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Article ; Online: FLYWCH1, a Multi-Functional Zinc Finger Protein Contributes to the DNA Repair Pathway.

Almozyan, Sheema / Coulton, James / Babaei-Jadidi, Roya / Nateri, Abdolrahman S

2021 Volume 10, Issue 4

Abstract: Over recent years, several Cys2-His2 (C2H2) domain-containing proteins have emerged as critical players in repairing DNA-double strand breaks. Human FLYWCH1 is a newly characterised nuclear transcription factor with (C2H2)-type zinc-finger DNA-binding ... ...

Abstract	Over recent years, several Cys2-His2 (C2H2) domain-containing proteins have emerged as critical players in repairing DNA-double strand breaks. Human FLYWCH1 is a newly characterised nuclear transcription factor with (C2H2)-type zinc-finger DNA-binding domains. Yet, our knowledge about FLYWCH1 is still in its infancy. This study explores the expression, role and regulation of FLYWCH1 in the context of DNA damage and repair. We provide evidence suggesting a potential contribution of FLYWCH1 in facilitating the recruitment of DNA-damage response proteins (DDRPs). We found that FLYWCH1 colocalises with γH2AX in normal fibroblasts and colorectal cancer (CRC) cell lines. Importantly, our results showed that enforced expression of FLYWCH1 induces the expression of γH2AX, ATM and P53 proteins. Using an
MeSH term(s)	Ataxia Telangiectasia Mutated Proteins/deficiency ; Ataxia Telangiectasia Mutated Proteins/genetics ; Cell Line ; Cell Line, Tumor ; Cisplatin/pharmacology ; DNA/genetics ; DNA/metabolism ; DNA Damage ; DNA Repair ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Fibroblasts/cytology ; Fibroblasts/drug effects ; Fibroblasts/metabolism ; Gene Expression Regulation ; Genes, Reporter ; Green Fluorescent Proteins/genetics ; Green Fluorescent Proteins/metabolism ; HCT116 Cells ; Histones/genetics ; Histones/metabolism ; Humans ; Phosphorylation ; Ribonuclease III/genetics ; Ribonuclease III/metabolism ; Signal Transduction ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	DNA-Binding Proteins ; FLYWCH1 protein, human ; H2AX protein, human ; Histones ; Tumor Suppressor Protein p53 ; Green Fluorescent Proteins (147336-22-9) ; DNA (9007-49-2) ; ATM protein, human (EC 2.7.11.1) ; Ataxia Telangiectasia Mutated Proteins (EC 2.7.11.1) ; DROSHA protein, human (EC 3.1.26.3) ; Ribonuclease III (EC 3.1.26.3) ; Cisplatin (Q20Q21Q62J)
Language	English
Publishing date	2021-04-13
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells10040889
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Article ; Online: Cross talk between LAM cells and fibroblasts may influence alveolar epithelial cell behavior in lymphangioleiomyomatosis.

Clements, Debbie / Miller, Suzanne / Babaei-Jadidi, Roya / Adam, Mike / Potter, S Steven / Johnson, Simon R

American journal of physiology. Lung cellular and molecular physiology

2021 Volume 322, Issue 2, Page(s) L283–L293

Abstract: Lymphangioleiomyomatosis (LAM) is a female-specific cystic lung disease in which tuberous sclerosis complex 2 (TSC2)-deficient LAM cells, LAM-associated fibroblasts (LAFs), and other cell types infiltrate the lungs. LAM lesions can be associated with ... ...

Abstract	Lymphangioleiomyomatosis (LAM) is a female-specific cystic lung disease in which tuberous sclerosis complex 2 (TSC2)-deficient LAM cells, LAM-associated fibroblasts (LAFs), and other cell types infiltrate the lungs. LAM lesions can be associated with type II alveolar epithelial (AT2) cells. We hypothesized that the behavior of AT2 cells in LAM is influenced locally by LAFs. We tested this hypothesis in the patient samples and in vitro. In human LAM lung, nodular AT2 cells show enhanced proliferation when compared with parenchymal AT2 cells, demonstrated by increased Ki67 expression. Furthermore, nodular AT2 cells express proteins associated with epithelial activation in other disease states including matrix metalloproteinase 7, and fibroblast growth factor 7 (FGF7). In vitro, LAF-conditioned medium is mitogenic and positively chemotactic for epithelial cells, increases the rate of epithelial repair, and protects against apoptosis. In vitro, LAM patient-derived
MeSH term(s)	Female ; Humans ; Alveolar Epithelial Cells/metabolism ; Fibroblasts/metabolism ; Lung Neoplasms/pathology ; Lymphangioleiomyomatosis/metabolism ; Tuberous Sclerosis ; Tuberous Sclerosis Complex 2 Protein/metabolism ; Tumor Suppressor Proteins/metabolism
Chemical Substances	Tuberous Sclerosis Complex 2 Protein ; Tumor Suppressor Proteins
Language	English
Publishing date	2021-12-22
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1013184-x
ISSN	1522-1504 ; 1040-0605
ISSN (online)	1522-1504
ISSN	1040-0605
DOI	10.1152/ajplung.00351.2021
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Zs.A 2749: 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)

