Ignet

Gene Information

Gene symbol: KHDRBS1

Gene name: KH domain containing, RNA binding, signal transduction associated 1

HGNC ID: 18116

Synonyms: Sam68, p62, FLJ34027

Related Genes

#	Gene Symbol	Number of hits
1	AKT1	1 hits
2	ATG5	1 hits
3	ATG7	1 hits
4	BAX	1 hits
5	BCL2	1 hits
6	BECN1	1 hits
7	CASP3	1 hits
8	FIS1	1 hits
9	GJA1	1 hits
10	GPR137B	1 hits
11	HMOX1	1 hits
12	KEAP1	1 hits
13	MAP1LC3A	1 hits
14	MATN1	1 hits
15	MFN2	1 hits
16	NFE2L2	1 hits
17	NPHS1	1 hits
18	PIK3CA	1 hits
19	PINK1	1 hits
20	PVRL1	1 hits
21	RORC	1 hits
22	SQSTM1	1 hits
23	SYNPO	1 hits

Related Sentences

#	PMID	Sentence
1	26081285	Previously, we reported that high glucose induced podocyte injury through upregulation of the (pro)renin receptor (PRR).
2	26081285	We hypothesized that increasing PRR reduces autophagy and increases apoptosis of mouse podocytes exposed to high glucose via activation of the PI3K/Akt/mTOR signaling pathway.
3	26081285	High glucose significantly increased mRNA and protein levels of PRR, phosphorylation of PI3K/Akt/mTOR, and p62.
4	26081285	In the absence of PRR, activation of Akt with sc-79 or mTOR with MHY-1485 increased p62 accumulation.
5	26081285	Based on these data, we conclude that high glucose decreases autophagy and increases apoptosis in mouse podocytes through the PRR/PI3K/Akt/mTOR signaling pathway.
6	26764202	Autophagy was evaluated by measuring the expressions of light chain 3, p62, beclin-1, and autophagy-related gene 5.
7	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.
8	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.
9	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.
10	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.
11	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.
12	31116585	We hypothesized that a functional apolipoprotein LI (APOL1)-miR193a axis (inverse relationship) preserves, but disruption alters, the podocyte molecular phenotype through the modulation of autophagy flux.
13	31116585	G0-, G1-, and G2-podocytes showed enhanced expression of light chain (LC) 3-II and beclin-1, but a disparate expression of p62 (low in wild-type but high in risk alleles).
14	31116585	Docking, protein-protein interaction, and immunoprecipitation studies with antiautophagy-related gene (ATG)14L, anti-UV radiation resistance-associated gene (UVRAG), or Rubicon antibodies suggested the formation of ATG14L complex I and UVRAG complex II in G0-podocytes and the formation of Rubicon complex III in G1- and G2-podocytes.
15	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.
16	31363726	The results showed that CMP suppressed the expressions of CD68, IL-1β, IL-6, and MCP-1 mRNA induced by STZ.
17	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.
18	31485651	Sam68 mediates high glucose‑induced podocyte apoptosis through modulation of Bax/Bcl‑2.
19	31485651	Furthermore, HG increased Bax and decreased Bcl‑2 protein expression in cultured podocytes, and this effect was blocked by Sam68 knockdown.
20	31485651	The results of the present study revealed that Sam68 mediated HG‑induced podocyte apoptosis, probably through the Bax/Bcl‑2 signaling pathway, and thus may be a potential therapeutic target for DN.
21	31485651	Sam68 mediates high glucose‑induced podocyte apoptosis through modulation of Bax/Bcl‑2.
22	31485651	Furthermore, HG increased Bax and decreased Bcl‑2 protein expression in cultured podocytes, and this effect was blocked by Sam68 knockdown.
23	31485651	The results of the present study revealed that Sam68 mediated HG‑induced podocyte apoptosis, probably through the Bax/Bcl‑2 signaling pathway, and thus may be a potential therapeutic target for DN.
24	31485651	Sam68 mediates high glucose‑induced podocyte apoptosis through modulation of Bax/Bcl‑2.
25	31485651	Furthermore, HG increased Bax and decreased Bcl‑2 protein expression in cultured podocytes, and this effect was blocked by Sam68 knockdown.
26	31485651	The results of the present study revealed that Sam68 mediated HG‑induced podocyte apoptosis, probably through the Bax/Bcl‑2 signaling pathway, and thus may be a potential therapeutic target for DN.
27	31545399	We observed that HG induced podocyte injury, accompanied by increases in Cx43 expression and impaired autophagic flux, as evidenced by the accumulation of LC3II/LC3I and p62.
28	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).
29	32482387	Moreover, inhibition of TM7SF1 expression did not increase the mRNA level of SQSTM1/P62.
30	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.
31	33204708	Curcumin Improves the Renal Autophagy in Rat Experimental Membranous Nephropathy via Regulating the PI3K/AKT/mTOR and Nrf2/HO-1 Signaling Pathways.
32	33204708	Western blot analyzed the levels of apoptosis, autophagy, PI3K/AKT/mTOR, and Nrf2/HO-1 pathway-associated proteins.
33	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.
34	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.
35	33441223	[Down-regulation of PHLPP1 expression ameliorates high glucose-induced autophagy inhibition and apoptosis promotion of podocytes by activating PI3K/AKT/mTOR pathway].
36	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.
37	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.
38	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.
39	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.
40	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.
41	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.
42	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.
43	33796024	AS II also partially restored the renal expression of mitochondrial dynamics-related and autophagy-related proteins, including Mfn2, Fis1, P62, and LC3.
44	33796024	These results suggested that AS II ameliorated podocyte injury and mitochondrial dysfunction in diabetic rats partly through regulation of Nrf2 and PINK1 pathway.
45	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.
46	33796024	AS II also partially restored the renal expression of mitochondrial dynamics-related and autophagy-related proteins, including Mfn2, Fis1, P62, and LC3.
47	33796024	These results suggested that AS II ameliorated podocyte injury and mitochondrial dysfunction in diabetic rats partly through regulation of Nrf2 and PINK1 pathway.
48	34253875	We showed that wogonin (4, 8, 16 μM) dose-dependently alleviated high glucose (HG)-induced MPC5 cell damage, accompanied by increased expression of WT-1, nephrin, and podocin proteins, and decreased expression of TNF-α, MCP-1, IL-1β as well as phosphorylated p65.
49	34253875	Wogonin reversed HG-suppressed autophagy in MPC5 cells, evidenced by increased ATG7, LC3-II, and Beclin-1 protein, and decreased p62 protein.