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Richard J Flannery et al.
American journal of physiology. Renal physiology, 309(8), F697-F707 (2015-08-21)
Defects in primary cilia lead to a variety of human diseases. One of these, polycystic kidney disease, can be caused by defects in a Ca²⁺-gated ion channel (TRPP2) found on the cilium. Other ciliary functions also contribute to cystogenesis, and
Hongxia Li et al.
Human molecular genetics, 24(25), 7295-7307 (2015-10-16)
Spinal muscular atrophy (SMA), a heritable neurodegenerative disease, results from insufficient levels of the survival motor neuron (SMN) protein. α-COP binds to SMN, linking the COPI vesicular transport pathway to SMA. Reduced levels of α-COP restricted development of neuronal processes
Behzad Torabi et al.
Apoptosis : an international journal on programmed cell death, 23(1), 65-78 (2017-12-14)
Sp1 is a ubiquitous transcription factor that regulates many genes involved in apoptosis and senescence. Sp1 also has a role in the DNA damage response; at low levels of DNA damage, Sp1 is phosphorylated by ATM and localizes to double-strand
Monika Oberhuber et al.
Molecular systems biology, 16(4), e9247-e9247 (2020-04-24)
Prostate cancer (PCa) has a broad spectrum of clinical behavior; hence, biomarkers are urgently needed for risk stratification. Here, we aim to find potential biomarkers for risk stratification, by utilizing a gene co-expression network of transcriptomics data in addition to
Mutant huntingtin alters cell fate in response to microtubule depolymerization via the GEF-H1-RhoA-ERK pathway
Varma H, et al.
The Journal of Biological Chemistry, 285(48), 37445-37457 (2010)
Cynthia M Quintero et al.
Journal of molecular biology, 430(21), 4168-4182 (2018-08-29)
Activation of the retinoic acid (RA) signaling pathway is important for controlling embryonic stem cell differentiation and development. Modulation of this pathway occurs through the recruitment of different epigenetic regulators at the retinoic acid receptors (RARs) located at RA-responsive elements
Yasmin A Kadry et al.
Journal of cell science, 131(20) (2018-09-27)
The integrin-associated adaptor proteins integrin-linked kinase (ILK) and kindlin-2 play central roles in integrin signaling and control of cell morphology. A direct ILK-kindlin-2 interaction is conserved across species and involves the F2PH subdomain of kindlin-2 and the pseudokinase domain (pKD)
Sang Hun Shin et al.
Experimental & molecular medicine, 46, e104-e104 (2014-07-06)
Prostate cancer is the most frequently diagnosed malignancy and the second leading cause of cancer mortality among men in the United States. Accumulating evidence suggests that lysophosphatidic acid (LPA) serves as an autocrine/paracrine mediator to affect initiation, progression and metastasis
Loredana Cifaldi et al.
Cancer research, 75(5), 824-834 (2015-01-17)
The endoplasmic reticulum aminopeptidase ERAP1 regulates innate and adaptive immune responses by trimming peptides for presentation by MHC class I (MHC-I) molecules. Herein, we demonstrate that genetic or pharmacological inhibition of ERAP1 on human tumor cell lines perturbs their ability
Downregulation of the Polycomb-Associated Methyltransferase Ezh2 during Maturation of Hippocampal Neurons Is Mediated by MicroRNAs Let-7 and miR-124.
Guajardo, et al.
International Journal of Molecular Sciences, 21 (2021)
Dipongkor Saha et al.
Journal for immunotherapy of cancer, 8(1) (2020-05-28)
Temozolomide (TMZ) chemotherapy is a current standard of care for glioblastoma (GBM), however it has only extended overall survival by a few months. Because it also modulates the immune system, both beneficially and negatively, understanding how TMZ interacts with immunotherapeutics
Bing Ma et al.
Cancer research, 75(3), 487-496 (2014-12-17)
The prototypic chitinase-like protein Chi3l1 is induced in cancers and portends a poor prognosis, but whether it contributes to cancer progression is unknown. To address this gap in knowledge, we investigated the production of Chi3l1 in melanoma lung metastases. We
Li Zhao et al.
Current HIV research, 16(6), 384-395 (2019-02-19)
Understanding of the restriction of HIV-1 transcription in resting CD4+ Tcells is critical to find a cure for AIDS. Although many negative factors causing HIV-1 transcription blockage in resting CD4+ T-cells have been found, there are still unknown mechanisms to
Jose Miguel Ramos Pittol et al.
Gastroenterology, 159(5), 1853-1865 (2020-07-28)
The nuclear receptor subfamily 1 group H member 4 (NR1H4, also called FXR) is a ligand-activated transcription factor that, upon binding of bile acids, regulates the expression of genes involved in bile acid, fat, sugar, and amino acid metabolism. Transcript
Chirantani Mukherjee et al.
Nature communications, 10(1), 3287-3287 (2019-07-25)
Homologous recombination (HR) and Fanconi Anemia (FA) pathway proteins in addition to their DNA repair functions, limit nuclease-mediated processing of stalled replication forks. However, the mechanism by which replication fork degradation results in genome instability is poorly understood. Here, we
Rajeev Singh et al.