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Article ; Online: Evolution of lung pathology in lymphangioleiomyomatosis: associations with disease course and treatment response.

Miller, Suzanne / Stewart, Iain D / Clements, Debbie / Soomro, Irshad / Babaei-Jadidi, Roya / Johnson, Simon R

The journal of pathology. Clinical research

2020 Volume 6, Issue 3, Page(s) 215–226

Abstract: Lymphangioleiomyomatosis (LAM) is a rare multisystem disease with a variable clinical course. The lungs are infiltrated by nodules of LAM cells, stromal cells and inflammatory cells, causing lung cysts and respiratory failure. We used immunohistochemical ...

Abstract	Lymphangioleiomyomatosis (LAM) is a rare multisystem disease with a variable clinical course. The lungs are infiltrated by nodules of LAM cells, stromal cells and inflammatory cells, causing lung cysts and respiratory failure. We used immunohistochemical markers in lung biopsy and transplant samples from a national cohort of women with LAM with linked clinical data to understand how LAM nodule cell populations changed with disease progression. Marker distribution was examined qualitatively by dual immunohistochemistry, and markers for LAM cells, fibroblasts, lymphatics, mast cells, proliferation, cathepsin K and mTOR pathway activity were quantitated in LAM nodules and compared with clinical features and prospective lung function loss. The LAM cell marker PNL2 was more extensively expressed in those with higher forced expiratory volume in one second (FEV
MeSH term(s)	Adult ; Antigens, Neoplasm/metabolism ; Biomarkers, Tumor/metabolism ; Cathepsin K/metabolism ; Disease Progression ; Female ; Fibroblasts/metabolism ; Fibroblasts/pathology ; Humans ; Immunohistochemistry ; Lung/metabolism ; Lung/pathology ; Lung Neoplasms/metabolism ; Lung Neoplasms/pathology ; Lymphangioleiomyomatosis/metabolism ; Lymphangioleiomyomatosis/pathology ; Middle Aged ; Perivascular Epithelioid Cell Neoplasms/metabolism ; Perivascular Epithelioid Cell Neoplasms/pathology ; Prospective Studies ; TOR Serine-Threonine Kinases/metabolism
Chemical Substances	Antigens, Neoplasm ; Biomarkers, Tumor ; PNL2 tumor biomarker ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Cathepsin K (EC 3.4.22.38)
Language	English
Publishing date	2020-04-30
Publishing country	England
Document type	Journal Article
ZDB-ID	2814357-7
ISSN	2056-4538 ; 2056-4538
ISSN (online)	2056-4538
ISSN	2056-4538
DOI	10.1002/cjp2.162
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Article ; Online: Targeting alternative splicing as a new cancer immunotherapy-phosphorylation of serine arginine-rich splicing factor (SRSF1) by SR protein kinase 1 (SRPK1) regulates alternative splicing of PD1 to generate a soluble antagonistic isoform that prevents T cell exhaustion.

Wahid, Mussarat / Pratoomthai, Benjamart / Egbuniwe, Isioma U / Evans, Hannah R / Babaei-Jadidi, Roya / Amartey, Jason O / Erdelyi, Viola / Yacqub-Usman, Kiren / Jackson, Andrew M / Morris, Jonathan C / Patel, Poulam M / Bates, David O

Cancer immunology, immunotherapy : CII

2023 Volume 72, Issue 12, Page(s) 4001–4014

Abstract: Background: Regulation of alternative splicing is a new therapeutic approach in cancer. The programmed cell death receptor 1 (PD-1) is an immunoinhibitory receptor expressed on immune cells that binds to its ligands, PD-L1 and PD-L2 expressed by cancer ... ...

