment options for CCMs underscore the importance of prognostic biomarkers to predict the likelihood of hemorrhagic events, aiding in treatment decisions and identifying potential pharmacological targets. This study aimed to identify blood biomarkers capable of diagnosing and predicting the risk of hemorrhage in CCM1 patients, establishing an initial set of circulating biomarker signatures. By analyzing proteomic profiles from both human and mouse CCM models and conducting pathway enrichment analyses, we compared groups to identify potential blood biomarkers with statistical significance. Specific candidate biomarkers primarily associated with metabolism and blood clotting pathways were identified. These biomarkers show promise as prognostic indicators for CCM1 deficiency and the risk of hemorrhagic stroke, strongly correlating with the likelihood of hemorrhagic cerebral cavernous malformations (CCMs). This lays the groundwork for further investigation into blood biomarkers to assess the risk of hemorrhagic CCMs.
MeSH term(s)	Hemangioma, Cavernous, Central Nervous System/blood ; Hemangioma, Cavernous, Central Nervous System/diagnosis ; Humans ; Animals ; Mice ; Prognosis ; Biomarkers/blood ; Proteomics/methods ; Cerebral Hemorrhage/blood ; Cerebral Hemorrhage/diagnosis ; KRIT1 Protein/blood ; Disease Models, Animal ; Female ; Male
Chemical Substances	Biomarkers ; KRIT1 Protein
Language	English
Publishing date	2024-04-26
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms25094740
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Article ; Online: Vertebrate Models to Investigate CCM Pathogenesis: The Zebrafish and Mouse Model.

Abou-Fadel, Johnathan / Zhang, Jun

Methods in molecular biology (Clifton, N.J.)

2020 Volume 2152, Page(s) 225–251

Abstract: The use of vertebrate models allows researchers to investigate mechanisms of CCM pathogenesis in vivo, to investigate discrepancies between observations seen in the lab with in vitro experiments and how they translate into animal models; these in vivo ... ...

Abstract	The use of vertebrate models allows researchers to investigate mechanisms of CCM pathogenesis in vivo, to investigate discrepancies between observations seen in the lab with in vitro experiments and how they translate into animal models; these in vivo models are more relevant in terms of CCM pathogenesis seen in humans than the in vitro counterparts. The use of CCM-deficient Zebrafish model offers advantages given their optical clarity during embryogenesis, short generation time, and high fecundity. When looking at the in vivo mouse model, gene conservation among CCM1, CCM2, and CCM3 is much higher among mammals (>92%), offering higher relevance in terms of similarities between what is seen in a mouse compared to human CCM pathogenesis. With both models, deficiencies in CCM1, CCM2, and CCM3 demonstrate perturbed cardiovascular development and underlying mechanisms of CCM pathogenesis at multiple stages seen in humans. The optimized methods described in this chapter allow researchers to benefit from both in vivo models, investigating impacts of deficiencies in CCM gene expression and its effect on angiogenesis and other signaling cascades, offering a much wider view of the molecular and cellular mechanisms in CCM progression.
MeSH term(s)	Alleles ; Animals ; Blood-Brain Barrier/metabolism ; Disease Models, Animal ; Disease Susceptibility ; Endothelial Cells/metabolism ; Fluorescent Antibody Technique ; Genomics/methods ; Hemangioma, Cavernous, Central Nervous System/etiology ; Hemangioma, Cavernous, Central Nervous System/metabolism ; Hemangioma, Cavernous, Central Nervous System/pathology ; Immunophenotyping ; In Situ Hybridization ; Mice ; Mice, Knockout ; Microtubule-Associated Proteins/genetics ; Microtubule-Associated Proteins/metabolism ; Mutation ; Neovascularization, Pathologic/genetics ; Neovascularization, Pathologic/metabolism ; Phenotype ; Proteomics/methods ; Vertebrates ; Zebrafish
Chemical Substances	Microtubule-Associated Proteins
Language	English
Publishing date	2020-06-10
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-0640-7_17
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Systems Wide Analysis of CCM Signaling Complex Alterations in CCM-Deficient Models Using Omics Approaches.

Abou-Fadel, Johnathan / Zhang, Jun

Methods in molecular biology (Clifton, N.J.)

2020 Volume 2152, Page(s) 325–344

Abstract: Omics research has garnered popularity recently to integrate in-depth analysis of alterations at the molecular level to elucidate observable phenotypes resulting from knockdown/knockout models. Genomics, performed through RNA-seq, allows the user to ... ...

Abstract	Omics research has garnered popularity recently to integrate in-depth analysis of alterations at the molecular level to elucidate observable phenotypes resulting from knockdown/knockout models. Genomics, performed through RNA-seq, allows the user to evaluate alterations at the transcription level, oftentimes more sensitive than other types of analysis, especially when attempting to understand lack of observation of an expected phenotype. Proteomics facilitates an understanding of mechanisms being altered at the translational level allowing for an understanding of multiple layers of regulation occurring, elucidating discrepancies between what is seen at the RNA level compared to what is translated to a functional protein. Here we describe the methods currently being used to evaluate CCM-deficient strains in human brain microvascular endothelial cells (HBMVEC), zebrafish embryos as well as in vivo mouse model to evaluate impacts on various signaling cascades resulting from deficiencies in KRIT1 (CCM1), MGC4607 (CCM2), and PDCD10 (CCM3). The integration of data from genomics and proteomics analysis allows for the composition of interactomes, elucidating systems wide impacts resulting from disruption of the CCM signaling complex (CSC).
MeSH term(s)	Animals ; Chromatin Immunoprecipitation Sequencing ; Chromatography, Liquid ; Computational Biology/instrumentation ; Computational Biology/methods ; Disease Models, Animal ; Genomics/instrumentation ; Genomics/methods ; Hemangioma, Cavernous, Central Nervous System/etiology ; Hemangioma, Cavernous, Central Nervous System/metabolism ; Humans ; Mice ; Microtubule-Associated Proteins/genetics ; Microtubule-Associated Proteins/metabolism ; Protein Binding ; Protein Interaction Mapping ; Proteomics/instrumentation ; Proteomics/methods ; Signal Transduction ; Tandem Mass Spectrometry ; Zebrafish
Chemical Substances	Microtubule-Associated Proteins
Language	English
Publishing date	2020-06-10
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-0640-7_24
Database	MEDical Literature Analysis and Retrieval System OnLINE

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