Ignet

Gene Information

Gene symbol: MAP1LC3A

Gene name: microtubule-associated protein 1 light chain 3 alpha

HGNC ID: 6838

Synonyms: MAP1BLC3, MAP1ALC3, LC3, LC3A, ATG8E

Related Genes

#	Gene Symbol	Number of hits
1	AKT1	1 hits
2	ALB	1 hits
3	APOL1	1 hits
4	ARHGDIB	1 hits
5	ATG16L2	1 hits
6	ATG5	1 hits
7	ATG7	1 hits
8	ATIC	1 hits
9	BAX	1 hits
10	BCL2	1 hits
11	BECN1	1 hits
12	CACNA1E	1 hits
13	CASP3	1 hits
14	CCL26	1 hits
15	CDKN1B	1 hits
16	CLEC16A	1 hits
17	CYBA	1 hits
18	CYBB	1 hits
19	FIS1	1 hits
20	HGF	1 hits
21	HMOX1	1 hits
22	IFNA1	1 hits
23	IGF2BP2	1 hits
24	INS	1 hits
25	IRGM	1 hits
26	JAK1	1 hits
27	JAK2	1 hits
28	JUN	1 hits
29	KEAP1	1 hits
30	KHDRBS1	1 hits
31	KIT	1 hits
32	LAMP1	1 hits
33	LAP3	1 hits
34	LDLR	1 hits
35	LRRK2	1 hits
36	MAP1A	1 hits
37	MAP1LC3B	1 hits
38	MAPK8	1 hits
39	MATN1	1 hits
40	MFN2	1 hits
41	MT-CYB	1 hits
42	MTMR3	1 hits
43	NFE2L2	1 hits
44	NPHS1	1 hits
45	NPHS2	1 hits
46	PIK3CA	1 hits
47	PINK1	1 hits
48	PRKAA1	1 hits
49	PRKAA2	1 hits
50	RHOD	1 hits
51	RORC	1 hits
52	RPS6KB1	1 hits
53	SLC2A4	1 hits
54	SQSTM1	1 hits
55	STAT1	1 hits
56	STAT3	1 hits
57	STAT5A	1 hits
58	STAT6	1 hits
59	SYNPO	1 hits
60	TSC1	1 hits
61	TWIST1	1 hits
62	ULK1	1 hits
63	VIM	1 hits
64	WT1	1 hits

