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1 ccumulates within the islet to contribute to cellular dysfunction.
2 ls of mitochondrial fusion and escaped major cellular dysfunction.
3 ential as a therapeutic target to ameliorate cellular dysfunction.
4 racellular aggregates that initiate profound cellular dysfunction.
5 ds may impair normal cell signaling, causing cellular dysfunction.
6  together with lipofuscin, may contribute to cellular dysfunction.
7 terocyte viability, increased apoptosis, and cellular dysfunction.
8 l significance of these reaction pathways to cellular dysfunction.
9 ey then penetrate these live cells and cause cellular dysfunction.
10 at disrupts RNA splicing, causing widespread cellular dysfunction.
11 ures, leading to altered gene expression and cellular dysfunction.
12 sh due to the widespread consequences of its cellular dysfunction.
13  proteins and DNA, causing mitochondrial and cellular dysfunction.
14 sosomal hydrolases, leading to lysosomal and cellular dysfunction.
15 on, frequently resulting in immune and other cellular dysfunction.
16  rupture under various stressors, leading to cellular dysfunction.
17 o the biology underlying progeria-associated cellular dysfunction.
18  amyloid beta peptide and delays adult-onset cellular dysfunction.
19  they are formed and proliferate to generate cellular dysfunction.
20 ent observed phenotypes represent reversible cellular dysfunction.
21 d when excessive lipid accumulation leads to cellular dysfunction.
22 e is enriched, OXPHOS declines, resulting in cellular dysfunction.
23 nstead are part of a coordinated response to cellular dysfunction.
24 ir capacity to cause membrane disruption and cellular dysfunction.
25 ral role for PRC in the adaptive response to cellular dysfunction.
26 ransient dysynchrony without whole heart and cellular dysfunction.
27 nce, two major protective mechanisms against cellular dysfunction.
28 mal trafficking, substrate accumulation, and cellular dysfunction.
29 ation of spurious oxidative damage can cause cellular dysfunction.
30  endothelial cells, which is associated with cellular dysfunction.
31 (GPCRs) involved in host defense and sensing cellular dysfunction.
32 e arise from Purkinje cell death rather than cellular dysfunction.
33 ceptors involved in host defense and sensing cellular dysfunction.
34 ffness is altered in disease and can lead to cellular dysfunction(9-11).
35  comprise a catalytic A-subunit that induces cellular dysfunction and a B-pentamer that recognizes ho
36      Genomic instability leads to mutations, cellular dysfunction and aberrant phenotypes at the tiss
37 ansduction pathways, which can contribute to cellular dysfunction and age-related reductions in stres
38 sruption is a novel mechanism to account for cellular dysfunction and apoptosis in T2DM.
39 e stress in islet beta cells, giving rise to cellular dysfunction and apoptosis.
40  delicate quality-control system can lead to cellular dysfunction and apoptosis.
41 mitochondrial Ca(2+) homeostasis can lead to cellular dysfunction and apoptosis.
42 c role of p53 in the mitochondria-associated cellular dysfunction and behavioral abnormalities of Hun
43 hat lipotoxicity in Schwann cells results in cellular dysfunction and cell death that involves a robu
44       This lipid overload is associated with cellular dysfunction and cell death, which contribute to
45 nergistic disruptive mechanisms that lead to cellular dysfunction and cell death.
46 hronic diseases and has been associated with cellular dysfunction and cell death.
47 ss ROS reduces lifespan by causing extensive cellular dysfunction and damage, birds are remarkably lo
48 ellular calcium may play a role in mediating cellular dysfunction and death following central nervous
49                                   Hepatocyte cellular dysfunction and death induced by lipids and mac
50 euronal signaling but can also contribute to cellular dysfunction and death under pathological condit
51             Inadequate oxygenation can cause cellular dysfunction and death.
52 an overproduction of ceramide and consequent cellular dysfunction and death.
53 echanisms whereby mutant huntingtin leads to cellular dysfunction and death.