Abstract	Background: Regulation of alternative splicing is a new therapeutic approach in cancer. The programmed cell death receptor 1 (PD-1) is an immunoinhibitory receptor expressed on immune cells that binds to its ligands, PD-L1 and PD-L2 expressed by cancer cells forming a dominant immune checkpoint pathway in the tumour microenvironment. Targeting this pathway using blocking antibodies (nivolumab and pembrolizumab) is the mainstay of anti-cancer immunotherapies, restoring the function of exhausted T cells. PD-1 is alternatively spliced to form isoforms that are either transmembrane signalling receptors (flPD1) that mediate T cell death by binding to the ligand, PD-L1 or an alternatively spliced, soluble, variant that lacks the transmembrane domain. Methods: We used PCR and western blotting on primary peripheral blood mononuclear cells (PBMCs) and Jurkat T cells, IL-2 ELISA, flow cytometry, co-culture of melanoma and cholangiocarcinoma cells, and bioinformatics analysis and molecular cloning to examine the mechanism of splicing of PD1 and its consequence. Results: The soluble form of PD-1, generated by skipping exon 3 (∆Ex3PD1), was endogenously expressed in PBMCs and T cells and prevents cancer cell-mediated T cell repression. Multiple binding sites of SRSF1 are adjacent to PD-1 exon 3 splicing sites. Overexpression of phosphomimic SRSF1 resulted in preferential expression of flPD1. Inhibition of SRSF1 phosphorylation both by SRPK1 shRNA knockdown and by a selective inhibitor, SPHINX31, resulted in a switch in splicing to ∆Ex3PD1. Cholangiocarcinoma cell-mediated repression of T cell IL-2 expression was reversed by SPHINX31 (equivalent to pembrolizumab). Conclusions: These results indicate that switching of the splicing decision from flPD1 to ∆Ex3PD1 by targeting SRPK1 could represent a potential novel mechanism of immune checkpoint inhibition in cancer.
MeSH term(s)	Humans ; Alternative Splicing ; Phosphorylation ; B7-H1 Antigen/genetics ; B7-H1 Antigen/metabolism ; Protein Serine-Threonine Kinases/genetics ; RNA Splicing Factors/genetics ; RNA Splicing Factors/metabolism ; Arginine/genetics ; Arginine/metabolism ; Serine/chemistry ; Serine/genetics ; Serine/metabolism ; T-Cell Exhaustion ; Interleukin-2/genetics ; Leukocytes, Mononuclear/metabolism ; Programmed Cell Death 1 Receptor/metabolism ; Serine-Arginine Splicing Factors/genetics ; Protein Isoforms/genetics ; Protein Isoforms/metabolism ; Immunotherapy ; Cholangiocarcinoma
Chemical Substances	B7-H1 Antigen ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; RNA Splicing Factors ; Arginine (94ZLA3W45F) ; Serine (452VLY9402) ; Interleukin-2 ; Programmed Cell Death 1 Receptor ; Serine-Arginine Splicing Factors (170974-22-8) ; Protein Isoforms ; SRPK1 protein, human (EC 2.7.1.-) ; SRSF1 protein, human
Language	English
Publishing date	2023-11-16
Publishing country	Germany
Document type	Journal Article
ZDB-ID	195342-4
ISSN	1432-0851 ; 0340-7004
ISSN (online)	1432-0851
ISSN	0340-7004
DOI	10.1007/s00262-023-03534-z
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Zs.A 1237: Show issues

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Article: Anti-miR-135/SPOCK1 axis antagonizes the influence of metabolism on drug response in intestinal/colon tumour organoids.

Babaei-Jadidi, Roya / Kashfi, Hossein / Alelwani, Walla / Karimi Bakhtiari, Ashkan / Kattan, Shahad W / Mansouri, Omniah A / Mukherjee, Abhik / Lobo, Dileep N / Nateri, Abdolrahman S

Oncogenesis

2022 Volume 11, Issue 1, Page(s) 4

Abstract: Little is known about the role of microRNAs (miRNAs) in rewiring the metabolism within tumours and adjacent non-tumour bearing normal tissue and their potential in cancer therapy. This study aimed to investigate the relationship between deregulated ... ...

Abstract	Little is known about the role of microRNAs (miRNAs) in rewiring the metabolism within tumours and adjacent non-tumour bearing normal tissue and their potential in cancer therapy. This study aimed to investigate the relationship between deregulated miRNAs and metabolic components in murine duodenal polyps and non-polyp-derived organoids (mPOs and mNPOs) from a double-mutant Apc
Language	English
Publishing date	2022-01-19
Publishing country	United States
Document type	Journal Article
ZDB-ID	2674437-5
ISSN	2157-9024
ISSN	2157-9024
DOI	10.1038/s41389-021-00376-1
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Article ; Online: ATM Regulated PTEN Degradation Is XIAP E3 Ubiquitin Ligase Mediated in p85α Deficient Cancer Cells and Influence Platinum Sensitivity.

