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JOURNAL ARTICLE
Panan Suntornsaratoon, Jayson M Antonio, Juan Flores, Ravij Upadhyay, John Veltri, Sheila Bandyopadhyay, Rhema Dadala, Michael Kim, Yue Liu, Iyshwarya Balasubramanian, Jerrold R Turner, Xiaoyang Su, Wei Vivian Li, Nan Gao, Ronaldo P Ferraris
BACKGROUND & AIMS: Lacticaseibacillus rhamnosus GG (LGG) is the world's most consumed probiotic but its mechanism of action on intestinal permeability and differentiation along with its interactions with an essential source of signaling metabolites, dietary tryptophan, are unclear. METHODS: Untargeted metabolomic and transcriptomic analyses were performed in LGG mono-colonized germ-free (GF) mice fed tryptophan (trp)-free or -sufficient diets. LGG-derived metabolites were profiled in vitro under anaerobic and aerobic conditions...
April 17, 2024: Cellular and Molecular Gastroenterology and Hepatology
#2
REVIEW
Tomás Alejandro Suárez Vázquez, Nallely López López, Mario César Salinas Carmona
Mast cells have long been recognized for their involvement in allergic pathology through the immunoglobulin E (IgE)-mediated degranulation mechanism. However, there is growing evidence of other "non-canonical" degranulation mechanisms activated by certain pathogen recognition receptors. Mast cells release several mediators, including histamine, cytokines, chemokines, prostaglandins, and leukotrienes, to initiate and enhance inflammation. The chemical nature of activating stimuli influences receptors, triggering mechanisms for the secretion of formed and new synthesized mediators...
2024: Frontiers in Immunology
#3
JOURNAL ARTICLE
Shanhui Liu, Kanak Joshi, Lei Zhang, Wenyan Li, Ryan Mack, Austin Runde, Patrick A Hagen, Kevin Barton, Peter Breslin, Hong-Long Ji, Ameet R Kini, Zhiping Wang, Jiwang Zhang
Myelodysplastic syndromes (MDS) are a heterogeneous group of pre-leukemic hematopoietic disorders characterized by cytopenia in peripheral blood due to ineffective hematopoiesis and normo- or hypercellularity and morphologic dysplasia in bone marrow (BM). An inflammatory BM microenvironment and programmed cell death of hematopoietic stem/progenitor cells (HSPCs) are thought to be the major causes of ineffective hematopoiesis in MDS. Pyroptosis, apoptosis and necroptosis (collectively, PANoptosis) are observed in BM tissues of MDS patients, suggesting an important role of PANoptosis in MDS pathogenesis...
April 18, 2024: Cell Death & Disease
#4
REVIEW
Samantha Messina
RAS oncogenes are master regulator genes in many cancers. In general, RAS-driven cancers have an oncogenic RAS mutation that promotes disease progression (colon, lung, pancreas). In contrast, brain tumors are not necessarily RAS-driven cancers because RAS mutations are rarely observed. In particular, glioblastomas (the most lethal brain tumor) do not appear to have dominant genetic mutations that are suitable for targeted therapy. Standard treatment for most brain tumors continues to focus on maximal surgical resection, radiotherapy and chemotherapy...
April 18, 2024: Molecular Biology Reports
#5
JOURNAL ARTICLE
Evelyn Katy Alvarez-Salazar, Arimelek Cortés-Hernández, Saúl Arteaga-Cruz, Gloria Soldevila
Regulatory T cells (Tregs) play a crucial role in the homeostasis of the immune response. Tregs are mainly generated in the thymus and are characterized by the expression of Foxp3, which is considered the Treg master transcription factor. In addition, Tregs can be induced from naïve CD4+ T cells to express Foxp3 under specific conditions both in vivo (pTregs) and in vitro (iTregs). Both subsets tTregs and pTregs are necessary for the establishment of immune tolerance to self and non-self antigens. Although it has been postulated that iTregs may be less stable compared to tTregs, mainly due to epigenetic differences, accumulating evidence in animal models shows that iTregs are stable in vivo and could be used for the treatment of inflammatory disorders including autoimmune diseases and allogeneic transplant rejection...
