LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 10 of total 27

Search options

  1. Article ; Online: Correction: Efficacy of GV1001 with gemcitabine/capecitabine in previously untreated patients with advanced pancreatic ductal adenocarcinoma having high serum eotaxin levels (KG4/2015): an open-label, randomised, Phase 3 trial.

    Jo, Jung Hyun / Kim, Yong-Tae / Choi, Ho Soon / Kim, Ho Gak / Lee, Hong Sik / Choi, Young Woo / Kim, Dong Uk / Lee, Kwang Hyuck / Kim, Eui Joo / Han, Joung-Ho / Lee, Seung Ok / Park, Chang-Hwan / Choi, Eun Kwang / Kim, Jae Woo / Cho, Jae Yong / Lee, Woo Jin / Moon, Hyungsik Roger / Park, Mi-Suk / Kim, Sangjae /
    Song, Si Young

    British journal of cancer

    2023  Volume 130, Issue 1, Page(s) 163

    Language English
    Publishing date 2023-12-04
    Publishing country England
    Document type Published Erratum
    ZDB-ID 80075-2
    ISSN 1532-1827 ; 0007-0920
    ISSN (online) 1532-1827
    ISSN 0007-0920
    DOI 10.1038/s41416-023-02520-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  2. Article ; Online: Efficacy of GV1001 with gemcitabine/capecitabine in previously untreated patients with advanced pancreatic ductal adenocarcinoma having high serum eotaxin levels (KG4/2015): an open-label, randomised, Phase 3 trial.

    Jo, Jung Hyun / Kim, Yong-Tae / Choi, Ho Soon / Kim, Ho Gak / Lee, Hong Sik / Choi, Young Woo / Kim, Dong Uk / Lee, Kwang Hyuck / Kim, Eui Joo / Han, Joung-Ho / Lee, Seung Ok / Park, Chang-Hwan / Choi, Eun Kwang / Kim, Jae Woo / Cho, Jae Yong / Lee, Woo Jin / Moon, Hyungsik Roger / Park, Mi-Suk / Kim, Sangjae /
    Song, Si Young

    British journal of cancer

    2023  Volume 130, Issue 1, Page(s) 43–52

    Abstract: Background: The TeloVac study indicated GV1001 did not improve the survival of advanced pancreatic ductal adenocarcinoma (PDAC). However, the cytokine examinations suggested that high serum eotaxin levels may predict responses to GV1001. This Phase III ... ...

    Abstract Background: The TeloVac study indicated GV1001 did not improve the survival of advanced pancreatic ductal adenocarcinoma (PDAC). However, the cytokine examinations suggested that high serum eotaxin levels may predict responses to GV1001. This Phase III trial assessed the efficacy of GV1001 with gemcitabine/capecitabine for eotaxin-high patients with untreated advanced PDAC.
    Methods: Patients recruited from 16 hospitals received gemcitabine (1000 mg/m
    Results: Total 148 patients were randomly assigned to the GV1001 (n = 75) and control groups (n = 73). The GV1001 group showed improved median OS (11.3 vs. 7.5 months, P = 0.021) and TTP (7.3 vs. 4.5 months, P = 0.021) compared to the control group. Grade >3 adverse events were reported in 77.3% and 73.1% in the GV1001 and control groups (P = 0.562), respectively.
    Conclusions: GV1001 plus gemcitabine/capecitabine improved OS and TTP compared to gemcitabine/capecitabine alone in eotaxin-high patients with advanced PDAC.
    Clinical trial registration: NCT02854072.
    MeSH term(s) Humans ; Gemcitabine ; Capecitabine/adverse effects ; Deoxycytidine/adverse effects ; Antineoplastic Combined Chemotherapy Protocols/adverse effects ; Pancreatic Neoplasms/pathology ; Adenocarcinoma/chemically induced
    Chemical Substances Gemcitabine ; Capecitabine (6804DJ8Z9U) ; Deoxycytidine (0W860991D6)
    Language English
    Publishing date 2023-10-30
    Publishing country England
    Document type Randomized Controlled Trial ; Clinical Trial, Phase III ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80075-2
    ISSN 1532-1827 ; 0007-0920
    ISSN (online) 1532-1827
    ISSN 0007-0920
    DOI 10.1038/s41416-023-02474-w
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  3. Article: Anti-cancer effects of lucidadiol against malignant melanoma cells

    Shin, Seong-Ah / Lee, Jun Seob / Joo, Byeong Jun / Ryu, Gyoungah / Han, Minjoo / Kim, Huiji / An, Jangeun / Koo, Man Hyung / Youn, Ui Joung / Lee, Jun Hyuck / Park, Hyun Ho / Lee, Chang Sup

    Applied biological chemistry. 2021 Dec., v. 64, no. 1

    2021  

    Abstract: Melanoma is one of the most aggressive and lethal skin cancers. Lucidadiol is a triterpenoid isolated from Ganoderma lucidum and is known to have various biological functions, including antibacterial effects. However, the anti-cancer effects and ... ...

