Ignet

Gene Information

Gene symbol: PPP2R4

Gene name: protein phosphatase 2A activator, regulatory subunit 4

HGNC ID: 9308

Synonyms: PTPA, PR53

Related Genes

#	Gene Symbol	Number of hits
1	AKT1	1 hits
2	AQP2	1 hits
3	BAX	1 hits
4	BCL2	1 hits
5	CRTC1	1 hits
6	DES	1 hits
7	FOXO1	1 hits
8	INS	1 hits
9	ITK	1 hits
10	MAP4	1 hits
11	MAPK1	1 hits
12	NPHS1	1 hits
13	PPP5C	1 hits
14	RCA1	1 hits
15	SIRT1	1 hits
16	TP53	1 hits
17	VIM	1 hits

Related Sentences

#	PMID	Sentence
1	34629746	Expressions of podocytes injury-, apoptosis- and epithelial-to-mesenchymal transition (EMT)- and JNK-interacting protein 4/p38-Mitogen-Activated Protein Kinase (JIP4/p38-MAPK) pathway-related factors were measured using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot as needed.
2	34629746	Expressions of podocytes injury-, apoptosis- and epithelial-to-mesenchymal transition (EMT)- and JNK-interacting protein 4/p38-Mitogen-Activated Protein Kinase (JIP4/p38-MAPK) pathway-related factors were measured using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot as needed.
3	34629746	Expressions of podocytes injury-, apoptosis- and epithelial-to-mesenchymal transition (EMT)- and JNK-interacting protein 4/p38-Mitogen-Activated Protein Kinase (JIP4/p38-MAPK) pathway-related factors were measured using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot as needed.
4	34629746	Expressions of podocytes injury-, apoptosis- and epithelial-to-mesenchymal transition (EMT)- and JNK-interacting protein 4/p38-Mitogen-Activated Protein Kinase (JIP4/p38-MAPK) pathway-related factors were measured using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot as needed.
5	34629746	Interaction between PP2A and JIP4/MAPK pathway was confirmed using co-immunoprecipitation (Co-Ip) assay.
6	34629746	Interaction between PP2A and JIP4/MAPK pathway was confirmed using co-immunoprecipitation (Co-Ip) assay.
7	34629746	Interaction between PP2A and JIP4/MAPK pathway was confirmed using co-immunoprecipitation (Co-Ip) assay.
8	34629746	Interaction between PP2A and JIP4/MAPK pathway was confirmed using co-immunoprecipitation (Co-Ip) assay.
9	34629746	In podocytes, ADR inhibited PP2A, Nephrin and Wilms' tumor (WT) 1 expressions yet upregulated apoptosis and Desmin expression, and suppressing PP2A expressionenhanced the effects.
10	34629746	In podocytes, ADR inhibited PP2A, Nephrin and Wilms' tumor (WT) 1 expressions yet upregulated apoptosis and Desmin expression, and suppressing PP2A expressionenhanced the effects.
11	34629746	In podocytes, ADR inhibited PP2A, Nephrin and Wilms' tumor (WT) 1 expressions yet upregulated apoptosis and Desmin expression, and suppressing PP2A expressionenhanced the effects.
12	34629746	In podocytes, ADR inhibited PP2A, Nephrin and Wilms' tumor (WT) 1 expressions yet upregulated apoptosis and Desmin expression, and suppressing PP2A expressionenhanced the effects.
13	34629746	Additionally, in ADR-treated podocytes, PP2A suppression enhanced the effects of ADR, yet silencing of JIP4 reversed the effects of PP2A suppression on regulating p38-MAPK pathway-, apoptosis- and EMT-related factors expressions and apoptosis, with upregulations of B-cell lymphoma-2 (Bcl-2) and E-cadherin and down-regulations of Bcl-2 associated protein X (Bax), cleaved (C)-casapse-3, N-cadherin, Vimentin and Snail.
14	34629746	Additionally, in ADR-treated podocytes, PP2A suppression enhanced the effects of ADR, yet silencing of JIP4 reversed the effects of PP2A suppression on regulating p38-MAPK pathway-, apoptosis- and EMT-related factors expressions and apoptosis, with upregulations of B-cell lymphoma-2 (Bcl-2) and E-cadherin and down-regulations of Bcl-2 associated protein X (Bax), cleaved (C)-casapse-3, N-cadherin, Vimentin and Snail.
15	34629746	Additionally, in ADR-treated podocytes, PP2A suppression enhanced the effects of ADR, yet silencing of JIP4 reversed the effects of PP2A suppression on regulating p38-MAPK pathway-, apoptosis- and EMT-related factors expressions and apoptosis, with upregulations of B-cell lymphoma-2 (Bcl-2) and E-cadherin and down-regulations of Bcl-2 associated protein X (Bax), cleaved (C)-casapse-3, N-cadherin, Vimentin and Snail.