Ali, Reem / Alabdullah, Muslim / Miligy, Islam / Normatova, Makhliyo / Babaei-Jadidi, Roya / Nateri, Abdolrahman S / Rakha, Emad A / Madhusudan, Srinivasan

Cells

2019 Volume 8, Issue 10

Abstract: Ataxia-telegiectasia mutated (ATM), phosphatase and tensin homolog (PTEN), and p85α are key tumour suppressors. Whether ATM regulates PTEN expression and influence platinum sensitivity is unknown. We generated ATM knockdowns (KD) and CRISPR knock outs ( ... ...

Abstract	Ataxia-telegiectasia mutated (ATM), phosphatase and tensin homolog (PTEN), and p85α are key tumour suppressors. Whether ATM regulates PTEN expression and influence platinum sensitivity is unknown. We generated ATM knockdowns (KD) and CRISPR knock outs (KO) in glioblastoma (LN18, LN229) and ovarian cancer cells (OVCAR3, OVCAR4). Doxycycline inducible PTEN expression was generated in LN18 and LN229 cells. Transient KD of p85α, CK2, and XIAP was accomplished using siRNAs. Stable p85α knock-in was isolated in LN18 cells. Molecular biology assays included proteasome activity assays, PCR, flow cytometry analysis (cell cycle, double strand break accumulation, apoptosis), immunofluorescence, co-immunoprecipitation, clonogenic, invasion, migration, and 3D neurosphere assays. The clinicopathological significance of ATM, PTEN, p85α, and XIAP (X-linked inhibitor of apoptosis protein) was evaluated in 525 human ovarian cancers using immunohistochemistry. ATM regulated PTEN is p85α dependant. ATM also controls CK2α level which in turn phosphorylates and stabilizes PTEN. In addition, p85α physically interacts with CK2α and protects CK2α from ATM regulated degradation. ATM deficiency resulted in accumulation of XIAP/p-XIAP levels which ubiquitinated PTEN and CK2α thereby directing them to degradation. ATM depletion in the context of p85α deficiency impaired cancer cell migration and invasion reduced 3D-neurosphere formation and increased toxicity to cisplatin chemotherapy. Increased sensitivity to platinum was associated with DNA double strand breaks accumulation, cell cycle arrest, and induction of autophagy. In ovarian cancer patients, ATM, PTEN, p85α, and XIAP protein levels predicted better progression free survival after platinum therapy. We unravel a previously unknown function of ATM in the regulation of PTEN throμgh XIAP mediated proteasome degradation.
MeSH term(s)	Ataxia Telangiectasia Mutated Proteins/genetics ; Ataxia Telangiectasia Mutated Proteins/metabolism ; Blotting, Western ; Caspase 3/genetics ; Caspase 3/metabolism ; Caspase 7/genetics ; Caspase 7/metabolism ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Proliferation/genetics ; Cisplatin/therapeutic use ; Doxycycline/therapeutic use ; Female ; Flow Cytometry ; HeLa Cells ; Humans ; Ovarian Neoplasms/drug therapy ; Ovarian Neoplasms/genetics ; Ovarian Neoplasms/metabolism ; PTEN Phosphohydrolase/genetics ; PTEN Phosphohydrolase/metabolism ; Plasmids/genetics ; Platinum/therapeutic use ; Protein Stability/drug effects ; Real-Time Polymerase Chain Reaction ; Tissue Array Analysis ; Ubiquitin-Protein Ligases/genetics ; Ubiquitin-Protein Ligases/metabolism ; X-Linked Inhibitor of Apoptosis Protein/genetics ; X-Linked Inhibitor of Apoptosis Protein/metabolism
Chemical Substances	X-Linked Inhibitor of Apoptosis Protein ; Platinum (49DFR088MY) ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Ataxia Telangiectasia Mutated Proteins (EC 2.7.11.1) ; PTEN Phosphohydrolase (EC 3.1.3.67) ; Caspase 3 (EC 3.4.22.-) ; Caspase 7 (EC 3.4.22.-) ; Doxycycline (N12000U13O) ; Cisplatin (Q20Q21Q62J)
Language	English
Publishing date	2019-10-18
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells8101271
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Article ; Online: Increased FLYWCH1 Expression is Negatively Correlated with Wnt/β-catenin Target Gene Expression in Acute Myeloid Leukemia Cells.