    Abstract Melanoma is one of the most aggressive and lethal skin cancers. Lucidadiol is a triterpenoid isolated from Ganoderma lucidum and is known to have various biological functions, including antibacterial effects. However, the anti-cancer effects and mechanism of action of lucidadiol in malignant melanoma are unknown. In this study, lucidadiol significantly reduced B16 melanoma cell viability in a dose- and time-dependent manner. In addition, lucidadiol induced apoptosis and suppressed cell mobility in B16 melanoma cells. Moreover, our findings revealed that lucidadiol remarkably downregulated phospho-Akt/ERK/JNK, but not p38. Taken together, our results suggest that lucidadiol could exerts its anti-cancer effects by inducing apoptosis via modulation of the Akt/MAPK pathway. Therefore, lucidadiol may be a potential cancer therapeutic agent for malignant melanoma.
    Keywords Ganoderma lucidum ; apoptosis ; cell viability ; mechanism of action ; melanoma ; therapeutics ; triterpenoids
    Language English
    Dates of publication 2021-12
    Size p. 75.
    Publishing place Springer Singapore
    Document type Article
    ZDB-ID 2846955-0
    ISSN 2468-0842 ; 2468-0834
    ISSN (online) 2468-0842
    ISSN 2468-0834
    DOI 10.1186/s13765-021-00647-w
    Database NAL-Catalogue (AGRICOLA)

    More links

    Kategorien

  4. Article ; Online: Molecular mechanisms involved in farnesol-induced apoptosis.

    Joo, Joung Hyuck / Jetten, Anton M

    Cancer letters

    2009  Volume 287, Issue 2, Page(s) 123–135

    Abstract: The isoprenoid alcohol farnesol is an effective inducer of cell cycle arrest and apoptosis in a variety of carcinoma cell types. In addition, farnesol has been reported to inhibit tumorigenesis in several animal models suggesting that it functions as a ... ...

    Abstract The isoprenoid alcohol farnesol is an effective inducer of cell cycle arrest and apoptosis in a variety of carcinoma cell types. In addition, farnesol has been reported to inhibit tumorigenesis in several animal models suggesting that it functions as a chemopreventative and anti-tumor agent in vivo. A number of different biochemical and cellular processes have been implicated in the growth-inhibitory and apoptosis-inducing effects of farnesol. These include regulation of 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase and CTP:phosphocholine cytidylyltransferase alpha (CCTalpha), rate-limiting enzymes in the mevalonate pathway and phosphatidylcholine biosynthesis, respectively, and the generation of reactive oxygen species. In some cell types the action of farnesol is mediated through nuclear receptors, including activation of farnesoid X receptor (FXR) and peroxisome proliferator-activated receptors (PPARs). Recent studies have revealed that induction of endoplasmic reticulum (ER) stress and the subsequent activation of the unfolded protein response (UPR) play a critical role in the induction of apoptosis by farnesol in lung carcinoma cells. This induction was found to be dependent on the activation of the MEK1/2-ERK1/2 pathway. In addition, farnesol induces activation of the NF-kappaB signaling pathway and a number of NF-kappaB target genes. Optimal activation of NF-kappaB was reported to depend on the phosphorylation of p65/RelA by the MEK1/2-MSK1 signaling pathway. In a number of cells farnesol-induced apoptosis was found to be linked to activation of the apoptosome. This review provides an overview of the biochemical and cellular processes regulated by farnesol in relationship to its growth-inhibitory, apoptosis-promoting, and anti-tumor effects.
    MeSH term(s) Animals ; Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Apoptosomes/metabolism ; Cell Proliferation ; Cytidine Diphosphate Choline/metabolism ; Endoplasmic Reticulum/metabolism ; Farnesol/metabolism ; Farnesol/pharmacology ; Humans ; Hydroxymethylglutaryl CoA Reductases/metabolism ; Mitogen-Activated Protein Kinases/metabolism ; NF-kappa B/metabolism ; Neoplasms/metabolism ; Neoplasms/pathology ; Oxidative Stress ; PPAR gamma/metabolism ; Receptors, Cytoplasmic and Nuclear/metabolism ; Signal Transduction/drug effects ; Thyroid Hormone Receptors beta/metabolism ; Unfolded Protein Response
    Chemical Substances Antineoplastic Agents ; Apoptosomes ; NF-kappa B ; PPAR gamma ; Receptors, Cytoplasmic and Nuclear ; Thyroid Hormone Receptors beta ; farnesoid X-activated receptor (0C5V0MRU6P) ; Farnesol (4602-84-0) ; Cytidine Diphosphate Choline (536BQ2JVC7) ; Hydroxymethylglutaryl CoA Reductases (EC 1.1.1.-) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24)
    Language English
    Publishing date 2009-06-10
    Publishing country Ireland
    Document type Journal Article ; Research Support, N.I.H., Intramural ; Review
    ZDB-ID 195674-7
    ISSN 1872-7980 ; 0304-3835
    ISSN (online) 1872-7980
    ISSN 0304-3835
    DOI 10.1016/j.canlet.2009.05.015
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  5. Article: Retinoid-related Orphan Receptors (RORs): Roles in Cellular Differentiation and Development.

