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Showing 1-30 of 321 results for "M7449" within Papers
Tao Shen et al.
The Journal of clinical investigation, 131(4) (2021-02-16)
Prostate cancer (PCa) is the second leading cause of cancer death in American men. Androgen receptor (AR) signaling is essential for PCa cell growth/survival and remains a key therapeutic target for lethal castration-resistant PCa (CRPC). GATA2 is a pioneer transcription
Guru Prasad Sharma et al.
Toxicology in vitro : an international journal published in association with BIBRA, 60, 420-436 (2019-06-09)
Metastatic prostate cancer, with no effective treatment, is among the leading causes of cancer-associated deaths in men. Overexpression of p38αMAPK has been observed in neuroendocrine prostate cancer patients and in both DU145 and PC-3 cell lines and represents a good
Miran Rada et al.
Oncotarget, 8(63), 106639-106647 (2018-01-02)
p53 is a tumour suppressor that is activated in response to various types of stress. It is regulated by a complex pattern of over 50 different post-translational modifications, including ubiquitination by the E3 ligase MDM2, which leads to its proteasomal
Lilli T E Bay et al.
Bio-protocol, 13(8), e4659-e4659 (2023-04-28)
RNA polymerase II (RNAPII) transcribes DNA into mRNA and thereby plays a critical role in cellular protein production. In addition, RNAPII plays a central role in DNA damage responses. Measurements of RNAPII on chromatin may thus give insight into several
Keith Dadson et al.
Scientific reports, 7, 41490-41490 (2017-02-06)
Cardiac homeostasis requires proper control of protein turnover. Protein degradation is principally controlled by the Ubiquitin-Proteasome System. Mule is an E3 ubiquitin ligase that regulates cellular growth, DNA repair and apoptosis to maintain normal tissue architecture. However, Mule's function in
Sha Li et al.
Scientific reports, 7(1), 2009-2009 (2017-05-19)
The placental transcription factors Distal-less 3 (DLX3) and Glial cell missing-1 (GCM1) have been shown to coordinate the specific regulation of PGF in human trophoblast cell lines. While both factors independently have a positive effect on PGF gene expression, when
Shubo Zhao et al.
Nucleic acids research, 49(2), 902-915 (2020-12-22)
Repair of covalent DNA-protein crosslinks (DPCs) by the metalloprotease SPRTN prevents genome instability, premature aging and carcinogenesis. SPRTN is specifically activated by DNA structures containing single- and double-stranded features, but degrades the protein components of DPCs promiscuously and independent of
Chung-Han Hsieh et al.
Cell metabolism, 30(6), 1131-1140 (2019-10-01)
The identification of molecular targets and pharmacodynamic markers for Parkinson's disease (PD) will empower more effective clinical management and experimental therapies. Miro1 is localized on the mitochondrial surface and mediates mitochondrial motility. Miro1 is removed from depolarized mitochondria to facilitate
Wenjuan Li et al.
Cell death & disease, 9(5), 482-482 (2018-05-01)
Deubiquitinases (DUBs) play essential roles in normal cell proliferation and tumor growth. However, the molecular mechanisms of DUBs on hepatocellular carcinoma (HCC) remains largely unknown. In this study, based on analysis of several HCC datasets, we found that the USP21
Sabateeshan Mathavarajah et al.
Nucleic acids research, 51(7), 3185-3204 (2023-03-14)
We have uncovered a role for the promyelocytic leukemia (PML) gene and novel PML-like DEDDh exonucleases in the maintenance of genome stability through the restriction of LINE-1 (L1) retrotransposition in jawed vertebrates. Although the mammalian PML protein forms nuclear bodies
Rulu Pan et al.
Cell death & disease, 14(6), 373-373 (2023-06-25)
Phosphodiesterase 4D interacting protein (PDE4DIP) is a centrosome/Golgi protein associated with cyclic nucleotide phosphodiesterases. PDE4DIP is commonly mutated in human cancers, and its alteration in mice leads to a predisposition to intestinal cancer. However, the biological function of PDE4DIP in
Neha Dhar et al.
Biotechnology and bioengineering, 117(2), 362-371 (2019-11-12)
Protein abnormalities are the major cause of neurodegenerative diseases such as spinocerebellar ataxia (SCA). Protein misfolding and impaired degradation leads to the build-up of protein aggregates inside the cell, which may further cause cellular degeneration. Reducing levels of either the
Elisa Cappuyns et al.
Cell cycle (Georgetown, Tex.), 17(9), 1068-1075 (2018-06-19)
Truncating de novo mutations in ADNP have been identified in patients with the Helsmoortel-Van der Aa syndrome. However correlations between the distinct mutations and their impact on the protein have not been studied before. Here we report the effect of
Silvia Sberna et al.
Cells, 12(20) (2023-10-27)
TAZ (WWTR1) is a transcriptional co-activator regulated by Hippo signaling, mechano-transduction, and G-protein couple receptors. Once activated, TAZ and its paralogue, YAP1, regulate gene expression programs promoting cell proliferation, survival, and differentiation, thus controlling embryonic development, tissue regeneration, and aging.
Young Ik Koh et al.
Autophagy, 18(11), 2593-2614 (2022-03-08)
Intracellular accumulation of mutant proteins causes proteinopathies, which lack targeted therapies. Autosomal dominant hearing loss (DFNA67) is caused by frameshift mutations in OSBPL2. Here, we show that DFNA67 is a toxic proteinopathy. Mutant OSBPL2 accumulated intracellularly and bound to macroautophagy/autophagy
Devon R Blake et al.