Almars, Amany / Chondrou, Panagiota S / Onyido, Emenike K / Almozyan, Sheema / Seedhouse, Claire / Babaei-Jadidi, Roya / Nateri, Abdolrahman S

International journal of molecular sciences

2019 Volume 20, Issue 11

Abstract: Acute myeloid leukaemia (AML) is a heterogeneous clonal malignancy of hematopoietic progenitor cells. The Wnt pathway and its downstream targets are tightly regulated by β-catenin. We recently discovered a new protein, FLYWCH1, which can directly bind ... ...

Abstract	Acute myeloid leukaemia (AML) is a heterogeneous clonal malignancy of hematopoietic progenitor cells. The Wnt pathway and its downstream targets are tightly regulated by β-catenin. We recently discovered a new protein, FLYWCH1, which can directly bind nuclear β-catenin. Herein, we studied the FLYWCH1/β-catenin pathway in AML cells using qRT-PCR, Western blot, and immunofluorescence assays. In addition, the stemness activity and cell cycle were analysed by the colony-forming unit (CFU) using methylcellulose-based and Propidium iodide/flow cytometry assays. We found that FLYWCH1 mRNA and protein were differentially expressed in the AML cell lines. C-Myc, cyclin D1, and c-Jun expression decreased in the presence of higher FLYWCH1 expression, and vice versa. There appeared to be the loss of FLYWCH1 expression in dividing cells. The sub-G0 phase was prolonged and shortened in the low and high FLYWCH1 expression cell lines, respectively. The G0/G1 arrest correlated with FLYWCH1-expression, and these cell lines also formed colonies, whereas the low FLYWCH1 expression cell lines could not. Thus, FLYWCH1 functions as a negative regulator of the Wnt/β-catenin pathway in AML.
MeSH term(s)	Cell Cycle/genetics ; Cell Line, Tumor ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Fluorescent Antibody Technique ; Gene Expression Regulation, Leukemic ; Humans ; Leukemia, Myeloid, Acute/genetics ; Leukemia, Myeloid, Acute/metabolism ; Neoplastic Stem Cells/metabolism ; RNA, Messenger/genetics ; Wnt Proteins/metabolism ; Wnt Signaling Pathway ; beta Catenin/metabolism
Chemical Substances	DNA-Binding Proteins ; FLYWCH1 protein, human ; RNA, Messenger ; Wnt Proteins ; beta Catenin
Language	English
Publishing date	2019-06-04
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/ijms20112739
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Article: Repurposing Antibacterial AM404 as a Potential Anticancer Drug for Targeting Colorectal Cancer Stem-Like Cells.

Ahmed, Mehreen / Jinks, Nicholas / Babaei-Jadidi, Roya / Kashfi, Hossein / Castellanos-Uribe, Marcos / May, Sean T / Mukherjee, Abhik / Nateri, Abdolrahman S

Cancers

2019 Volume 12, Issue 1

Abstract: Tumour-promoting inflammation is involved in colorectal cancer (CRC) development and therapeutic resistance. However, the antibiotics and antibacterial drugs and signalling that regulate the potency of anticancer treatment upon forced differentiation of ... ...

Abstract	Tumour-promoting inflammation is involved in colorectal cancer (CRC) development and therapeutic resistance. However, the antibiotics and antibacterial drugs and signalling that regulate the potency of anticancer treatment upon forced differentiation of cancer stem-like cell (CSC) are not fully defined yet. We screened an NIH-clinical collection of the small-molecule compound library of antibacterial/anti-inflammatory agents that identified potential candidate drugs targeting CRC-SC for differentiation. Selected compounds were validated in both in vitro organoids and ex vivo colon explant models for their differentiation induction, impediment on neoplastic cell growth, and to elucidate the mechanism of their anticancer activity. We initially focused on AM404, an anandamide uptake inhibitor. AM404 is a metabolite of acetaminophen with antibacterial activity, which showed high potential in preventing CRC-SC features, such as stemness/de-differentiation, migration and drug-resistance. Furthermore, AM404 suppressed the expression of
Language	English
Publishing date	2019-12-31
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers12010106
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Article ; Online: The streptavidin/biotinylated DNA/protein bound complex protocol for determining the association of c-JUN protein with NANOG promoter.

