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Showing 1-30 of 297 results for "SHC002" within Papers
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
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
Gulizar Issa Ameen et al.
The Journal of endocrinology, 236(1), 29-41 (2017-11-09)
Obesity leads to adipose tissue dysfunction, insulin resistance and diabetes. Adipose tissue produces adipokines that contribute to regulate insulin sensitivity. In turn, insulin stimulates the production and release of some adipokines. Casitas-b-lymphoma proteins (c-Cbl, Cbl-b and Cbl3) are intracellular adaptor
Kai Wu et al.
Proceedings of the National Academy of Sciences of the United States of America, 115(42), E9889-E9898 (2018-10-03)
Human CMV (HCMV) exhibits a broad cell tropism that depends on two virion glycoprotein complexes: a trimeric complex (gH/gL/gO) that facilitates viral infection primarily in fibroblasts and a pentameric complex (gH/gL/pUL128-pUL130-pUL131A) that mediates infection in epithelial and endothelial cells. We
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
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
Xiao Tang et al.
Journal of immunology (Baltimore, Md. : 1950), 195(3), 1191-1201 (2015-06-28)
Bioactive peptide LL-37/hCAP18, the only human member of the cathelicidin family, plays important roles in killing various pathogens, as well as in immune modulation. We demonstrate that LL-37 is internalized by human macrophages in a time-, dose-, temperature-, and peptide
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
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
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
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
Tess Orvis et al.
Cancer research, 74(22), 6486-6498 (2014-08-15)
SWI/SNF chromatin remodeling complexes regulate critical cellular processes, including cell-cycle control, programmed cell death, differentiation, genomic instability, and DNA repair. Inactivation of this class of chromatin remodeling complex has been associated with a variety of malignancies, including lung, ovarian, renal
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
Wenchao Zhou et al.
Oncotarget, 6(35), 37300-37315 (2015-10-30)
Glioblastoma multiforme (GBM) is the most lethal brain tumor. Tumor relapse in GBM is inevitable despite maximal therapeutic interventions. Glioma stem cells (GSCs) have been found to be critical players in therapeutic resistance and tumor recurrence. Therapeutic drugs targeting GSCs
Jacqueline Nguyen et al.
Bone, 131, 115148-115148 (2019-11-13)
Many signaling pathways involved in bone homeostasis also participate in the anabolic response of bone to mechanical loading. For example, TGFβ signaling coordinates the maintenance of bone mass and bone quality through its effects on osteoblasts, osteoclasts, and osteocytes. TGFβ
Xiuxing Wang et al.
Cancer research, 77(18), 4947-4960 (2017-07-22)
Metabolic dysregulation drives tumor initiation in a subset of glioblastomas harboring isocitrate dehydrogenase (IDH) mutations, but metabolic alterations in glioblastomas with wild-type IDH are poorly understood. MYC promotes metabolic reprogramming in cancer, but targeting MYC has proven notoriously challenging. Here
Irina Shakhova et al.
Molecular carcinogenesis, 58(3), 426-435 (2018-11-21)
We previously identified a gain-of-function mutation in PPP3CB in a neuroblastoma (NB) with MYCN amplification. Here we investigated the functional and clinical role of PPP3CB in NB. High PPP3CB expression was an independent indicator predicting poor prognosis of NB. Overexpression
L-W Ding et al.
Oncogene, 34(11), 1463-1474 (2014-04-08)
LNK (SH2B3) is an adaptor protein studied extensively in normal and malignant hematopoietic cells. In these cells, it downregulates activated tyrosine kinases at the cell surface resulting in an antiproliferative effect. To date, no studies have examined activities of LNK
Zherong Xu et al.
Journal of cachexia, sarcopenia and muscle, 8(5), 808-823 (2017-04-19)
Ageing skeletal muscle undergoes chronic denervation, and the neuromuscular junction (NMJ), the key structure that connects motor neuron nerves with muscle cells, shows increased defects with ageing. Previous studies in various species have shown that with ageing, type II fast-twitch
NCYM, a Cis-antisense gene of MYCN, encodes a de novo evolved protein that inhibits GSK3? resulting in the stabilization of MYCN in human neuroblastomas.
Suenaga Y, Islam SM, Alagu J, et al.
PLoS Genetics, 10(1), e1003996-e1003996 (2014)
Monique D Appelman et al.
Cells, 9(4) (2020-04-23)
The sodium taurocholate cotransporting polypeptide (NTCP) is expressed at the basolateral membrane of hepatocytes, where it mediates the uptake of conjugated bile acids and forms the hepatocyte entry receptor for the hepatitis B and D virus. Here, we aimed to
Kruppel-like factor 4 mediates lysophosphatidic acid-stimulated migration and proliferation of PC3M prostate cancer cells.
Shin SH, Kwon YW, Heo SC, et al.
Experimental & Molecular Medicine, 46, e104-e104 (2014)
J K Liu et al.
Cell death and differentiation, 21(8), 1325-1339 (2014-05-17)
Glioblastoma is the most common primary intrinsic brain tumor and remains incurable despite maximal therapy. Glioblastomas display cellular hierarchies with self-renewing glioma-initiating cells (GICs) at the apex. To discover new GIC targets, we used in vivo delivery of phage display
Functional Interplay between Histone H2B ADP-Ribosylation and Phosphorylation Controls Adipogenesis.
Dan Huang et al.
Molecular cell, 79(6), 934-949 (2020-08-22)
Although ADP-ribosylation of histones by PARP-1 has been linked to genotoxic stress responses, its role in physiological processes and gene expression has remained elusive. We found that NAD+-dependent ADP-ribosylation of histone H2B-Glu35 by small nucleolar RNA (snoRNA)-activated PARP-1 inhibits AMP
Stephen C Mack et al.
Nature, 553(7686), 101-105 (2017-12-21)
Genomic sequencing has driven precision-based oncology therapy; however, the genetic drivers of many malignancies remain unknown or non-targetable, so alternative approaches to the identification of therapeutic leads are necessary. Ependymomas are chemotherapy-resistant brain tumours, which, despite genomic sequencing, lack effective
Osteoclast-derived complement component 3a stimulates osteoblast differentiation.
Matsuoka K, Park KA, Ito M, et al.
Journal of Bone and Mineral Research, 29(7), 1522-1530 (2014)
Genetic and epigenetic characteristics of FSHD-associated 4q and 10q D4Z4 that are distinct from non-4q/10q D4Z4 homologs.
Zeng W, Chen YY, Newkirk DA, et al.
Human Mutation, 35(8), 998-1010 (2014)
Patrick J Cimino et al.
Genes & development, 32(7-8), 512-523 (2018-04-11)
Glioblastoma is the most frequently occurring and invariably fatal primary brain tumor in adults. The vast majority of glioblastomas is characterized by chromosomal copy number alterations, including gain of whole chromosome 7 and loss of whole chromosome 10. Gain of
Gang Zhang et al.
Cell death & disease, 10(6), 419-419 (2019-05-31)
Despite significant advances in the treatment of human immunodeficiency virus type-1 (HIV) infection, antiretroviral therapy only suppresses viral replication but is unable to eliminate infection. Thus, discontinuation of antiretrovirals results in viral reactivation and disease progression. A major reservoir of
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