{"entity": "journal", "iuid": "673ec6194f4d4686a8dcdf602be9da2d", "timestamp": "2026-08-22T06:51:57.497Z", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/journal/Life%20%28Basel%29.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/journal/Life%20%28Basel%29"}}, "title": "Life (Basel)", "issn": "2075-1729", "issn-l": null, "publications_count": 3, "publications": [{"entity": "publication", "iuid": "18f55f7d966e4c2a88047cb28c65b222", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/18f55f7d966e4c2a88047cb28c65b222.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/18f55f7d966e4c2a88047cb28c65b222"}}, "title": "Role of ZNF143 and Its Association with Gene Expression Patterns, Noncoding Mutations, and the Immune System in Human Breast Cancer.", "authors": [{"family": "Saddeek", "given": "Salma", "initials": "S", "orcid": "0000-0002-3207-1837", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/4224c75f6f6342659458f28302a5cafb.json"}}, {"family": "Almassabi", "given": "Rehab", "initials": "R", "orcid": "0000-0003-2639-6384", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/0c829d07299b4595b75f11a6801cf7ff.json"}}, {"family": "Mobashir", "given": "Mohammad", "initials": "M", "orcid": "0000-0002-5385-4048", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/8e961b3a2fe94cb3acc1fa8f718cd97c.json"}}], "type": "journal article", "published": "2022-12-22", "journal": {"title": "Life (Basel)", "issn": "2075-1729", "volume": "13", "issue": "1", "issn-l": null}, "abstract": "The function of noncoding sequence variations at ZNF143 binding sites in breast cancer cells is currently not well understood. Distal elements and promoters, also known as cis-regulatory elements, control the expression of genes. They may be identified by functional genomic techniques and sequence conservation, and they frequently show cell- and tissue-type specificity. The creation, destruction, or modulation of TF binding and function may be influenced by genetic modifications at TF binding sites that affect the binding affinity. Therefore, noncoding mutations that affect the ZNF143 binding site may be able to alter the expression of some genes in breast cancer. In order to understand the relationship among ZNF143, gene expression patterns, and noncoding mutations, we adopted an integrative strategy in this study and paid close attention to putative immunological signaling pathways. The immune system-related pathways ErbB, HIF1a, NF-kB, FoxO, JAK-STAT, Wnt, Notch, cell cycle, PI3K-AKT, RAP1, calcium signaling, cell junctions and adhesion, actin cytoskeleton regulation, and cancer pathways are among those that may be significant, according to the overall analysis.", "doi": "10.3390/life13010027", "pmid": "36675976", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC9865137"}, {"db": "pii", "key": "life13010027"}], "notes": [], "created": "2026-08-21T13:04:04.690Z", "modified": "2026-08-21T13:04:04.813Z"}, {"entity": "publication", "iuid": "61e386329419404897582dedb033ae5c", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/61e386329419404897582dedb033ae5c.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/61e386329419404897582dedb033ae5c"}}, "title": "NF-kB in Signaling Patterns and Its Temporal Dynamics Encode/Decode Human Diseases.", "authors": [{"family": "Almowallad", "given": "Sanaa", "initials": "S", "orcid": "0000-0001-6317-4065", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/ba5088a953384eaf92f910fef81a2de0.json"}}, {"family": "Alqahtani", "given": "Leena S", "initials": "LS", "orcid": "0000-0003-1789-2239", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/1285b072b3804ad6a66f47793a0cf686.json"}}, {"family": "Mobashir", "given": "Mohammad", "initials": "M", "orcid": "0000-0002-5385-4048", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/8e961b3a2fe94cb3acc1fa8f718cd97c.json"}}], "type": "journal article", "published": "2022-12-02", "journal": {"title": "Life (Basel)", "issn": "2075-1729", "volume": "12", "issue": "12", "issn-l": null}, "abstract": "Defects in signaling pathways are the root cause of many disorders. These malformations come in a wide variety of types, and their causes are also very diverse. Some of these flaws can be brought on by pathogenic organisms and viruses, many of which can obstruct signaling processes. Other illnesses are linked to malfunctions in the way that cell signaling pathways work. When thinking about how errors in signaling pathways might cause disease, the idea of signalosome remodeling is helpful. The signalosome may be conveniently divided into two types of defects: phenotypic remodeling and genotypic remodeling. The majority of