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Gene Information

Gene symbol: SQSTM1

Gene name: sequestosome 1

HGNC ID: 11280

Synonyms: p62, p60, p62B, A170

Related Genes

# Gene Symbol Number of hits
1 ATP6AP2 1 hits
2 BECN1 1 hits
3 CCDC91 1 hits
4 EGFR 1 hits
5 FKBP5 1 hits
6 GPR137B 1 hits
7 HGF 1 hits
8 IGKV1-27 1 hits
9 IL8 1 hits
10 INS 1 hits
11 IRF3 1 hits
12 KHDRBS1 1 hits
13 MAP1LC3A 1 hits
14 MAPK3 1 hits
15 NFKB1 1 hits
16 PVRL1 1 hits

Related Sentences

# PMID Sentence
1 33239448 We have now determined that in cultured podocytes, high glucose led to increases in activation of EGFR signaling but decreases in autophagy activity as indicated by decreased beclin-1 and inhibition of LC3B autophagosome formation as well as increased rubicon (an autophagy inhibitor) and SQSTM1 (autophagy substrate).
2 32827692 HGF protected against diabetic nephropathy via autophagy-lysosome pathway in podocyte by modulating PI3K/Akt-GSK3β-TFEB axis.
3 32827692 Diabetic mice treated with HGF had markedly reduced ratio of kidney weight to body weight, urinary albumin excretion, podocyte loss and matrix expansion compared with that in the non-treated counterpart.
4 32827692 Simultaneously, HGF-treated diabetic mice exhibited increased autophagy activity as indicated by the decreased accumulation of sequestosome 1 (SQSTM1/ p62) and increased microtubule-associated proteins 1 light chains 3 (LC3) II/LC3I ratio.
5 32827692 These beneficial effects of HGF were blocked by HGF/c-Met inhibitor Crizotinib or phosphatidylinositide 3-kinases (PI3K) inhibitor LY294002.
6 32827692 Moreover, HGF treatment obviously prevented inactivation of the protein kinase B (Akt)-glycogen synthase kinase 3 beta (GSK3β)-transcription factor EB (TFEB) axis in high glucose-stimulated podocytes, which was associated with improved lysosome function and autophagy.
7 32827692 These results suggested that HGF protected against diabetic nephropathy through restoring podocyte autophagy, which at least partially involved PI3K/Akt-GSK3β-TFEB axis-mediated lysosomal function improvement.
8 32482387 Interestingly, we detected an increase in LC3BII and SQSTM1/P62 in MPC5 through inhibiting TM7SF1, and which can be completely corrected after blocking the autolysosome degradation with chloroquine (CQ).
9 32482387 Interestingly, we detected an increase in LC3BII and SQSTM1/P62 in MPC5 through inhibiting TM7SF1, and which can be completely corrected after blocking the autolysosome degradation with chloroquine (CQ).
10 32482387 Interestingly, we detected an increase in LC3BII and SQSTM1/P62 in MPC5 through inhibiting TM7SF1, and which can be completely corrected after blocking the autolysosome degradation with chloroquine (CQ).
11 32482387 Moreover, inhibition of TM7SF1 expression did not increase the mRNA level of SQSTM1/P62.
12 32482387 Moreover, inhibition of TM7SF1 expression did not increase the mRNA level of SQSTM1/P62.
13 32482387 Moreover, inhibition of TM7SF1 expression did not increase the mRNA level of SQSTM1/P62.
14 32482387 Theses results suggested that inhibition of TM7SF1 led to impaired degradation of autophagy products, which manifest as an abnormal accumulation of LC3BII and SQSTM1/P62.
15 32482387 Theses results suggested that inhibition of TM7SF1 led to impaired degradation of autophagy products, which manifest as an abnormal accumulation of LC3BII and SQSTM1/P62.
16 32482387 Theses results suggested that inhibition of TM7SF1 led to impaired degradation of autophagy products, which manifest as an abnormal accumulation of LC3BII and SQSTM1/P62.
17 28600173 Moreover, autophagy upregulation by Sequestosome 1 (p62/SQSM1) knockdown ameliorated this cell injury and relieved insulin resistance.
18 28450279 Autophagy upregulates (pro)renin receptor expression via reduction of P62/SQSTM1 and activation of ERK1/2 signaling pathway in podocytes.
19 28450279 Autophagy upregulates (pro)renin receptor expression via reduction of P62/SQSTM1 and activation of ERK1/2 signaling pathway in podocytes.
20 28450279 Autophagy upregulates (pro)renin receptor expression via reduction of P62/SQSTM1 and activation of ERK1/2 signaling pathway in podocytes.