54 is known to induce lipotoxicity resulting in cellular dysfunction and death.
55 ely results in global oxidative stress (OS), cellular dysfunction and death.
56  sources of oxidative stress and triggers of cellular dysfunction and death.
57 ygen and nitrogen species capable of causing cellular dysfunction and death.
58 ation despite clear evidence for progressive cellular dysfunction and degeneration.
59 how metabolic stress causally contributes to cellular dysfunction and diabetes pathogenesis.
60 ed as a key mechanism underlying age-related cellular dysfunction and disease progression.
61 be cytoprotective, it can also contribute to cellular dysfunction and disease progression.
62  cellular components that may play a role in cellular dysfunction and disease.
63 tion of aberrant proteins, which can lead to cellular dysfunction and disease.
64 al imbalances within a cell can also lead to cellular dysfunction and diseases.
65 ry incurred during liver surgery can lead to cellular dysfunction and elevations in proinflammatory c
66 mation of oxidized LDL in the artery wall to cellular dysfunction and formation of lesions.
67 change to create without inducing unintended cellular dysfunction and how to deliver this technology
68 sult of cell death per se, but the result of cellular dysfunction and morphological alterations that
69 of the mutant protein is expected to prevent cellular dysfunction and neurodegeneration in HD.
70 llular compartments may coordinately lead to cellular dysfunction and neurodegeneration in PD.
71 s valuable new insight into mTORC1-dependent cellular dysfunction and neurodevelopmental disorders.
72 ts to nuclear proteins eventually leading to cellular dysfunction and neuronal death.
73 eta42) lead to a series of events that cause cellular dysfunction and neuronal death.
74 gical mechanisms do not explain the basis of cellular dysfunction and organ failure, the ultimate cau
75 understanding into how these defects lead to cellular dysfunction and organ pathology is still incomp
76 dation may play a role in the development of cellular dysfunction and other complications of diabetes
77 anisms by which protein aggregation mediates cellular dysfunction and overt cell death are unknown.
78 ation of misfolded proteins and to potential cellular dysfunction and pathological consequences.
79 perturbations in histone balance may lead to cellular dysfunction and pathologies.
80 prevent Abeta42 aggregation protects against cellular dysfunction and reduces the production/accumula
81 ial stress, inflammation, pulmonary vascular cellular dysfunction and structural dysregulation, iron
82 of genetically distinct, projection-specific cellular dysfunction and that dysregulated lateral MB ne
83  are considered as toxic metabolites causing cellular dysfunction and tissue damage, the enzymology o
84                                              Cellular dysfunction and tissue pathology can result fro
85 their deregulation is associated with severe cellular dysfunction and various diseases.
86 lar NAD(+) and subsequently, ATP, leading to cellular dysfunction and, ultimately, cell death.
87 er-ordered aggregates, and cause a myriad of cellular dysfunctions and neuronal death.
88 n (AL-LC) proteins provoke oxidative stress, cellular dysfunction, and apoptosis in isolated adult ca
89 y attenuated AL-LC-induced oxidative stress, cellular dysfunction, and apoptosis.
90 alcineurin inhibitors benefit axonal damage, cellular dysfunction, and cognitive outcomes in animal m
91                                    Fibrosis, cellular dysfunction, and gap junction protein alteratio
92 sequent activation of inflammatory pathways, cellular dysfunction, and lipoapoptosis.
93 nditions, may help in identifying markers of cellular dysfunction, and more broadly in cell phenotypi
94 ptor activation with subsequent induction of cellular dysfunction, apoptosis, and arrhythmias.
95     Accumulated protein damage and resultant cellular dysfunction are consequences of limited protein
96 e and untreatable, and mechanisms underlying cellular dysfunction are poorly understood.
97 r and less efficient connectivity as well as cellular dysfunction are the substrate of the weaker exc
98  by which this toxic PARP1 activity triggers cellular dysfunction are unclear.