    Jetten, Anton M / Joo, Joung Hyuck

    Advances in developmental biology (Amsterdam, Netherlands)

    2008  Volume 16, Page(s) 313–355

    Abstract: Retinoid-related orphan receptors RORalpha, -beta, and -gamma are transcription factors belonging to the steroid hormone receptor superfamily. During embryonic development RORs are expressed in a spatial and temporal manner and are critical in the ... ...

    Abstract Retinoid-related orphan receptors RORalpha, -beta, and -gamma are transcription factors belonging to the steroid hormone receptor superfamily. During embryonic development RORs are expressed in a spatial and temporal manner and are critical in the regulation of cellular differentiation and the development of several tissues. RORalpha plays a key role in the development of the cerebellum particularly in the regulation of the maturation and survival of Purkinje cells. In RORalpha-deficient mice, the reduced production of sonic hedgehog by these cells appears to be the major cause of the decreased proliferation of granule cell precursors and the observed cerebellar atrophy. RORalpha has been implicated in the regulation of a number of other physiological processes, including bone formation. RORbeta expression is largely restricted to several regions of the brain, the retina, and pineal gland. Mice deficient in RORbeta develop retinal degeneration that results in blindness. RORgamma is essential for lymph node organogenesis. In the intestine RORgamma is required for the formation of several other lymphoid tissues: Peyer's patches, cryptopatches, and isolated lymphoid follicles. RORgamma plays a key role in the generation of lymphoid tissue inducer (LTi) cells that are essential for the development of these lymphoid tissues. In addition, RORgamma is a critical regulator of thymopoiesis. It controls the differentiation of immature single-positive thymocytes into double-positive thymocytes and promotes the survival of double-positive thymocytes by inducing the expression of the anti-apoptotic gene Bcl-X(L). Interestingly, all three ROR receptors appear to play a role in the control of circadian rhythms. RORalpha positively regulates the expression of Bmal1, a transcription factor that is critical in the control of the circadian clock. This review intends to provide an overview of the current status of the functions RORs have in these biological processes.
    Language English
    Publishing date 2008-04-07
    Publishing country Netherlands
    Document type Journal Article
    ISSN 1574-3349
    ISSN 1574-3349
    DOI 10.1016/S1574-3349(06)16010-X
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  6. Article: NF-kappaB-dependent transcriptional activation in lung carcinoma cells by farnesol involves p65/RelA(Ser276) phosphorylation via the MEK-MSK1 signaling pathway.

    Joo, Joung Hyuck / Jetten, Anton M

    The Journal of biological chemistry

    2008  Volume 283, Issue 24, Page(s) 16391–16399

    Abstract: In this study, we demonstrate that treatment of human lung adenocarcinoma H460 cells with farnesol induces the expression of a number of immune response and inflammatory genes, including IL-6, CXCL3, IL-1alpha, and COX-2. This response was dependent on ... ...