significant illnesses that affect people, including high blood pressure, heart disease, diabetes, and many types of mental illness, appear to be caused by minute phenotypic changes in signaling pathways. Such phenotypic remodeling modifies cell behavior and subverts normal cellular processes, resulting in illness. There has not been much progress in creating efficient therapies since it has been challenging to definitively confirm this connection between signalosome remodeling and illness. The considerable redundancy included into cell signaling systems presents several potential for developing novel treatments for various disease conditions. One of the most important pathways, NF-\u03baB, controls several aspects of innate and adaptive immune responses, is a key modulator of inflammatory reactions, and has been widely studied both from experimental and theoretical perspectives. NF-\u03baB contributes to the control of inflammasomes and stimulates the expression of a number of pro-inflammatory genes, including those that produce cytokines and chemokines. Additionally, NF-\u03baB is essential for controlling innate immune cells and inflammatory T cells' survival, activation, and differentiation. As a result, aberrant NF-\u03baB activation plays a role in the pathogenesis of several inflammatory illnesses. The activation and function of NF-\u03baB in relation to inflammatory illnesses was covered here, and the advancement of treatment approaches based on NF-\u03baB inhibition will be highlighted. This review presents the temporal behavior of NF-\u03baB and its potential relevance in different human diseases which will be helpful not only for theoretical but also for experimental perspectives.", "doi": "10.3390/life12122012", "pmid": "36556376", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC9788026"}, {"db": "pii", "key": "life12122012"}], "notes": [], "created": "2026-08-21T13:04:02.474Z", "modified": "2026-08-21T13:04:02.584Z"}, {"entity": "publication", "iuid": "2c974b2ab0604c4a94f8c55f981d657c", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/2c974b2ab0604c4a94f8c55f981d657c.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/2c974b2ab0604c4a94f8c55f981d657c"}}, "title": "CRISPRi as a Tool to Repress Multiple Copies of Extracellular Polymeric Substances (EPS)-Related Genes in the Cyanobacterium Synechocystis sp. PCC 6803.", "authors": [{"family": "Santos", "given": "Marina", "initials": "M"}, {"family": "Pacheco", "given": "Catarina C", "initials": "CC", "orcid": "0000-0002-0741-1529", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/0ab56c9690354e4e9157b01af1ffffe6.json"}}, {"family": "Yao", "given": "Lun", "initials": "L"}, {"family": "Hudson", "given": "Elton P", "initials": "EP"}, {"family": "Tamagnini", "given": "Paula", "initials": "P", "orcid": "0000-0003-4396-2122", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/e31a40f4dd6a44cd8623e64bfd1c2929.json"}}], "type": "journal article", "published": "2021-11-06", "journal": {"title": "Life (Basel)", "issn": "2075-1729", "volume": "11", "issue": "11", "issn-l": null}, "abstract": "The use of the versatile cyanobacterial extracellular polymeric substances (EPS) for biotechnological/biomedical applications implies an extensive knowledge of their biosynthetic pathways to improve/control polymer production yields and characteristics. The multiple copies of EPS-related genes, scattered throughout cyanobacterial genomes, adds another layer of complexity, making these studies challenging and time-consuming. Usually, this issue would be tackled by generating deletion mutants, a process that in cyanobacteria is also hindered by the polyploidy. Thus, the use of the CRISPRi multiplex system constitutes an efficient approach to addressing this redundancy. Here, three putative Synechocystis sp. PCC 6803 kpsM homologues (slr0977, slr2107, and sll0574) were repressed using this methodology. The characterization of the 3-sgRNA mutant in terms of fitness/growth and total carbohydrates, released and capsular polysaccharides, and its comparison with previously generated single knockout mutants pointed towards Slr0977 being the key KpsM player in Synechocystis EPS production. This work validates CRISPRi as a powerful tool to unravel cyanobacterial complex EPS biosynthetic pathways expediting this type of studies.", "doi": "10.3390/life11111198", "pmid": "34833074", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC8620461"}, {"db": "pii", "key": "life11111198"}], "notes": [], "created": "2026-08-20T13:42:08.384Z", "modified": "2026-08-20T13:42:08.557Z"}], "created": "2026-08-20T13:42:08.514Z", "modified": "2026-08-20T13:42:08.514Z"}