99 NA foci, and their relative contributions to cellular dysfunction, are unclear.
100 esis and outcomes, unifying diverse modes of cellular dysfunction around core actionable mechanisms.
101 iapoptotic effects on beta-cells and prevent cellular dysfunction associated with mitoNEET overexpres
102 to irreversible pathological aggregation and cellular dysfunction associated with the onset and devel
103 leviates the transcriptional, molecular, and cellular dysfunctions associated with DS.
104  and their aberrant accumulation can lead to cellular dysfunctions associated with neurodegenerative
105 g of the relative contribution of reversible cellular dysfunction at different stages in disease.
106 ing that the DA subgenomic segment can cause cellular dysfunction but not death, possibly similar to
107 ave implicated altered DDX6 in molecular and cellular dysfunction, but clinical consequences and path
108 survival in stress-inducing environments and cellular dysfunction, but constitutive activation of SKN
109 ations to a variety of stress conditions and cellular dysfunction, but how the energetic demands are
110 ontaining expanded CUG or CCUG repeats cause cellular dysfunction by altering the processing or metab
111 f mutant huntingtin in the nucleus may cause cellular dysfunction by binding to Sp1 and thus reducing
112             We propose a novel mechanism for cellular dysfunction by the HD mutation arising from the
113 twi/twi Schwann cells that may be reflecting cellular dysfunctions by inhibition of the PKC.
114 ease hypothesis that protein aggregation and cellular dysfunction can occur at a threshold of approxi
115 would broaden COE applications to understand cellular dysfunction, cell communication, and the target
116 om the fatty liver-is the engine that drives cellular dysfunction, cell death, and deleterious remode
117 d organisms in complex ways that can lead to cellular dysfunction, cell death, inflammation, and dise
118                                    Aging and cellular dysfunction compromise the survival and re-acti
119                                    Aging and cellular dysfunction compromise the survival and reactiv
120   Mutant HTT expression leads to a myriad of cellular dysfunctions culminating in neuronal loss and c
121                   In addition to its role in cellular dysfunction during metabolic stress, the period
122 d to identify new drugs targeting Ca-related cellular dysfunction (eg, cardiac arrhythmias).
123 deficiencies contribute to microvascular and cellular dysfunction following critical illness.
124 citotoxicity has been shown to contribute to cellular dysfunction following traumatic brain injury (T
125 s involving cells, chemokines and cytokines, cellular dysfunctions, growth factors, and viral protein
126                                Although many cellular dysfunctions have been described in cystinosis,
127                                   AD-related cellular dysfunctions have been linked to this ApoE4 mis
128 impairs neuronal energetics, contributing to cellular dysfunction in AD.
129 y, autophagy is tightly regulated to prevent cellular dysfunction in all eukaryotic cells.
130 fficiency as a key contributor to widespread cellular dysfunction in aneuploid HMECs with net copy nu
131 nigmatic molecule linking dietary factors to cellular dysfunction in cardiovascular, neurological, an
132 s to mitochondrial respiration contribute to cellular dysfunction in conditions of hypoxia and have b
133 nal MT stability and suggest a mechanism for cellular dysfunction in dynein-linked disease.
134 al mutant fragments that aggregate and cause cellular dysfunction in HD.
135 tect LDL oxidation and prevent oxLDL-induced cellular dysfunction in HUVECs.
136 ogenic aggregates and their implications for cellular dysfunction in NMDs.
137 contributes to free fatty acid (FFA)-induced cellular dysfunction in nonislet tissues in type 2 diabe
138  quantity of ectopic fat could contribute to cellular dysfunction in obesity and type 2 diabetes.
139 nisms and, potentially, provides a basis for cellular dysfunction in pathologic situations in which i
140 evealed as a potential molecular hub for DKD cellular dysfunction in several cross-linked pathways fe
141 portant questions about common mechanisms of cellular dysfunction in these disorders.
142                      The first indication of cellular dysfunction in treated SC cultures was a decrea
143 d risk of metabolic disorder development and cellular dysfunction in various species.