21 28450279 Autophagy upregulates (pro)renin receptor expression via reduction of P62/SQSTM1 and activation of ERK1/2 signaling pathway in podocytes.
22 28450279 Autophagy upregulates (pro)renin receptor expression via reduction of P62/SQSTM1 and activation of ERK1/2 signaling pathway in podocytes.
23 28450279 Autophagy upregulates (pro)renin receptor expression via reduction of P62/SQSTM1 and activation of ERK1/2 signaling pathway in podocytes.
24 28450279 Knockout of p62 enhanced extracellular signal-regulated kinases (ERK1/2) activity.
25 28450279 Knockout of p62 enhanced extracellular signal-regulated kinases (ERK1/2) activity.
26 28450279 Knockout of p62 enhanced extracellular signal-regulated kinases (ERK1/2) activity.
27 28450279 Knockout of p62 enhanced extracellular signal-regulated kinases (ERK1/2) activity.
28 28450279 Knockout of p62 enhanced extracellular signal-regulated kinases (ERK1/2) activity.
29 28450279 Knockout of p62 enhanced extracellular signal-regulated kinases (ERK1/2) activity.
30 28450279 (pro)renin receptor (PRR) is expressed in podocytes where it contributes to the homeostasis of these cells.
31 28450279 (pro)renin receptor (PRR) is expressed in podocytes where it contributes to the homeostasis of these cells.
32 28450279 (pro)renin receptor (PRR) is expressed in podocytes where it contributes to the homeostasis of these cells.
33 28450279 (pro)renin receptor (PRR) is expressed in podocytes where it contributes to the homeostasis of these cells.
34 28450279 (pro)renin receptor (PRR) is expressed in podocytes where it contributes to the homeostasis of these cells.
35 28450279 (pro)renin receptor (PRR) is expressed in podocytes where it contributes to the homeostasis of these cells.
36 28450279 We hypothesized that in podocytes, upregulation of autophagic activity increases PRR expression via reduction of p62 and stimulation of ERK1/2 signaling pathway.
37 28450279 We hypothesized that in podocytes, upregulation of autophagic activity increases PRR expression via reduction of p62 and stimulation of ERK1/2 signaling pathway.
38 28450279 We hypothesized that in podocytes, upregulation of autophagic activity increases PRR expression via reduction of p62 and stimulation of ERK1/2 signaling pathway.
39 28450279 We hypothesized that in podocytes, upregulation of autophagic activity increases PRR expression via reduction of p62 and stimulation of ERK1/2 signaling pathway.
40 28450279 We hypothesized that in podocytes, upregulation of autophagic activity increases PRR expression via reduction of p62 and stimulation of ERK1/2 signaling pathway.
41 28450279 We hypothesized that in podocytes, upregulation of autophagic activity increases PRR expression via reduction of p62 and stimulation of ERK1/2 signaling pathway.
42 28450279 Both rapamycin and EBSS significantly decreased p62 protein levels, increased ERK1/2 activation by phosphorylating pTpY185/187, and increased mRNA and protein expressions of PRR.
43 28450279 Both rapamycin and EBSS significantly decreased p62 protein levels, increased ERK1/2 activation by phosphorylating pTpY185/187, and increased mRNA and protein expressions of PRR.
44 28450279 Both rapamycin and EBSS significantly decreased p62 protein levels, increased ERK1/2 activation by phosphorylating pTpY185/187, and increased mRNA and protein expressions of PRR.
45 28450279 Both rapamycin and EBSS significantly decreased p62 protein levels, increased ERK1/2 activation by phosphorylating pTpY185/187, and increased mRNA and protein expressions of PRR.
46 28450279 Both rapamycin and EBSS significantly decreased p62 protein levels, increased ERK1/2 activation by phosphorylating pTpY185/187, and increased mRNA and protein expressions of PRR.
47 28450279 Both rapamycin and EBSS significantly decreased p62 protein levels, increased ERK1/2 activation by phosphorylating pTpY185/187, and increased mRNA and protein expressions of PRR.
48 28450279 Utilizing confocal microscopy demonstrated that rapamycin and EBSS significantly decreased p62/SQSTM1 and increased PRR protein expressions.
49 28450279 Utilizing confocal microscopy demonstrated that rapamycin and EBSS significantly decreased p62/SQSTM1 and increased PRR protein expressions.
