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1 sis leads to cell depletion and insufficient compensatory proliferation.
2 d into a liver undergoing chronic damage and compensatory proliferation.
3 es did not undergo spontaneous cell death or compensatory proliferation.
4 ugh removal of aberrant or damaged cells and compensatory proliferation.
5 oral control of damage-induced apoptosis and compensatory proliferation.
6 tissue regeneration, transdetermination and compensatory proliferation.
7 ession, PUMA-dependent hepatocyte death, and compensatory proliferation.
8 ogated PUMA induction, hepatocyte death, and compensatory proliferation.
9 ial cells and thus lead to apoptosis-induced compensatory proliferation.
10 ppears to be critical for both apoptosis and compensatory proliferation.
11 he activation of Hedgehog (Hh) signaling for compensatory proliferation.
12 ate the depleted crypt in a process known as compensatory proliferation.
13 ion through increased nutritional uptake and compensatory proliferation.
14 ptotic cells activate signaling cascades for compensatory proliferation.
15 to normal-looking adult wings as a result of compensatory proliferation.
16 tion is intricately linked to cell death and compensatory proliferation.
17 esis by inhibiting EGFR-dependent hepatocyte compensatory proliferation.
18 We discovered that Hippo signaling regulates compensatory proliferation after extensive cell death in
19 cess and damaged cells but can also initiate compensatory proliferation, an adaptive response that oc
20 o DEN-induced injury was sufficient to block compensatory proliferation and annihilate development of
22 ently in mature pancreatic cell types, since compensatory proliferation and possible mTORC2 activatio
23 y controlled in tissue regeneration to allow compensatory proliferation and prevent the intrinsic onc
24 xposure blocked prolonged JNK activation and compensatory proliferation and prevented excessive DEN-i
26 n abundant miRNA in the beta-cell, regulates compensatory proliferation and secretion during insulin
28 cancer in TGR5(-/-) mice, hepatocyte death, compensatory proliferation, and gene expression of certa
29 cyte and HSC apoptosis, resulting in reduced compensatory proliferation, and reduced replication stre
30 omotes chemical hepatocarcinogenesis through compensatory proliferation, and suggest apoptotic induce
31 umor development, suggesting that control of compensatory proliferation by high levels of p21 is crit
32 eltaHEP mice, there was hepatocyte death and compensatory proliferation, contributing to an inflammat
33 nucleotide (AICAR) and metformin, attenuated compensatory proliferation (days 6, 7, and 30) following
34 induced hepatocyte death and cytokine-driven compensatory proliferation, disruption of JNK1 abrogated
35 ep mice by inducing hepatocyte apoptosis and compensatory proliferation during early phases of tumori
36 at diploid cells in mosaic embryos undertake compensatory proliferation during the implantation stage
38 utive emergence of a fatty liver, apoptosis, compensatory proliferation, fibrosis, and cirrhosis that
39 r data support the hypothesis that increased compensatory proliferation following continued tissue da
40 es JNK-dependent apoptosis and JNK-dependent compensatory proliferation following radiation injury.
41 r targets of hepatocyte death in relation to compensatory proliferation have not been fully character
42 different caspases trigger distinct forms of compensatory proliferation in an apparent nonapoptotic f
43 lial injury-induced colitis showing impaired compensatory proliferation in crypts and extensive ulcer
45 s from differentiated hepatocytes undergoing compensatory proliferation in livers damaged by viruses
46 ute to tissue homeostasis by promoting local compensatory proliferation in response to cell death.
47 nes, which enhance cell survival and trigger compensatory proliferation in response to tissue injury.
48 , decreased levels of phosphorylated ERK and compensatory proliferation in the neighboring epithelial
49 In response to the induction of apoptosis, compensatory proliferation increased in the small intest
50 mice displayed spontaneous hepatocyte death, compensatory proliferation, inflammatory cell infiltrati
51 or grp mutants, suggesting that the need for compensatory proliferation is greater for checkpoint mut
52 egulatory networks controlling inflammation, compensatory proliferation, morphology and cell migratio
53 at increased hepatocyte death and associated compensatory proliferation observed in DEN-injured ERRal
54 t the potential for functionally significant compensatory proliferation of beta cells is retained in
56 evealed a new role for Drosophila p53 in the compensatory proliferation of cells that are needed to r
57 newing capacity of hepatocytes, resulting in compensatory proliferation of DDB1-expressing hepatocyte
58 -) hepatocytes into GS(+) hepatocytes and by compensatory proliferation of hepatocytes across liver z
59 pendently, directed hepatic fibrosis and the compensatory proliferation of hepatocytes and biliary ce
60 ndent RIPK1 phosphorylation in LPCs inhibits compensatory proliferation of hepatocytes and intrahepat
61 ORC1 by rapamycin effectively attenuates the compensatory proliferation of hepatocytes in CAMK2gamma(
62 is well recognized that lymphopenia induces compensatory proliferation of immune cells, generally te
64 dant-generating pollutants causes injury and compensatory proliferation of lung epithelium, but the s
65 ticellular organisms, apoptotic cells induce compensatory proliferation of neighboring cells to maint
66 as identified a link between dying cells and compensatory proliferation of neighbouring survivor cell
69 d hepatocyte death, giving rise to augmented compensatory proliferation of surviving hepatocytes.
71 ts importance, the mechanistic basis of such compensatory proliferation remains poorly understood.
73 larity complex influences both a physiologic compensatory proliferation response after irradiation in
76 rtance of JNK1-mediated hepatocyte death and compensatory proliferation, these results strongly sugge
77 hila wing imaginal disc, dying cells trigger compensatory proliferation through secretion of the mito
78 optosis, unaffected epithelial cells undergo compensatory proliferation to maintain the integrity of
79 mediated by JNK signaling, which also drives compensatory proliferation to maintain tissue integrity
80 elial progenitor cells to undergo sufficient compensatory proliferation to rescue the deficit in prog
82 bitory factor (Mif)-containing AEVs regulate compensatory proliferation via ERK signaling in epitheli
83 (TLR) ligands, as well as growth signals for compensatory proliferation, would also be key factors in