144 (mtHtt), and is associated with a variety of cellular dysfunctions including excessive mitochondrial
145 ty, leading to aberrant chromatin states and cellular dysfunction, including those related to morphog
146 g accumulation of amyloid A and for limiting cellular dysfunction induced by amyloid A.
147  consistent with the hypothesis that adipose cellular dysfunction is a primary contributor to systemi
148                                      A major cellular dysfunction is insufficient apical plasma membr
149 ing in displacement of normal structures and cellular dysfunction is the characteristic feature of sy
150 eef-building corals offer a clear example of cellular dysfunction leading to a dysbiosis that disrupt
151 ory pathways, resulting in mitochondrial and cellular dysfunction leading to multiorgan failure.
152 oteins, which occur naturally or result from cellular dysfunction, might be more common than recogniz
153 scription stress that, if unresolved, causes cellular dysfunction, neurodegeneration and ageing.
154 egeneration in SMA remain elusive, as global cellular dysfunction obscures the identification and cha
155                    These results demonstrate cellular dysfunction of C9orf72 HRE mutant microglia, an
156 ll enable us to directly test whether common cellular dysfunction or behavioural outcomes of a geneti
157 the application of gene products that reduce cellular dysfunction or death represent new therapeutic
158 ough reactive oxygen species toxicity) drive cellular dysfunction or demise.
159 cid alpha-glucosidase leading to progressive cellular dysfunction owing to the accumulation of glycog
160 ngton's disease (HD), cognitive symptoms and cellular dysfunction precede the onset of classical moto
161 the early cognitive deficits may be due to a cellular dysfunction rather than being a consequence of
162  nature of species responsible for mediating cellular dysfunction remain unclear.
163 echanisms translating genetic association to cellular dysfunction remain unknown.
164 ich was associated with their development of cellular dysfunction; second, when peritoneal macrophage
165 se cell death, but instead initiate discrete cellular dysfunctions.SIGNIFICANCE STATEMENT Public awar
166 pects of Alzheimer's disease (AD)-associated cellular dysfunction, suggesting a pivotal role for this
167 d or prolonged tissue injury, can exacerbate cellular dysfunction, suggesting that it may contribute
168                       Dystrophin loss causes cellular dysfunction that drives the loss of healthy ske
169 hronic exposure to hyperglycemia can lead to cellular dysfunction that may become irreversible over t
170 onal regulation is one of the main causes of cellular dysfunction that underlies different disease st
171 f hypothyroidism, is linked to metabolic and cellular dysfunctions that contribute to disease aetiopa
172 tion and parenchymal inflammation leading to cellular dysfunction, thrombosis, and fibrosis.
173  increased susceptibility to ethanol-induced cellular dysfunction through decreased bioenergetic stor
174 test whether environmental stress can induce cellular dysfunction through modulating RNA-chromatin in
175 y exposure to anesthesia may produce lasting cellular dysfunction through the induction of a sustaine
176 mia causes myocardial insulin resistance and cellular dysfunction via IRS1 and IRS2, we generated hea
177  GPCR/G protein interfaces and counteracting cellular dysfunctions via focused tuning of GPCR signali
178 HADH II enzymatic activity to Abeta-mediated cellular dysfunction was studied by site-directed mutage
179 ng several cellular biological mechanisms of cellular dysfunction, we and others have recently propos
180  the presence of misfolded proteins leads to cellular dysfunction, we employed Caenorhabditis elegans
181 d colleagues demonstrated a toxic cascade of cellular dysfunctions which may underlie Parkinson's dis
182 rce of increased plasma GDF15 levels in that cellular dysfunction with aging can be pleiotropic and h
183 L expression (which can persist) can lead to cellular dysfunction with survival.
184 protein, are responsible for a wide range of cellular dysfunctions within the vessel wall.
185 adily express protein aggregates, leading to cellular dysfunction without concomitant up-regulation o

 
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