Related Sentences

#	PMID	Sentence
1	34975320	GPR43 activation-mediated lipotoxicity contributes to podocyte injury in diabetic nephropathy by modulating the ERK/EGR1 pathway.
2	34975320	The protein expression of GPR43, LC3II, p62, beclin1, low-density lipoprotein receptor (LDLR) and early growth response protein 1 (EGR1) in kidney tissues and podocytes was measured by real-time PCR, immunofluorescent staining and Western blotting.
3	34975320	An in vitro study further demonstrated that acetate treatment induced cholesterol accumulation in high glucose-stimulated podocytes, which was correlated with increased cholesterol uptake mediated by LDLR and reduced cholesterol autophagic degradation, as characterized by the inhibition of LC3 maturation, p62 degradation and autophagosome formation.
4	34975320	Furthermore, GPR43 activation increased extracellular regulated protein kinases 1/2 (ERK1/2) activity and EGR1 expression in podocytes, which resulted in an increase in cholesterol influx and autophagy inhibition.
5	34975320	Conclusion: GPR43 activation-mediated lipotoxicity contributes to podocyte injury in DN by modulating the ERK/EGR1 pathway.
6	34408785	Yiqi Huoxue Recipe Regulates Autophagy through Degradation of Advanced Glycation End Products via mTOR/S6K1/LC3 Pathway in Diabetic Nephropathy.
7	33901462	In the present study, compared to controls, DKD mice showed glomerular hypertrophy, increased kidney weight/weight ratio, and increased urinary protein levels, as well as decreased desmin and synaptopodin expression.
8	33901462	Further, a lower number of autophagosomes, reduced expression of MAP1LC3 (LC3) in glomeruli, and increased expression of JAK/STAT pathway-related proteins, namely JAK1, JAK2, STAT1, STAT3, STAT5, and STAT6, were observed in DKD mice.
9	33796024	Expressions of mitochondrial dynamics-related and autophagy-related proteins, such as Mfn2, Fis1, P62, and LC3, as well as Nrf2, Keap1, PINK1, and Parkin, were examined by immunohistochemistry, western blot, and real-time PCR, respectively.
10	33796024	Expressions of mitochondrial dynamics-related and autophagy-related proteins, such as Mfn2, Fis1, P62, and LC3, as well as Nrf2, Keap1, PINK1, and Parkin, were examined by immunohistochemistry, western blot, and real-time PCR, respectively.
11	33796024	AS II also partially restored the renal expression of mitochondrial dynamics-related and autophagy-related proteins, including Mfn2, Fis1, P62, and LC3.
12	33796024	AS II also partially restored the renal expression of mitochondrial dynamics-related and autophagy-related proteins, including Mfn2, Fis1, P62, and LC3.
13	33796024	These results suggested that AS II ameliorated podocyte injury and mitochondrial dysfunction in diabetic rats partly through regulation of Nrf2 and PINK1 pathway.
14	33796024	These results suggested that AS II ameliorated podocyte injury and mitochondrial dysfunction in diabetic rats partly through regulation of Nrf2 and PINK1 pathway.
15	33441223	[Down-regulation of PHLPP1 expression ameliorates high glucose-induced autophagy inhibition and apoptosis promotion of podocytes by activating PI3K/AKT/mTOR pathway].
16	33441223	Objective To investigate the expression of pleckstrin homology(PH) domain leucine-rich repeats protein phosphatase 1 (PHLPP1) in renal tissue of patients with diabetic nephropathy (DN) and its effect on podocyte autophagy and apoptosis, and to explore its related mechanism.
17	33441223	Methods Immunohistochemistry was used to detect PHLPP1 expression in renal tissue of patients with DN and non-diabetes, and immunofluorescence histochemical staining was used to detect the co-expression of nephrin and PHLPP1 to determine the localization of PHLPP1 in podocytes.
18	33441223	The formation of autophagic vesicles was observed by transmission electron microscope, and the protein expression levels of LC3, P62, PI3K, mTOR, p-mTOR, cleaved caspase 3 (c-caspase-3), AKT, p-AKT were detected by Western blotting.
19	33441223	Compared with NG group, the autophagy level of podocytes, the expression of PI3K and the phosphorylation level of mTOR in the HG group, HG combined with si-PHLPP1 group and HG combined with HCQ group were significantly reduced; the apoptosis rate and c-caspase-3 protein expression level were significantly enhanced; the phosphorylation level of AKT in the HG combined with si-PHLPP1 group significantly increased, but it in the other two groups significantly decreased.
20	33441223	Compared with HG group, the apoptosis rate and c-caspase-3 protein expression in the HG combined with si-PHLPP1 group were significantly reduced, while autophagy level, PI3K protein expression and phosphorylation level of mTOR and Akt protein were significantly elevated.
21	33441223	Conclusion PHLPP1 is highly expressed in renal tissue of patients with DN, and the down-regulated expression of PHLPP1 in podocytes can promote the autophagy of podocytes and reduced the apoptosis of podocytes by activating PI3K/AKT/mTOR pathway.