April 17, 2024: Journal of Leukocyte Biology
#6
JOURNAL ARTICLE
Daniel Zechariah Paul Jebanesan, Raveen Stephen Stallon Illangeswaran, Bharathi M Rajamani, Rakhi Thalayattu Vidhyadharan, Saswati Das, Nayanthara K Bijukumar, Balaji Balakrishnan, Vikram Mathews, Shaji R Velayudhan, Poonkuzhali Balasubramanian
De novo acute myeloid leukemia (AML) patients with FMS-like tyrosine kinase 3 internal tandem duplications (FLT3-ITD) have worse treatment outcomes. Arsenic trioxide (ATO) used in the treatment of acute promyelocytic leukemia (APL) has been reported to be effective in degrading the FLT3 protein in AML cell lines and sensitizing non-APL AML patient samples in-vitro. We have previously reported that primary cells from FLT3-ITD mutated AML patients were sensitive to ATO in-vitro compared to other non-M3 AML and molecular/pharmacological inhibition of NF-E2 related factor 2 (NRF2), a master regulator of antioxidant response improved the chemosensitivity to ATO and daunorubicin even in non FLT3-ITD mutated cell lines and primary samples...
April 17, 2024: Annals of Hematology
#7
JOURNAL ARTICLE
Sophia Davidson, Yuri Shibata, Sophie Collard, Hongyu Zheng, Klara Kong, June M Sun, Pawat Laohamonthonkul, Anthony Cerra, Tobias Kratina, Margaret W Y Li, Carolyn Russell, Anna van Beek, Edwin P Kirk, Rebecca Walsh, Jubran Alqanatish, Abdullah Almojali, Wafaa Alsuwairi, Abdulrahman Alrasheed, Najoua Lalaoui, Paul E Gray, David Komander, Seth L Masters
OTU deubiquitinase with linear linkage specificity (OTULIN) regulates inflammation and cell death by deubiquitinating linear ubiquitin chains generated by the linear ubiquitin chain assembly complex (LUBAC). Biallelic loss-of-function mutations causes OTULIN-related autoinflammatory syndrome (ORAS), while OTULIN haploinsuffiency has not been associated with spontaneous inflammation. However, herein, we identify two patients with the heterozygous mutation p.Cys129Ser in OTULIN. Consistent with ORAS, we observed accumulation of linear ubiquitin chains, increased sensitivity to TNF-induced death, and dysregulation of inflammatory signaling in patient cells...
June 3, 2024: Journal of Experimental Medicine
#8
REVIEW
Gazmend Temaj, Silvia Chichiarelli, Pelin Telkoparan-Akillilar, Sarmistha Saha, Nexhibe Nuhii, Rifat Hadziselimovic, Luciano Saso
It is known that more than 10% of genetic diseases are caused by a mutation in protein-coding mRNA (premature termination codon; PTC). mRNAs with an early stop codon are degraded by the cellular surveillance process known as nonsense-mediated mRNA decay (NMD), which prevents the synthesis of C-terminally truncated proteins. Up-frameshift-1 (UPF1) has been reported to be involved in the downregulation of various cancers, and low expression of UPF1 was shown to correlate with poor prognosis. It is known that UPF1 is a master regulator of nonsense-mediated mRNA decay (NMD)...
April 13, 2024: Archives of Biochemistry and Biophysics
#9
REVIEW
Dario R Alessi, Suzanne R Pfeffer
Activating mutations in leucine-rich repeat kinase 2 (LRRK2) represent the most common cause of monogenic Parkinson's disease. LRRK2 is a large multidomain protein kinase that phosphorylates a specific subset of the ∼65 human Rab GTPases, which are master regulators of the secretory and endocytic pathways. After phosphorylation by LRRK2, Rabs lose the capacity to bind cognate effector proteins and guanine nucleotide exchange factors. Moreover, the phosphorylated Rabs cannot interact with their cognate prenyl-binding retrieval proteins (also known as guanine nucleotide dissociation inhibitors) and, thus, they become trapped on membrane surfaces...
April 15, 2024: Annual Review of Biochemistry
#10
JOURNAL ARTICLE
Ehab M Fahmy, Heba M Nageeb, Ahmed Sadek, Fatma H El Nouby, Loay I Aglan, Mohamed M Amin
T helper 17 (Th17) cells have been reported to be the most powerful factor in autoimmune disorder pathogenesis, which points to the Th17 master cytokine, interleukin (IL)-17A, as the crucial mediator. We aimed to determine the impact of IL-17A polymorphism in the -197 G/A promoter region on level of IL-17 and intensity of rheumatoid arthritis (RA) disease symptoms. This case-control study was conducted at the Department of Clinical Rheumatology of Aswan university Hospital and included 35 people suffering RA and 30 volunteer controls, matched for age and sex...