    Abstract In this study, we demonstrate that treatment of human lung adenocarcinoma H460 cells with farnesol induces the expression of a number of immune response and inflammatory genes, including IL-6, CXCL3, IL-1alpha, and COX-2. This response was dependent on the activation of the NF-kappaB signaling pathway. Farnesol treatment reduces the level of IkappaBalpha and induces translocation of p65/RelA to the nucleus, its phosphorylation at Ser(276), and transactivation of NF-kappaB-dependent transcription. Moreover, overexpression of IkappaBalpha or treatment with the NF-kappaB inhibitor caffeic acid phenethyl ester greatly diminishes the induction of inflammatory gene expression by farnesol. We provide evidence indicating that the farnesol-induced phosphorylation of p65/RelA at Ser(276) is important for optimal transcriptional activity of NF-kappaB. The MEK1/2 inhibitor U0126 and knockdown of MEK1/2 expression with small interfering RNAs effectively blocked the phosphorylation of p65/RelA(Ser(276)) but not that of Ser(536), suggesting that this phosphorylation is dependent on the activation of the MEK1/2-ERK1/2 pathway. We further show that inhibition of MSK1, a kinase acting downstream of MEK1/2-ERK1/2, by H89 or knockdown of MSK1 expression also inhibited phosphorylation of p65/RelA(Ser(276)), suggesting that this phosphorylation is dependent on MSK1. Knockdown of MEK1/2 or MSK1 expression inhibits farnesol-induced expression of CXCL3, IL-1alpha, and COX-2 mRNA. Our results indicate that the induction of inflammatory genes by farnesol is mediated by the activation of the NF-kappaB pathway and involves MEK1/2-ERK1/2-MSK1-dependent phosphorylation of p65/RelA(Ser(276)). The activation of the NF-kappaB pathway by farnesol might be part of a prosurvival response during farnesol-induced ER stress.
    MeSH term(s) Cell Line, Tumor ; Farnesol/pharmacology ; Gene Expression Regulation, Neoplastic ; Humans ; I-kappa B Proteins/metabolism ; Lung Neoplasms/metabolism ; Lung Neoplasms/pathology ; MAP Kinase Kinase 1/metabolism ; MAP Kinase Kinase 2/metabolism ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinase 3/metabolism ; NF-KappaB Inhibitor alpha ; NF-kappa B/metabolism ; Ribosomal Protein S6 Kinases, 90-kDa/metabolism ; Signal Transduction ; Transcription Factor RelA/metabolism ; Transcriptional Activation
    Chemical Substances I-kappa B Proteins ; NF-kappa B ; NFKBIA protein, human ; Transcription Factor RelA ; NF-KappaB Inhibitor alpha (139874-52-5) ; Farnesol (4602-84-0) ; MAP2K2 protein, human (EC 2.7.1.-) ; Ribosomal Protein S6 Kinases, 90-kDa (EC 2.7.11.1) ; mitogen and stress-activated protein kinase 1 (EC 2.7.11.1) ; Mitogen-Activated Protein Kinase 1 (EC 2.7.11.24) ; Mitogen-Activated Protein Kinase 3 (EC 2.7.11.24) ; MAP Kinase Kinase 1 (EC 2.7.12.2) ; MAP Kinase Kinase 2 (EC 2.7.12.2)
    Language English
    Publishing date 2008-04-18
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Intramural
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.M800945200
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  7. Article ; Online: Farnesol activates the intrinsic pathway of apoptosis and the ATF4-ATF3-CHOP cascade of ER stress in human T lymphoblastic leukemia Molt4 cells.

    Joo, Joung Hyuck / Ueda, Eiichiro / Bortner, Carl D / Yang, Xiao-Ping / Liao, Grace / Jetten, Anton M

    Biochemical pharmacology

    2015  Volume 97, Issue 3, Page(s) 256–268

    Abstract: In this study, we demonstrate that treatment of T lymphoblastic leukemic Molt4 cells with farnesol activates the apoptosome via the intrinsic pathway of apoptosis. This induction was associated with changes in the level of intracellular potassium and ... ...