Science signaling, 12(590) (2019-07-18)
Stabilization of the MYC oncoprotein by KRAS signaling critically promotes the growth of pancreatic ductal adenocarcinoma (PDAC). Thus, understanding how MYC protein stability is regulated may lead to effective therapies. Here, we used a previously developed, flow cytometry-based assay that
Shanfeng Li et al.
Molecular carcinogenesis, 62(11), 1686-1699 (2023-07-21)
TRIM16 has been identified as a tumor suppressor in hepatocellular carcinoma (HCC). This study aimed to investigate whether there are genetic variants in TRIM16 influencing HCC risk and/or prognosis and explore the mechanisms. We performed a gene-wide single-nucleotide polymorphism (SNP)
Chang-Quan Wang et al.
The Plant cell, 27(4), 1128-1139 (2015-04-05)
Hypocotyl elongation is a highly coordinated physiological response regulated by myriad internal and external cues. Here, we show that BBX19, a transcriptional regulator with two B-box motifs, is a positive regulator of growth; diminished BBX19 expression by RNA interference reduces
Kamalakshi Deka et al.
Cell death and differentiation, 28(2), 730-747 (2020-09-16)
Arginylation was previously found to promote stabilization of heat shock protein 70.3 (Hsp70.3) mRNA and cell survival in mouse embryonic fibroblasts (MEFs) on exposure to heat stress (HS). In search of a factor responsible for these phenomena, the current study
Zsuzsa Bartos et al.
Frontiers in cell and developmental biology, 9, 615729-615729 (2021-02-27)
Proper targeting of the urate and xenobiotic transporter ATP-binding transporter subfamily G member 2 (ABCG2) to the plasma membrane (PM) is essential for its normal function. The naturally occurring Q141K and M71V polymorphisms in ABCG2, associated with gout and hyperuricemia
Anbok Lee et al.
International journal of oncology, 60(1) (2021-12-17)
Myeloid cell leukemia sequence 1 (MCL‑1), an anti‑apoptotic B‑cell lymphoma 2 (BCL‑2) family molecule frequently amplified in various human cancer cells, is known to be critical for cancer cell survival. MCL‑1 has been recognized as a target molecule for cancer treatment. While
Shashank Srivastava et al.
Cell cycle (Georgetown, Tex.), 16(16), 1515-1525 (2017-08-02)
The ADA3 (Alteration/Deficiency in Activation 3) protein is an essential adaptor component of several Lysine Acetyltransferase (KAT) complexes involved in chromatin modifications. Previously, we and others have demonstrated a crucial role of ADA3 in cell cycle progression and in maintenance
Yeast Smy2 and its human homologs GIGYF1 and -2 regulate Cdc48/VCP function during transcription stress.
Lehner, et al.
Cell Reports, 41, 111536-111536 (2022)
Yu Chen Feng et al.
Nature communications, 11(1), 4980-4980 (2020-10-07)
The functions of the proto-oncoprotein c-Myc and the tumor suppressor p53 in controlling cell survival and proliferation are inextricably linked as "Yin and Yang" partners in normal cells to maintain tissue homeostasis: c-Myc induces the expression of ARF tumor suppressor
Jialiang Shao et al.
The EMBO journal, 40(20), e107480-e107480 (2021-07-17)
The mTORC1 pathway plays key roles in regulating various biological processes, including sensing amino acid deprivation and driving expression of ribosomal protein (RP)-coding genes. In this study, we observed that depletion of glutamate dehydrogenase 1 (GDH1), an enzyme that converts
Cody W Lewis et al.
Oncotarget, 8(43), 73705-73722 (2017-11-02)
Wee1 kinase is a crucial negative regulator of Cdk1/cyclin B1 activity and is required for normal entry into and exit from mitosis. Wee1 activity can be chemically inhibited by the small molecule MK-1775, which is currently being tested in phase
Hannah R Lewis et al.
Frontiers in physiology, 12, 732020-732020 (2021-09-28)
Aims: In cardiac myocytes, the sarcomeric Z-disc protein telethonin is constitutively bis-phosphorylated at C-terminal residues S157 and S161; however, the functional significance of this phosphorylation is not known. We sought to assess the significance of telethonin phosphorylation in vivo, using
Sanggenon C inhibits cell proliferation and induces apoptosis by regulating the MIB1/DAPK1 axis in glioblastoma.
Chang, et al.
MedComm, 4, e281-e281 (2023)
Hyun-Jung Kim et al.
Cell death & disease, 14(8), 576-576 (2023-08-31)
Peptidylarginine deiminase (PADI) 2 catalyzes the post-translational conversion of peptidyl-arginine to peptidyl-citrulline in a process called citrullination. However, the precise functions of PADI2 in bone formation and homeostasis remain unknown. In this study, our objective was to elucidate the function
Zichong Li et al.
PLoS pathogens, 15(1), e1007498-e1007498 (2019-01-16)
The establishment of HIV-1 latency gives rise to persistent chronic infection that requires life-long treatment. To reverse latency for viral eradiation, the HIV-1 Tat protein and its associated ELL2-containing Super Elongation Complexes (ELL2-SECs) are essential to activate HIV-1 transcription. Despite
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