Oncotarget, 8(1), 833-845 (2016-12-03)
Hedgehog (Hh) signaling plays important roles in embryonic development and in tumor formation. Apart from the well-established stimulation of the GLI family of transcription factors, Hh ligands promote the phosphorylation and activation of mTOR and AKT kinases, yet the molecular
Meriem Ladli et al.
Haematologica, 104(5), 907-918 (2018-10-13)
AMP-activated protein kinase (AMPK) is a heterotrimeric complex containing α, β, and γ subunits involved in maintaining integrity and survival of murine red blood cells. Indeed, Ampk α1-/- , Ampk β1-/- and Ampk γ1-/- mice develop hemolytic anemia and the
TRIM28 is an epigenetic barrier to induced pluripotent stem cell reprogramming
Miles DC, et al.
Stem Cells, 35(1), 147-157 (2017)
Marilena Pontoriero et al.
Journal of molecular medicine (Berlin, Germany), 97(5), 675-690 (2019-03-20)
The antigen-mediated triggering of B cell receptor (BCR) activates the transcription factor NF-κB that regulates the expression of genes involved in B cell differentiation, proliferation, and survival. The tyrosine kinase Btk is essentially required for the activation of NF-κB in
Hua Zhang et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 36(47), 11837-11850 (2016-11-25)
Mushroom dendritic spine structures are essential for memory storage and the loss of mushroom spines may explain memory defects in aging and Alzheimer's disease (AD). The stability of mushroom spines depends on stromal interaction molecule 2 (STIM2)-mediated neuronal-store-operated Ca2+ influx
Hawasatu Dumbuya et al.
FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 34(9), 11605-11623 (2020-07-14)
Exposure to high doses of solar long wavelength ultraviolet radiation (UVA) damages human skin via reactive oxygen species (ROS). Whether physiological UVA doses also generate ROS that has an effect on the skin remains unknown. We previously showed that in
Jun Lu et al.
EBioMedicine, 34, 85-93 (2018-08-07)
Uncoordinated 51-like kinase 1 (ULK1) plays a vital role in autophagy. ULK1 dysregulation has recently been found in several human cancers. mRNA expression levels of ULK1 and clinical information were analysed from The Cancer Genome Atlas data. ULK1 expression levels
Ana Rita Lourenço et al.
Nature communications, 11(1), 785-785 (2020-02-09)
Extracellular signals such as TGF-β can induce epithelial-to-mesenchymal transition (EMT) in cancers of epithelial origin, promoting molecular and phenotypical changes resulting in pro-metastatic characteristics. We identified C/EBPα as one of the most TGF-β-mediated downregulated transcription factors in human mammary epithelial
Vincent A van der Mark et al.
Cellular and molecular life sciences : CMLS, 74(4), 715-730 (2016-09-16)
P4-ATPases are lipid flippases that catalyze the transport of phospholipids to create membrane phospholipid asymmetry and to initiate the biogenesis of transport vesicles. Here we show, for the first time, that lipid flippases are essential to dampen the inflammatory response
Hélène Lazareth et al.
Nature communications, 10(1), 3303-3303 (2019-07-26)
The mechanisms driving the development of extracapillary lesions in focal segmental glomerulosclerosis (FSGS) and crescentic glomerulonephritis (CGN) remain poorly understood. A key question is how parietal epithelial cells (PECs) invade glomerular capillaries, thereby promoting injury and kidney failure. Here we
B Y Ahn et al.
Oncogene, 35(11), 1411-1422 (2015-06-30)
The invasive nature of glioblastoma renders them incurable by current therapeutic interventions. Using a novel invasive human glioma model, we previously identified the neurotrophin receptor p75(NTR) (aka CD271) as a mediator of glioma invasion. Herein, we provide evidence that preventing
Julia C Meier et al.
Cancer medicine, 4(2), 253-267 (2014-12-11)
Molecular mechanisms underlying the development of resistance to platinum-based treatment in patients with ovarian cancer remain poorly understood. This is mainly due to the lack of appropriate in vivo models allowing the identification of resistance-related factors. In this study, we
Anne-Sophie Thomas-Claudepierre et al.
The Journal of experimental medicine, 213(3), 303-312 (2016-02-24)
Immunoglobulin (Ig) class switch recombination (CSR) is initiated by the transcription-coupled recruitment of activation-induced cytidine deaminase (AID) to Ig switch regions (S regions). During CSR, the IgH locus undergoes dynamic three-dimensional structural changes in which promoters, enhancers, and S regions
Fabian Freisleben et al.
International journal of molecular sciences, 21(14) (2020-07-28)
Aberrant activation of the hedgehog (HH) pathway is observed in many neoplasms, including acute myeloid leukemia (AML). The glioma-associated oncogene homolog (GLI) transcription factors are the main downstream effectors of the HH signaling cascade and are responsible for the proliferation
Vladimir A Vigont et al.
Frontiers in cell and developmental biology, 9, 625231-625231 (2021-02-20)
Huntington's disease (HD) is a severe autosomal-dominant neurodegenerative disorder caused by a mutation within a gene, encoding huntingtin protein. Here we have used the induced pluripotent stem cell technology to produce patient-specific terminally differentiated GABA-ergic medium spiny neurons modeling a
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