50 28450279 Utilizing confocal microscopy demonstrated that rapamycin and EBSS significantly decreased p62/SQSTM1 and increased PRR protein expressions.
51 28450279 Utilizing confocal microscopy demonstrated that rapamycin and EBSS significantly decreased p62/SQSTM1 and increased PRR protein expressions.
52 28450279 Utilizing confocal microscopy demonstrated that rapamycin and EBSS significantly decreased p62/SQSTM1 and increased PRR protein expressions.
53 28450279 Utilizing confocal microscopy demonstrated that rapamycin and EBSS significantly decreased p62/SQSTM1 and increased PRR protein expressions.
54 28450279 Similarly, by enhancing autophagic activity by transfection with autophagy-related 5 (ATG5) cDNA or ATG7 cDNA, results similar to those observed with rapamycin and EBSS treatments were produced.
55 28450279 Similarly, by enhancing autophagic activity by transfection with autophagy-related 5 (ATG5) cDNA or ATG7 cDNA, results similar to those observed with rapamycin and EBSS treatments were produced.
56 28450279 Similarly, by enhancing autophagic activity by transfection with autophagy-related 5 (ATG5) cDNA or ATG7 cDNA, results similar to those observed with rapamycin and EBSS treatments were produced.
57 28450279 Similarly, by enhancing autophagic activity by transfection with autophagy-related 5 (ATG5) cDNA or ATG7 cDNA, results similar to those observed with rapamycin and EBSS treatments were produced.
58 28450279 Similarly, by enhancing autophagic activity by transfection with autophagy-related 5 (ATG5) cDNA or ATG7 cDNA, results similar to those observed with rapamycin and EBSS treatments were produced.
59 28450279 Similarly, by enhancing autophagic activity by transfection with autophagy-related 5 (ATG5) cDNA or ATG7 cDNA, results similar to those observed with rapamycin and EBSS treatments were produced.
60 28450279 ERK1/2 inhibitor U0126 significantly attenuated mRNA and protein expressions of PRR in podocytes treated with rapamycin.
61 28450279 ERK1/2 inhibitor U0126 significantly attenuated mRNA and protein expressions of PRR in podocytes treated with rapamycin.
62 28450279 ERK1/2 inhibitor U0126 significantly attenuated mRNA and protein expressions of PRR in podocytes treated with rapamycin.
63 28450279 ERK1/2 inhibitor U0126 significantly attenuated mRNA and protein expressions of PRR in podocytes treated with rapamycin.
64 28450279 ERK1/2 inhibitor U0126 significantly attenuated mRNA and protein expressions of PRR in podocytes treated with rapamycin.
65 28450279 ERK1/2 inhibitor U0126 significantly attenuated mRNA and protein expressions of PRR in podocytes treated with rapamycin.
66 28450279 In conclusion, upregulation of autophagy enhanced PRR expression through reduction of p62 and stimulation of ERK1/2 activity signaling pathway.
67 28450279 In conclusion, upregulation of autophagy enhanced PRR expression through reduction of p62 and stimulation of ERK1/2 activity signaling pathway.
68 28450279 In conclusion, upregulation of autophagy enhanced PRR expression through reduction of p62 and stimulation of ERK1/2 activity signaling pathway.
69 28450279 In conclusion, upregulation of autophagy enhanced PRR expression through reduction of p62 and stimulation of ERK1/2 activity signaling pathway.
70 28450279 In conclusion, upregulation of autophagy enhanced PRR expression through reduction of p62 and stimulation of ERK1/2 activity signaling pathway.
71 28450279 In conclusion, upregulation of autophagy enhanced PRR expression through reduction of p62 and stimulation of ERK1/2 activity signaling pathway.
72 23296190 In addition to these receptors, Toll-like receptor 3 (TLR3) and retinoic acid-inducible gene 1 (RIG-I)-like helicases (RLHs), podocytes express the collateral proteins required to support intracellular signaling.
73 23296190 The transcription factor interferon regulatory factor 3 (IRF3) and nuclear factor kappa B (NF-ĸB) are phosphorylated and translocate to the nucleus, and dsRNA increases synthesis of proteins driven by IRF3 (P54, P56 and P60) or NF-ĸB (interleukin 8 and A20).
74 23296190 Furthermore, dsRNA suppresses podocyte cell migration, alters the expression of a panel of podocyte essential proteins (nephrin, podocin and CD2-associated protein or CD2AP) and changes transepithelial albumin flux.