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METTL3-mediated HSPA9 m6A modification promotes malignant transformation and inhibits cellular senescence by regulating exosomal mortalin protein in cervical cancer.
Ao K, Yin M, Lyu X, Xiao Y, Chen X, Zhong S, Wen X, Yuan J, Ye M, Zhang J, Li X, Hao Y, Guo X. Ao K, et al. Cancer Lett. 2024 Apr 10;587:216658. doi: 10.1016/j.canlet.2024.216658. Epub 2024 Jan 20. Cancer Lett. 2024. PMID: 38253218
Furthermore, mortalin gained increased mRNA stability and enhanced translation efficiency via the m6A methylation in the HSPA9 mRNA 3'UTR, which was catalysed by METTL3 in CCa cells. Exosomal mortalin overexpression significantly promoted the proliferation, migration and i …
Furthermore, mortalin gained increased mRNA stability and enhanced translation efficiency via the m6A methylation in the HSPA9 mRNA 3 …
An Hsp70 family chaperone, mortalin/mthsp70/PBP74/Grp75: what, when, and where?
Wadhwa R, Taira K, Kaul SC. Wadhwa R, et al. Cell Stress Chaperones. 2002 Jul;7(3):309-16. doi: 10.1379/1466-1268(2002)007<0309:ahfcmm>2.0.co;2. Cell Stress Chaperones. 2002. PMID: 12482206 Free PMC article. Review.
It has been assigned to multiple subcellular sites and implicated in multiple functions ranging from stress response, intracellular trafficking, antigen processing, control of cell proliferation, differentiation, and tumorigenesis. The present article compiles and reviews …
It has been assigned to multiple subcellular sites and implicated in multiple functions ranging from stress response, intracellular traffick …
In vitro aging research in Japan.
Tsuji T, Miyazaki M, Sakaguchi M, Namba M. Tsuji T, et al. Exp Gerontol. 2000 May;35(3):291-8. doi: 10.1016/s0531-5565(00)00085-1. Exp Gerontol. 2000. PMID: 10832050 Review. No abstract available.
Steady-State Levels of Phosphorylated Mitogen-Activated Protein Kinase Kinase 1/2 Determined by Mortalin/HSPA9 and Protein Phosphatase 1 Alpha in KRAS and BRAF Tumor Cells.
Wu PK, Hong SK, Park JI. Wu PK, et al. Mol Cell Biol. 2017 Aug 28;37(18):e00061-17. doi: 10.1128/MCB.00061-17. Print 2017 Sep 15. Mol Cell Biol. 2017. PMID: 28674184 Free PMC article.
Therefore, additional mechanisms may exist to modulate MEK/ERK activity in favor of tumor cell proliferation. We previously reported that mortalin/HSPA9 can facilitate proliferation of certain KRAS and BRAF tumor cells by modulating MEK/ERK activity. ...
Therefore, additional mechanisms may exist to modulate MEK/ERK activity in favor of tumor cell proliferation. We previously reported …
Opposed arsenite-mediated regulation of p53-survivin is involved in neoplastic transformation, DNA damage, or apoptosis in human keratinocytes.
Li Y, Jiang R, Zhao Y, Xu Y, Ling M, Pang Y, Shen L, Zhou Y, Zhang J, Zhou J, Wang X, Liu Q. Li Y, et al. Toxicology. 2012 Oct 28;300(3):121-31. doi: 10.1016/j.tox.2012.06.004. Epub 2012 Jun 15. Toxicology. 2012. PMID: 22706169
Our present study shows that, for human keratinocytes (HaCaT) cells, a low concentration of arsenite activates extracellular signal-regulated kinases (ERKs), which leads to up-regulation of nuclear factor kappaB (NF-kappaB) binding to DNA and to elevated, NF-kappaB-dependent expr …
Our present study shows that, for human keratinocytes (HaCaT) cells, a low concentration of arsenite activates extracellular signal-regulate …
Identification of tumor necrosis factor signaling-related proteins during Epstein-Barr virus-induced B cell transformation.
Jeon JP, Kim JW, Park B, Nam HY, Shim SM, Lee MH, Han BG. Jeon JP, et al. Acta Virol. 2008;52(3):151-9. Acta Virol. 2008. PMID: 18999889
Epstein-Barr virus (EBV) infection in vitro transforms primary B cells into continuously proliferating lymphoblastoid cell lines (LCLs) that have been widely used as a genomic resource for variety of immunological and genetic studies. ...This study suggested that deregulat …
Epstein-Barr virus (EBV) infection in vitro transforms primary B cells into continuously proliferating lymphoblastoid cell lines (LCL …
mot-2-Mediated cross talk between nuclear factor-B and p53 is involved in arsenite-induced tumorigenesis of human embryo lung fibroblast cells.
Li Y, Xu Y, Ling M, Yang Y, Wang S, Li Z, Zhou J, Wang X, Liu Q. Li Y, et al. Environ Health Perspect. 2010 Jul;118(7):936-42. doi: 10.1289/ehp.0901677. Epub 2010 Mar 3. Environ Health Perspect. 2010. PMID: 20199942 Free PMC article.
OBJECTIVE: We investigated the molecular mechanisms underlying the inactivation of p53 and neoplastic transformation induced by arsenite in human embryo lung fibroblast (HELF) cells. METHODS: Anchorage-independent growth assays were performed, and tumorigenicity in …
OBJECTIVE: We investigated the molecular mechanisms underlying the inactivation of p53 and neoplastic transformation induced b …
Ubiquitin-like (UBX)-domain-containing protein, UBXN2A, promotes cell death by interfering with the p53-Mortalin interactions in colon cancer cells.
Sane S, Abdullah A, Boudreau DA, Autenried RK, Gupta BK, Wang X, Wang H, Schlenker EH, Zhang D, Telleria C, Huang L, Chauhan SC, Rezvani K. Sane S, et al. Cell Death Dis. 2014 Mar 13;5(3):e1118. doi: 10.1038/cddis.2014.100. Cell Death Dis. 2014. PMID: 24625977 Free PMC article.
The mot-2-dependent cytoprotective function enables cancer cells to support malignant transformation. Abrogating the p53-mot-2 interaction can control or slow down the growth of cancer cells. ...
The mot-2-dependent cytoprotective function enables cancer cells to support malignant transformation. Abrogating the p53-mot-2 intera …
The repressive effect of NF-kappaB on p53 by mot-2 is involved in human keratinocyte transformation induced by low levels of arsenite.
Li Y, Ling M, Xu Y, Wang S, Li Z, Zhou J, Wang X, Liu Q. Li Y, et al. Toxicol Sci. 2010 Jul;116(1):174-82. doi: 10.1093/toxsci/kfq109. Epub 2010 Apr 7. Toxicol Sci. 2010. PMID: 20375080
In the present study, molecular mechanisms underlying the inactivation of p53 function and the genomic instability in malignant transformation of the human keratinocyte cell line, HaCaT, induced by low levels of arsenic were investigated. ...Moreover, inactivation o …
In the present study, molecular mechanisms underlying the inactivation of p53 function and the genomic instability in malignant transform
14 results