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1 P1) regulation, suggesting a unique role for mortalin.
2 ation in a complex with the chaperon protein mortalin.
3 gen-responsive genes SOX5, RBM15, Dynein and Mortalin.
4 mediated nucleotide and substrate release by mortalin.
5                At 6 hours, the RNA level for mortalin-2, a pro-survival gene, was upregulated.
6                RT-PCR was performed for 18s, mortalin-2, cathepsins B, D, and L/V2.
7 ed and duplicated centrosomes, we identified mortalin, a member of heat shock protein family, as a pr
8                                              Mortalin [also known as heat shock protein family A (HSP
9 0-fold above normal clam hemocytes) of human mortalin, an Hsp70 family protein.
10 mmunoprecipitation we have demonstrated that mortalin and p53 proteins are complexed in the cytoplasm
11 tor of mortalin, disrupts the interaction of mortalin and p53 proteins, resulting in translocation of
12 cation requires physical interaction between mortalin and p53.
13  breast cancer exosome release and reinforce Mortalin and Vimentin as critical regulators and therape
14  SMRwt treatment reduced mesenchymal markers Mortalin and Vimentin expression, while the epithelial m
15                                              Mortalin and Vimentin knockdown was achieved through ant
16 nstrated that the SMR peptide interacts with Mortalin and Vimentin to inhibit pro-EMT exosome release
17 200b, miR-200c, and miR-217 as regulators of mortalin and, perhaps indirectly, of CD46 and CD55.
18  In human mitochondria, mitochondrial Hsp70 (mortalin) and the nucleotide exchange factor (GrpEL1) wo
19 ion in MEK/ERK-activated cancer and identify mortalin as a molecular switch that mediates the tumor-s
20 C cell survival and proliferation, proposing mortalin as a novel therapeutic target for MTC.
21 etion and HIV-1 virus release, we identified mortalin as an SMR-specific cellular protein.
22 Thus, our present findings not only identify mortalin as an upstream molecule of p53 but also provide
23  regulator of mortalin expression, the ESRRA-mortalin axis has higher significance in tumors with onc
24 in human and other animal cancers displaying mortalin-based cytoplasmic sequestration of the p53 tumo
25 these topoisomerase II poisons may result as mortalin-based cytoplasmic tethering is overwhelmed by d
26 odels for human cancers displaying a similar mortalin-based phenotype.
27                                 In addition, mortalin can potentially target the C8 and C9 complement
28          In this study, we demonstrated that mortalin can regulate MEK/ERK activity via protein phosp
29 tidyl-prolyl isomerase cyclophilin D (CypD), mortalin decreased mitochondrial permeability by inhibit
30 trates that p21(CIP1) has dual effects under mortalin-depleted conditions, i.e., mediating cell cycle
31                           Here, we show that mortalin depletion can selectively induce death of immor
32                                Nevertheless, mortalin depletion did not affect cellular PP1alpha leve
33                                    Moreover, mortalin depletion downregulated RET expression independ
34 erivative, phenocopied the lethal effects of mortalin depletion in K-Ras(G12V)-expressing IMR90E1A an
35                                      Indeed, mortalin depletion increased mitochondrial membrane perm
36                                       Hence, mortalin depletion increased mitochondrial permeability
37 fferent MEK/ERK-activated cancer cell lines, mortalin depletion induced cell death and growth arrest,
38                                Intriguingly, mortalin depletion induced growth arrest partly via the
39 nisms underlying these effects revealed that mortalin depletion induces transient MEK/ERK (extracellu
40 markably, MEK/ERK activity was necessary for mortalin depletion to induce p21(CIP1) expression in B-R
41                          Here, we found that mortalin depletion was selectively lethal to tumor and i
42  activity sensitizes cells to the effects of mortalin depletion, suggesting that mortalin has potenti
43 ocytes with MKT-077, a cationic inhibitor of mortalin, disrupts the interaction of mortalin and p53 p
44 t suppression of centrosome duplication, and mortalin-driven centrosome duplication requires physical
45 pacity against CDC relative to mitochondrial mortalin-EGFP.
46                                              Mortalin (encoded by HSPA9) is a mitochondrial chaperone
47                      Following transfection, mortalin-enhanced GFP (EGFP) is located primarily in mit
48 oncocytic characteristics, wherein ESRRA and mortalin exhibited relatively high functional overlap.
49 also effectively suppressed tumor growth and mortalin expression in the xenografts of oncocytic or ES
50  this correlation, ESRRA depletion decreased mortalin expression only in follicular thyroid tumor cel
51 a caspase-dependent apoptosis, which ectopic mortalin expression substantially abrogated.