22	33204708	Curcumin Improves the Renal Autophagy in Rat Experimental Membranous Nephropathy via Regulating the PI3K/AKT/mTOR and Nrf2/HO-1 Signaling Pathways.
23	33204708	Western blot analyzed the levels of apoptosis, autophagy, PI3K/AKT/mTOR, and Nrf2/HO-1 pathway-associated proteins.
24	33204708	In addition, curcumin downregulated the expression of Bax, Caspase-3, p62, PI3K, p-AKT, and p-mTOR proteins and upregulated the Bcl-2, beclin1, LC3, Nrf2, and HO-1 levels in this animal model.
25	33204708	The results provide a scientific basis that curcumin could significantly alleviate the development of MN by inducing autophagy and alleviating renal oxidative stress through the PI3K/AKT/mTOR and Nrf2/HO-1 pathways.
26	32827692	HGF protected against diabetic nephropathy via autophagy-lysosome pathway in podocyte by modulating PI3K/Akt-GSK3β-TFEB axis.
27	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.
28	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.
29	32827692	These beneficial effects of HGF were blocked by HGF/c-Met inhibitor Crizotinib or phosphatidylinositide 3-kinases (PI3K) inhibitor LY294002.
30	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.
31	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.
32	32765784	Lycopene attenuates high glucose-mediated apoptosis in MPC5 podocytes by promoting autophagy via the PI3K/AKT signaling pathway.
33	32765784	To explore the effects of Lyc on the PI3K/AKT signaling pathway and autophagy, LY294002 (LY) and 3-methyladenine (3-MA) were used as PI3K and autophagy inhibitors, respectively.
34	32765784	The expression levels of nephrin, podocin, apoptosis-related proteins (Bax, Bcl-2 and cleaved caspase-3), autophagy-related proteins [Beclin-1 and microtubule associated protein 1 light chain 3 (LC3)II/LC3I] and certain key proteins involved in the PI3K/AKT signaling pathway were measured via western blotting.
35	32765784	The results suggested that Lyc reversed the inhibitory effect of HG on cell viability, and the protein expression levels of nephrin and podocin, as well as the promoting effect of HG on MPC5 podocyte apoptosis.
36	32765784	In addition, under HG conditions, Lyc upregulated the phosphorylation levels of PI3K and AKT, and reduced HG- and LY-mediated MPC5 podocyte apoptosis.
37	32765784	Therefore, the present study suggested that Lyc may protect against HG-induced MPC5 podocyte apoptosis by promoting autophagy activity via activation of the PI3K/AKT signaling pathway.
38	31978139	The microtubule-associated protein 1 light chain 3 (LC3)-positive area was co-localized with the Wilms tumor 1 (WT1)-positive area on immunofluorescence microscopy, which suggested that autophagy occurred in the podocytes of patients with MCNS.
39	31865844	Instead we present data showing that autophagy in podocytes is mainly controlled by AMP-activated protein kinase (AMPK) and ULK1 (unc-51 like kinase 1).
40	31865844	Abbreviations: AICAR: 5-aminoimidazole-4-carboxamide ribonucleotide; AMPK: AMP-activated protein kinase; ATG: autophagy related; BW: body weight; Cq: chloroquine; ER: endoplasmic reticulum; ESRD: end stage renal disease; FACS: fluorescence activated cell sorting; GFP: green fluorescent protein; i.p.: intra peritoneal; MAP1LC3/LC3: microtubule-associated protein 1 light chain 3; MTOR: mechanistic target of rapamycin kinase; NPHS1: nephrosis 1, nephrin; NPHS2: nephrosis 2, podocin; PLA: proximity-ligation assay; PRKAA: 5'-AMP-activated protein kinase catalytic subunit alpha; RPTOR/RAPTOR: regulatory associated protein of MTOR, complex 1; RFP: red fluorescent protein; TSC1: tuberous sclerosis 1; ULK1: unc-51 like kinase 1.
41	31741405	Furthermore, curcumin upregulated the expression of E-cadherin and LC3 proteins and downregulated the vimentin, TWIST1, p62, p-mTOR, p-Akt and P13K levels in DN rats and MPC5 cells.
42	31741405	Discussion and conclusions: The protection against development of DN by curcumin treatment involved changes in inducing autophagy and alleviating podocyte EMT, through the PI3k/Akt/mTOR pathway, providing the scientific basis for further research and clinical applications of curcumin.
43	31363726	CD68 expression was measured by immunohistochemistry analysis, and the expressions of IL-1β, IL-6, and MCP-1 mRNA were measured by qRT-PCR.
44	31363726	The results showed that CMP suppressed the expressions of CD68, IL-1β, IL-6, and MCP-1 mRNA induced by STZ.
45	31363726	The results showed that the administration of CMP was able to overcome the STZ-treated autophagy deficiency, significantly increase the rate of autophagy in the kidney, promote the expression of Atg5, beclin1 and LC3 protein, and reduce the expression of p62 protein.