Ibrahim, Elsayed E / Babaei-Jadidi, Roya / Nateri, Abdolrahman S

Current protocols in stem cell biology

2013 Volume Chapter 1, Page(s) Unit 1B.10

Abstract: Chromatin immunoprecipitation (ChIP) is a widely used and pre-eminent technique for detecting the association of an individual protein or a particular protein complex with its specific DNA sequence(s) in vivo. Herein we introduce a novel and simple ... ...

Abstract	Chromatin immunoprecipitation (ChIP) is a widely used and pre-eminent technique for detecting the association of an individual protein or a particular protein complex with its specific DNA sequence(s) in vivo. Herein we introduce a novel and simple biotinylated-oligonucleotide-mediated ChIP method for testing specific binding of the c-JUN protein to the M1-DNA-regulatory element in the NANOG promoter. We prepared a 260-bp DNA PCR amplicon containing -300 bp to -59 bp, relative to the transcriptional start site of the human NANOG gene, which was transfected into mouse embryonic fibroblasts (MEF) containing wild-type (c-jun(+/+)) or knockout c-jun (c-jun(-/-)) alleles. Whole cells that were cross-linked using formaldehyde and protein-DNA interactions were immunoprecipitated using streptavidin-coupled Dynabeads. Protein-DNA cross-links were reversed during incubation at 95°C, and protein samples were visualized using SDS-PAGE electrophoresis and western blotting. This streptavidin/biotinylated DNA/protein-bound complex protocol can be used for detecting the interactions between multiple transcription factors and their DNA binding sites.
MeSH term(s)	Animals ; Biotinylation/drug effects ; Blotting, Western ; Chromatin Immunoprecipitation/methods ; Cross-Linking Reagents/pharmacology ; DNA/metabolism ; DNA-Binding Proteins/metabolism ; Embryo, Mammalian/cytology ; Fibroblasts/drug effects ; Fibroblasts/metabolism ; Homeodomain Proteins/genetics ; Humans ; Mice ; Nanog Homeobox Protein ; Polymerase Chain Reaction ; Promoter Regions, Genetic ; Protein Binding/drug effects ; Proto-Oncogene Proteins c-jun/metabolism ; Streptavidin/metabolism
Chemical Substances	Cross-Linking Reagents ; DNA-Binding Proteins ; Homeodomain Proteins ; NANOG protein, human ; Nanog Homeobox Protein ; Proto-Oncogene Proteins c-jun ; DNA (9007-49-2) ; Streptavidin (9013-20-1)
Language	English
Publishing date	2013-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1938-8969
ISSN (online)	1938-8969
DOI	10.1002/9780470151808.sc01b10s25
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Article ; Online: Mast-Cell Tryptase Release Contributes to Disease Progression in Lymphangioleiomyomatosis.

Babaei-Jadidi, Roya / Dongre, Arundhati / Miller, Suzanne / Castellanos Uribe, Marcos / Stewart, Ian D / Thompson, Zoe M / Nateri, Abdolrahman S / Bradding, Peter / May, Sean T / Clements, Debbie / Johnson, Simon R

American journal of respiratory and critical care medicine

2021 Volume 204, Issue 4, Page(s) 431–444

Abstract: Rationale: ...

Abstract	Rationale:
MeSH term(s)	Adult ; Animals ; Biomarkers, Tumor/genetics ; Biomarkers, Tumor/metabolism ; Chemokines/metabolism ; Disease Progression ; Fibroblasts/metabolism ; Fibroblasts/pathology ; Gene Expression Regulation, Neoplastic ; Humans ; Lung Neoplasms/genetics ; Lung Neoplasms/metabolism ; Lung Neoplasms/pathology ; Lymphangioleiomyomatosis/genetics ; Lymphangioleiomyomatosis/metabolism ; Lymphangioleiomyomatosis/pathology ; Mast Cells/metabolism ; Mast Cells/pathology ; Mice ; Mice, Inbred C57BL ; Middle Aged ; Spheroids, Cellular ; Tryptases/metabolism ; Tumor Cells, Cultured
Chemical Substances	Biomarkers, Tumor ; Chemokines ; Tryptases (EC 3.4.21.59)
Language	English
Publishing date	2021-04-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1180953-x
ISSN	1535-4970 ; 0003-0805 ; 1073-449X
ISSN (online)	1535-4970
ISSN	0003-0805 ; 1073-449X
DOI	10.1164/rccm.202007-2854OC
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