    Abstract In this study, we demonstrate that treatment of T lymphoblastic leukemic Molt4 cells with farnesol activates the apoptosome via the intrinsic pathway of apoptosis. This induction was associated with changes in the level of intracellular potassium and calcium, the dissipation of the mitochondrial and plasma membrane potential, release of cytochrome c, activation of several caspases, and PARP cleavage. The induction of apoptosis by farnesol was inhibited by the addition of the pan-caspase inhibitor Z-VAD-fmk and by the exogenous expression of the anti-apoptotic protein Bcl2. Analysis of the gene expression profiles by microarray analysis revealed that farnesol increased the expression of several genes related to the unfolded protein response (UPR), including CHOP and CHAC1. This induction was associated with the activation of the PERK-eIF2α-ATF3/4 cascade, but not the XBP-1 branch of the UPR. Although farnesol induced activation of the ERK1/2, p38, and JNK pathways, inhibition of these MAPKs had little effect on farnesol-induced apoptosis or the induction of UPR-related genes. Our data indicate that the induction of apoptosis in leukemic cells by farnesol is mediated through a pathway that involves activation of the apoptosome via the intrinsic pathway and induction of the PERK-eIF2α-ATF3/4 cascade in a manner that is independent of the farnesol-induced activation of MAPKs.
    MeSH term(s) Activating Transcription Factor 3/metabolism ; Activating Transcription Factor 4/metabolism ; Anticarcinogenic Agents/pharmacology ; Apoptosis/drug effects ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Farnesol/pharmacology ; Humans ; MAP Kinase Signaling System/drug effects ; Membrane Potential, Mitochondrial/drug effects ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/metabolism ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/pathology ; Proto-Oncogene Proteins c-bcl-2/genetics ; Reactive Oxygen Species/metabolism ; Transcription Factor CHOP/metabolism ; Transcriptome/drug effects ; Transfection
    Chemical Substances ATF3 protein, human ; ATF4 protein, human ; Activating Transcription Factor 3 ; Anticarcinogenic Agents ; DDIT3 protein, human ; Proto-Oncogene Proteins c-bcl-2 ; Reactive Oxygen Species ; Activating Transcription Factor 4 (145891-90-3) ; Transcription Factor CHOP (147336-12-7) ; Farnesol (4602-84-0)
    Language English
    Publishing date 2015-08-11
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 208787-x
    ISSN 1873-2968 ; 0006-2952
    ISSN (online) 1873-2968
    ISSN 0006-2952
    DOI 10.1016/j.bcp.2015.08.086
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  8. Article ; Online: Long-Term Outcomes Following Trabeculectomy Combined with 25-Gauge Transconjunctival Sutureless Vitrectomy in Uveitis Patients.

    Kim, Bo Hyuck / Shin, Joo Young / Lee, Min Joung / Kim, Suk Hwan / Yu, Hyeong Gon

    Ocular immunology and inflammation

    2015  Volume 23, Issue 3, Page(s) 212–218

    Abstract: Purpose: To evaluate the efficacy of combined trabeculectomy (TLE) and 25-gauge transconjunctival sutureless vitrectomy (TSV-25) for uveitis patients.: Methods: Combined TSV-25/TLE was performed in 9 eyes of 6 patients with vitreoretinal ... ...

    Abstract Purpose: To evaluate the efficacy of combined trabeculectomy (TLE) and 25-gauge transconjunctival sutureless vitrectomy (TSV-25) for uveitis patients.
    Methods: Combined TSV-25/TLE was performed in 9 eyes of 6 patients with vitreoretinal complications and intractable glaucoma. Visual acuity, intraocular pressure (IOP), inflammatory control, and number of hypotensive medications were evaluated.
    Results: Visual acuity improved in 7 of 9 eyes and inflammation was controlled with a decreased oral anti-inflammatory agent dosage in all eyes. Mean IOP, which was 28.11 ± 4.83 mmHg preoperatively, was significantly reduced (15.77 ± 2.68 mmHg) 5 years after surgery (p = 0.008). The mean number of IOP-lowering medications was 3.33 ± 0.71 before surgery and 1.11 ± 0.92 5 years after surgery (p = 0.007). Two eyes required implant of an Ahmed drainage valve during the follow-up period.
    Conclusion: Combined TSV-25/TLE can be effective in managing vitreoretinal complications and elevated IOP in uveitis patients.
    MeSH term(s) Adult ; Conjunctiva/surgery ; Female ; Follow-Up Studies ; Glaucoma/complications ; Glaucoma/physiopathology ; Glaucoma/surgery ; Humans ; Intraocular Pressure ; Male ; Middle Aged ; Retrospective Studies ; Suture Techniques ; Time Factors ; Trabeculectomy/methods ; Treatment Outcome ; Uveitis/complications ; Uveitis/physiopathology ; Uveitis/surgery ; Visual Acuity ; Vitrectomy/methods
    Language English
    Publishing date 2015-06
    Publishing country England
    Document type Journal Article
    ZDB-ID 1193873-0
    ISSN 1744-5078 ; 0927-3948
    ISSN (online) 1744-5078
    ISSN 0927-3948
    DOI 10.3109/09273948.2014.892626
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  9. Article ; Online: ULK1 and ULK2 Regulate Stress Granule Disassembly Through Phosphorylation and Activation of VCP/p97.