46	30755075	Abbreviations: ALB: albumin; ARHGDIB: Rho GDP dissociation inhibitor beta; APOL1: apolipoprotein L1; ATG5: autophagy related 5; ATG7: autophagy related 7; ATG16L2: autophagy related 16 like 2; BECN1: beclin 1; CDKN1B: cyclin dependent kinase inhibitor 1B; CLEC16A, C-type lectin domain containing 16A; CYBB: cytochrome b-245 beta chain; DC: dendritic cell; DRAM1: DNA damage regulated autophagy modulator 1; eQTL: expression quantitative trait loci; GWAS: genome-wide association study; IFNA: interferon alpha; IRGM: immunity related GTPase M; LRRK2: leucine rich repeat kinase 2; MAP1LC3B: microtubule associated protein 1 light chain 3 beta; MTMR3: myotubularin related protein 3; LAP" LC3-associated phagocytosis; LN: lupus nephritis; NOD: non-obese diabetic; NPHS2: NPHS2, podocin; PBMC: peripheral blood mononuclear cell; RUBCN: rubicon autophagy regulator; SLE: systemic lupus erythematosus.
47	30283057	Activation of autophagy by c-kit⁺ progenitor/stem cells also contributed to kidney regeneration and intracellular homeostasis (autophagosomes and autophagolysosomes number and LC3A/B-I and LC3A/B-II expression were higher in the c-kit group vs saline treated animals, P = 0.0031 and P = 0.0009, respectively).
48	30221708	Multiple methods were utilized to detect autophagic activity including western blot analysis to measure the levels of microtubule‑associated protein 1 light chain 3 (LC3) II and beclin1, reverse transcription‑quantitative polymerase chain reaction was performed to evaluate the levels of LC3 mRNA and transmission electron microscopy was conducted to observe autophagosomes.
49	30210600	The expression and distribution of microtubule-associated proteins 1A/1B light chain 3B (LC3), LC3-I, LC3-II, beclin-1, PI3K and mTOR were determined using immunohistochemistry and western blotting.
50	30210600	The expression and distribution of microtubule-associated proteins 1A/1B light chain 3B (LC3), LC3-I, LC3-II, beclin-1, PI3K and mTOR were determined using immunohistochemistry and western blotting.
51	30210600	The number of autophagosomes was significantly decreased and the expression of beclin-1, LC3, LC3-I and LC3-II was inhibited following MHCD treatment compared with the model group (P<0.05).
52	30210600	The number of autophagosomes was significantly decreased and the expression of beclin-1, LC3, LC3-I and LC3-II was inhibited following MHCD treatment compared with the model group (P<0.05).
53	30186468	After 24 h of treatment, MPC5 cells were collected to measure autophagy-related protein levels, including microtubule-associated protein light chain 3 (LC3), p62, cluster of differentiation (CD)63, phosphorylated-protein kinase B (Akt), Akt, p-mammalian target of rapamycin (mTOR), and mTOR, via western blotting, immunofluorescence or both, and to determine apoptosis by flow cytometry.
54	29999001	Genistein is derived from a leguminous plant, and MyD88 and TRIF are adaptor molecules in the Toll-like receptor (TLR) signaling pathway, which may play a role in autophagy.
55	29999001	In this study, we utilized an in vitro high glucose (HG)-treated podocyte model to investigate the effects and underlying mechanisms of Genistein and MyD88 or TRIF siRNA induced autophagy and renal protection.
56	29999001	MATERIAL AND METHODS An immortalized mouse podocyte cell line was treated with HG, Genistein, chloroquine, and/or transfected with specific Myd88 and TRIF siRNAs.
57	29999001	The expression of autophagy-related factors and podocyte structure and functional markers, including LC3, p62, p-mTOR, synaptopodin, and nephrin, were measured by Western blot, and LC3 and p-mTOR expression were also assessed by immunofluorescence.
58	29070572	Fasting blood glucose and insulin and the expression of podocin, nephrin, phosphoinositide 3-kinase (PI3K), glucose transporter type (Glut4), and microtubule-associated protein 1A/1B-light chain 3 (LC3) were assayed.
59	29070572	The decreased translocation of Glut4 to the plasma membrane and excess autophagy seen in mice fed a high-fat diet and in PA-treated cultured podocytes were attenuated by GLP-1.
60	29070572	GLP-1 restored insulin sensitivity and ameliorated renal injury by decreasing the level of autophagy.
61	28428258	Levels of microtubule-associated protein 1A/1B-light chain 3 (LC3)-II expression and c-Jun N-terminal kinase-1 phosphorylation were decreased in IRE1α-deletion glomeruli, in keeping with reduced autophagy.
62	27077005	Autophagy related proteins LC3, Beclin, and p62 as well as nephrin, a podocyte injury marker, were assessed using western blot and immunofluorescence staining.
63	25412249	Autophagy was investigated by immunofluorescence staining for LC3 puncta and Western blotting for LC3, Atg5, p-AMPK, p-mTOR and its substrates.
64	24238063	Treatment with the mTOR inhibitor, rapamycin, increased LC3-II and the content of both APs detected by Cyto-ID Green staining and autophagolysosomes (APLs) measured by acridine orange staining and colocalization of LC3 and Lamp1.