April 2024: Egyptian Journal of Immunology
#11
REVIEW
Chandra Shekhar Boosani, Laxminarayana Burela
TNF-α functions as a master regulator of inflammation, and it plays a prominent role in several immunological diseases. By promoting important cellular mechanisms, such as cell proliferation, migration, and phenotype switch, TNF-α induces its exacerbating effects, which are the underlying cause of many proliferative diseases such as cancer and cardiovascular disease. TNF-α primarily alters the immune component of the disease, which subsequently affects normal functioning of the cells. Monoclonal antibodies and synthetic drugs that can target TNF-α and impair its effects have been developed and are currently used in the treatment of a few select human diseases...
April 8, 2024: Cancers
#12
JOURNAL ARTICLE
Paula Ayuso-García, Alejandro Sánchez-Rueda, Sergio Velasco-Avilés, Miguel Tamayo-Caro, Aroa Ferrer-Pinós, Cecilia Huarte-Sebastian, Vanesa Alvarez, Cristina Riobello, Selene Jiménez-Vega, Izaskun Buendia, Jorge Cañas-Martin, Héctor Fernández-Susavila, Adrián Aparicio-Rey, Eva M Esquinas-Román, Carlos Rodríguez Ponte, Romane Guhl, Nicolas Laville, Encarni Pérez-Andrés, José L Lavín, Monika González-Lopez, Nuria Macías Cámara, Ana M Aransay, Juan José Lozano, James D Sutherland, Rosa Barrio, María Luz Martinez-Chantar, Mikel Azkargorta, Félix Elortza, Mario Soriano-Navarro, Carlos Matute, María Victoria Sánchez-Gómez, Laura Bayón-Cordero, Alberto Pérez-Samartín, Susana B Bravo, Thimo Kurz, Tomas Lama-Díaz, Miguel G Blanco, Saif Haddad, Christopher J Record, Peter M van Hasselt, Mary M Reilly, Marta Varela-Rey, Ashwin Woodhoo
Myelination is essential for neuronal function and health. In peripheral nerves, >100 causative mutations have been identified that cause Charcot-Marie-Tooth disease, a disorder that can affect myelin sheaths. Among these, a number of mutations are related to essential targets of the posttranslational modification neddylation, although how these lead to myelin defects is unclear. Here, we demonstrate that inhibiting neddylation leads to a notable absence of peripheral myelin and axonal loss both in developing and regenerating mouse nerves...
April 12, 2024: Science Advances
#13
REVIEW
Charlotte Lauren Burton, Alessandra Longaretti, Andjela Zlatanovic, Guilherme Monteiro Gomes, Raffaella Tonini
Animals often behave repetitively and predictably. These repetitive behaviors can have a component that is learned and ingrained as habits, which can be evolutionarily advantageous as they reduce cognitive load and the expenditure of attentional resources. Repetitive behaviors can also be conscious and deliberate, and may occur in the absence of habit formation, typically when they are a feature of normal development in children, or neuropsychiatric disorders. They can be considered pathological when they interfere with social relationships and daily activities...
2024: Frontiers in Cellular Neuroscience
#14
REVIEW
Mélanie Lavaud, Robel Tesfaye, Léa Lassous, Bénédicte Brounais, Marc Baud'huin, Franck Verrecchia, François Lamoureux, Steven Georges, Benjamin Ory
Precise spatiotemporal regulations of gene expression are essential for determining cells' fates and functions. Enhancers are cis -acting DNA elements that act as periodic transcriptional thrusters and their activities are cell type specific. Clusters of enhancers, called super-enhancers, are more densely occupied by transcriptional activators than enhancers, driving stronger expression of their target genes, which have prominent roles in establishing and maintaining cellular identities. Here we review the current knowledge on the composition and structure of super-enhancers to understand how they robustly stimulate the expression of cellular identity genes...
April 8, 2024: Epigenomics
#15
JOURNAL ARTICLE
Kelvin Yin, Maren Büttner, Ioannis K Deligiannis, Mateusz Strzelecki, Liwei Zhang, Carlos Talavera-López, Fabian Theis, Duncan T Odom, Celia P Martinez-Jimenez
BACKGROUND & AIMS: Polyploidy in hepatocytes has been proposed as a genetic mechanism to buffer against transcriptional dysregulation. Here, we aim to demonstrate the role of polyploidy in modulating gene regulatory networks in hepatocytes during ageing. METHODS: We performed single-nucleus RNA-sequencing in hepatocyte nuclei of different ploidy levels isolated from young and old wild-type mice. Changes in the gene expression and regulatory network were compared to three independent haploinsufficient strains for HNF4A, CEBPA or CTCF, representing non-deleterious perturbations...