    Wang, Bo / Maxwell, Brian A / Joo, Joung Hyuck / Gwon, Youngdae / Messing, James / Mishra, Ashutosh / Shaw, Timothy I / Ward, Amber L / Quan, Honghu / Sakurada, Sadie Miki / Pruett-Miller, Shondra M / Bertorini, Tulio / Vogel, Peter / Kim, Hong Joo / Peng, Junmin / Taylor, J Paul / Kundu, Mondira

    Molecular cell

    2019  Volume 74, Issue 4, Page(s) 742–757.e8

    Abstract: Disturbances in autophagy and stress granule dynamics have been implicated as potential mechanisms underlying inclusion body myopathy (IBM) and related disorders. Yet the roles of core autophagy proteins in IBM and stress granule dynamics remain poorly ... ...

    Abstract Disturbances in autophagy and stress granule dynamics have been implicated as potential mechanisms underlying inclusion body myopathy (IBM) and related disorders. Yet the roles of core autophagy proteins in IBM and stress granule dynamics remain poorly characterized. Here, we demonstrate that disrupted expression of the core autophagy proteins ULK1 and ULK2 in mice causes a vacuolar myopathy with ubiquitin and TDP-43-positive inclusions; this myopathy is similar to that caused by VCP/p97 mutations, the most common cause of familial IBM. Mechanistically, we show that ULK1/2 localize to stress granules and phosphorylate VCP, thereby increasing VCP's activity and ability to disassemble stress granules. These data suggest that VCP dysregulation and defective stress granule disassembly contribute to IBM-like disease in Ulk1/2-deficient mice. In addition, stress granule disassembly is accelerated by an ULK1/2 agonist, suggesting ULK1/2 as targets for exploiting the higher-order regulation of stress granules for therapeutic intervention of IBM and related disorders.
    MeSH term(s) Adenosine Triphosphatases/genetics ; Animals ; Autophagy/genetics ; Autophagy-Related Protein-1 Homolog/genetics ; DNA-Binding Proteins/genetics ; Disease Models, Animal ; Humans ; Inclusion Bodies/genetics ; Inclusion Bodies/pathology ; Lysosomal Storage Diseases/genetics ; Lysosomal Storage Diseases/metabolism ; Lysosomal Storage Diseases/pathology ; Mice ; Muscular Diseases/genetics ; Muscular Diseases/metabolism ; Muscular Diseases/pathology ; Phosphorylation/genetics ; Protein-Serine-Threonine Kinases/genetics ; Stress, Physiological/genetics ; Ubiquitin/genetics ; Valosin Containing Protein/genetics
    Chemical Substances DNA-Binding Proteins ; TDP-43 protein, mouse ; Ubiquitin ; Ulk2 protein, mouse (EC 2.7.1.11) ; Autophagy-Related Protein-1 Homolog (EC 2.7.11.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; Ulk1 protein, mouse (EC 2.7.11.1) ; Adenosine Triphosphatases (EC 3.6.1.-) ; Valosin Containing Protein (EC 3.6.4.6) ; Vcp protein, mouse (EC 3.6.4.6)
    Language English
    Publishing date 2019-04-09
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1415236-8
    ISSN 1097-4164 ; 1097-2765
    ISSN (online) 1097-4164
    ISSN 1097-2765
    DOI 10.1016/j.molcel.2019.03.027
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  10. Article ; Online: The Noncanonical Role of ULK/ATG1 in ER-to-Golgi Trafficking Is Essential for Cellular Homeostasis.

    Joo, Joung Hyuck / Wang, Bo / Frankel, Elisa / Ge, Liang / Xu, Lu / Iyengar, Rekha / Li-Harms, XiuJie / Wright, Christopher / Shaw, Timothy I / Lindsten, Tullia / Green, Douglas R / Peng, Junmin / Hendershot, Linda M / Kilic, Fusun / Sze, Ji Ying / Audhya, Anjon / Kundu, Mondira

    Molecular cell

    2016  Volume 62, Issue 6, Page(s) 982

    Language English
    Publishing date 2016-06-16
    Publishing country United States
    Document type Journal Article ; Published Erratum
    ZDB-ID 1415236-8
    ISSN 1097-4164 ; 1097-2765
    ISSN (online) 1097-4164
    ISSN 1097-2765
    DOI 10.1016/j.molcel.2016.05.030
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

To top