52  that ESRRA is a tumor-specific regulator of mortalin expression, the ESRRA-mortalin axis has higher
53 on and in vitro binding assays revealed that mortalin facilitates PP1alpha-mediated MEK1/2 dephosphor
54 ily chaperones could not effectively replace mortalin for p21(CIP1) regulation, suggesting a unique r
55 ly, increased MEK-ERK signaling activity and mortalin function converged opposingly on the regulation
56                           One interactor was mortalin/GRP75, a homolog of the yeast ssq1 chaperone th
57                                              Mortalin/GRP75, the mitochondrial heat shock protein 70,
58 rocess involving the mitochondrial chaperone mortalin/GRP75.
59 to determine structures of full-length human mortalin-GrpEL1 complexes in previously unobserved state
60 ons allow us to delineate specific roles for mortalin-GrpEL1 interfaces and to identify steps in GrpE
61        These findings suggest that targeting mortalin has potential as a selective therapeutic strate
62 fects of mortalin depletion, suggesting that mortalin has potential as a selective therapeutic target
63            The mitochondrial HSP70 chaperone mortalin (HSPA9/GRP75) is often upregulated and mislocal
64                                We found that mortalin (HSPA9/GRP75), a member of HSP70 family, is upr
65                          Here we report that mortalin (HSPA9/GRP75/PBP74) is a novel negative regulat
66                  We previously reported that mortalin/HSPA9 can facilitate proliferation of certain K
67 ation, suggesting a nonconventional role for mortalin in promoting PP1alpha-MEK1/2 interaction.
68 on between C5b-9 deposition and the level of mortalin in the cell.
69 body inhibition we demonstrated that the Nef/mortalin interaction is necessary for exNef secretion.
70 eriments with full-length Nef confirmed that mortalin interacts with Nef via Nef's SMR motif and that
71                  These data demonstrate that mortalin is a key regulator of multiple signaling and me
72                                We found that mortalin is present in the MEK1/MEK2 proteome and is upr
73                                       Direct Mortalin knockdown paralleled the results of SMR peptide
74 emia cells to CDC, whereas overexpression of mortalin leads to their resistance to CDC.
75               Further analysis revealed that mortalin localized to centrosomes in late G1 before cent
76 strated that, to compensate for reduction in mortalin mRNA level, the cells increased the rate of syn
77  for miR-200b, miR-200c, or miR-217 enhanced mortalin mRNA level.
78 -200b/c or miR-217 lowered the expression of mortalin mRNA.
79  miR-217 regulatory sites were identified in mortalin mRNA.
80 ial molecular chaperone GRP75, also known as mortalin/mthsp70/PBP74, directly interacts with frataxin
81 express its full protective effect from CDC, mortalin must first reach the mitochondria.
82 cell types exhibiting normal MEK/ERK status, mortalin overexpression suppressed B-Raf(V600E)- or Delt
83                            Overexpression of mortalin overrides the p53-dependent suppression of cent
84 lites or the mitochondrial chaperone mtHsp75/mortalin partially reverses the inflammation-associated
85                                    Moreover, mortalin promotes dissociation of p53 from centrosomes t
86 rrelation between exNef secretion levels and mortalin protein expression.
87 iRNA modulators had no significant effect on mortalin protein level.
88 the cells increased the rate of synthesis of mortalin protein.
89 n leukemic clam hemocytes, wild-type p53 and mortalin proteins co-localize in the cytoplasm.
90 nced its release from the cells and promoted mortalin relocation to the plasma membrane.
91 p53 mutant that lacks the ability to bind to mortalin remains at centrosomes, and suppresses centroso
92     Overexpression and microRNA knockdown of mortalin revealed a positive correlation between exNef s
93 translocase 3 (ANT3) as a previously unknown mortalin substrate and cell survival/death effector.
94 bitor derivatives that effectively inhibited mortalin suppressed the proliferation of B-Raf(V600E) tu
95             As shown here, interference with mortalin synthesis enhances sensitivity of K562 erythrol
96                            Similar to intact mortalin, the ATPase domain, but not the substrate-bindi
97                    Two functional domains of mortalin, the N-terminal ATPase domain and the C-termina
98                                   Binding of mortalin to complement C9 and C8 occurs through an ionic
99  cancer biopsy specimens in correlation with mortalin upregulation.
100  regulation of the peptide-binding domain in mortalin was critical to cell survival or death.
101                                              Mortalin was previously shown by us to bind to component
102 rate-binding cavity and the substrate lid of mortalin were necessary for these physical interactions,
103  cancers p53 is tethered in the cytoplasm by mortalin when the latter protein is overexpressed.
104 have a role in tumorigenesis in concert with mortalin, which affects MEK/ERK activity in tumor cells.

 
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