April 5, 2024: Journal of Hepatology
#16
JOURNAL ARTICLE
Tim E Moors, Martino L Morella, Cesc Bertran-Cobo, Hanneke Geut, Vinod Udayar, Evelien Timmermans-Huisman, Angela M T Ingrassia, John J P Brevé, John G J M Bol, Vincenzo Bonifati, Ravi Jagasia, Wilma D J van de Berg
Transcription factor EB (TFEB) is a master regulator of genes involved in the maintenance of autophagic and lysosomal homeostasis, processes which have been implicated in the pathogenesis of GBA-related and sporadic Parkinson's disease (PD), and dementia with Lewy bodies (DLB). TFEB activation results in its translocation from the cytosol to the nucleus. Here, we investigated TFEB subcellular localization and its relation to intracellular alpha-synuclein (aSyn) accumulation in post-mortem human brain of individuals with either incidental Lewy body disease (iLBD), GBA-related PD/DLB (GBA-PD/DLB) or sporadic PD/DLB (sPD/DLB), compared to control subjects...
April 6, 2024: Acta Neuropathologica
#17
REVIEW
Camilla Ascanelli, Rowda Dahir, Catherine H Wilson
The Myc family of proto-oncogenes is a key node for the signal transduction of external pro-proliferative signals to the cellular processes required for development, tissue homoeostasis maintenance, and regeneration across evolution. The tight regulation of Myc synthesis and activity is essential for restricting its oncogenic potential. In this review, we highlight the central role that Myc plays in regeneration across the animal kingdom (from Cnidaria to echinoderms to Chordata) and how Myc could be employed to unlock the regenerative potential of non-regenerative tissues in humans for therapeutic purposes...
2024: Frontiers in Cell and Developmental Biology
#18
REVIEW
Shan-Shan Liu, Xiang Fang, Xin Wen, Ji-Shan Liu, Miribangvl Alip, Tian Sun, Yuan-Yuan Wang, Hong-Wei Chen
Mesenchymal stem cells (MSCs) are stem/progenitor cells capable of self-renewal and differentiation into osteoblasts, chondrocytes and adipocytes. The transformation of multipotent MSCs to adipocytes mainly involves two subsequent steps from MSCs to preadipocytes and further preadipocytes into adipocytes, in which the process MSCs are precisely controlled to commit to the adipogenic lineage and then mature into adipocytes. Previous studies have shown that the master transcription factors C/enhancer-binding protein alpha and peroxisome proliferation activator receptor gamma play vital roles in adipogenesis...
March 26, 2024: World Journal of Stem Cells
#19
JOURNAL ARTICLE
Chloe K Nagasawa, Aaron O Bailey, William Russell, Mariano A Garcia-Blanco
Forkhead box P3 (FOXP3) is the master fate-determining transcription factor in regulatory T (Treg) cells and is essential for their development, function and homeostasis. Mutations in FOXP3 cause immunodysregulation polyendocrinopathy enteropathy X-linked (IPEX) syndrome, and aberrant expression of FOXP3 has been implicated in other diseases such as multiple sclerosis and cancer. We previously demonstrated that pre-mRNA splicing of FOXP3 RNAs is highly sen-sitive to levels of DExD-box polypeptide 39B (DDX39B) and here we investigate the mechanism of this sensitivity...
April 4, 2024: RNA
#20
JOURNAL ARTICLE
James D Vasta, Ani Michaud, J Aaron Crapster, Matthew B Robers
Dysfunction of the RAS/mitogen-activated protein kinase (MAPK) pathway is a common driver of human cancers. As such, both the master regulator of the pathway, RAS, and its proximal kinase effectors, RAFs, have been of interest as drug targets for decades. Importantly, signaling within the RAS/MAPK pathway is highly coordinated due to the formation of a higher-order complex called the RAS/RAF signalosome, which may minimally contain dimers of both RAS and RAF protomers. In the disease state, RAS and RAF assemble in homo- and/or heterodimeric forms...
2024: Methods in Molecular Biology
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