16	34629746	Additionally, in ADR-treated podocytes, PP2A suppression enhanced the effects of ADR, yet silencing of JIP4 reversed the effects of PP2A suppression on regulating p38-MAPK pathway-, apoptosis- and EMT-related factors expressions and apoptosis, with upregulations of B-cell lymphoma-2 (Bcl-2) and E-cadherin and down-regulations of Bcl-2 associated protein X (Bax), cleaved (C)-casapse-3, N-cadherin, Vimentin and Snail.
17	34629746	PP2A protects ADR-treated podocytes against injury and EMT by suppressing JIP4/p38-MAPK pathway, showing their interaction in podocytes.
18	34629746	PP2A protects ADR-treated podocytes against injury and EMT by suppressing JIP4/p38-MAPK pathway, showing their interaction in podocytes.
19	34629746	PP2A protects ADR-treated podocytes against injury and EMT by suppressing JIP4/p38-MAPK pathway, showing their interaction in podocytes.
20	34629746	PP2A protects ADR-treated podocytes against injury and EMT by suppressing JIP4/p38-MAPK pathway, showing their interaction in podocytes.
21	34539832	Protein phosphatase 2A (PP2A), which is involved in renal development and the function of ion-transport proteins, aquaporin-2 and podocytes, is likely to serve an important role in renal processes.
22	34539832	Protein phosphatase 2A (PP2A), which is involved in renal development and the function of ion-transport proteins, aquaporin-2 and podocytes, is likely to serve an important role in renal processes.
23	34539832	How dysregulation of PP2A in the kidneys causes podocyte death and the inactivation of PP2A in renal carcinoma tissues is discussed.
24	34539832	How dysregulation of PP2A in the kidneys causes podocyte death and the inactivation of PP2A in renal carcinoma tissues is discussed.
25	25724269	Independent role of PP2A and mTORc1 in palmitate induced podocyte death.
26	25724269	Independent role of PP2A and mTORc1 in palmitate induced podocyte death.
27	25724269	Independent role of PP2A and mTORc1 in palmitate induced podocyte death.
28	25724269	Independent role of PP2A and mTORc1 in palmitate induced podocyte death.
29	25724269	Independent role of PP2A and mTORc1 in palmitate induced podocyte death.
30	25724269	This impairment in insulin signalling prevents insulin induced SIRT 1 expression and deacetylation of p53.
31	25724269	This impairment in insulin signalling prevents insulin induced SIRT 1 expression and deacetylation of p53.
32	25724269	This impairment in insulin signalling prevents insulin induced SIRT 1 expression and deacetylation of p53.
33	25724269	This impairment in insulin signalling prevents insulin induced SIRT 1 expression and deacetylation of p53.
34	25724269	This impairment in insulin signalling prevents insulin induced SIRT 1 expression and deacetylation of p53.
35	25724269	Further, palmitate treatment prevents insulin induced phosphorylation of PP2A and FOXO1 but it potentiates the phosphorylation of mTOR at Ser 2448.
36	25724269	Further, palmitate treatment prevents insulin induced phosphorylation of PP2A and FOXO1 but it potentiates the phosphorylation of mTOR at Ser 2448.
37	25724269	Further, palmitate treatment prevents insulin induced phosphorylation of PP2A and FOXO1 but it potentiates the phosphorylation of mTOR at Ser 2448.
38	25724269	Further, palmitate treatment prevents insulin induced phosphorylation of PP2A and FOXO1 but it potentiates the phosphorylation of mTOR at Ser 2448.
39	25724269	Further, palmitate treatment prevents insulin induced phosphorylation of PP2A and FOXO1 but it potentiates the phosphorylation of mTOR at Ser 2448.
40	25724269	Interestingly, selective inhibition of PP2A, by Okadaic acid at 5 nM, restored insulin induced phosphorylation of AKT, FOXO1, SIRT1 activity and p53 degradation.
41	25724269	Interestingly, selective inhibition of PP2A, by Okadaic acid at 5 nM, restored insulin induced phosphorylation of AKT, FOXO1, SIRT1 activity and p53 degradation.
42	25724269	Interestingly, selective inhibition of PP2A, by Okadaic acid at 5 nM, restored insulin induced phosphorylation of AKT, FOXO1, SIRT1 activity and p53 degradation.
43	25724269	Interestingly, selective inhibition of PP2A, by Okadaic acid at 5 nM, restored insulin induced phosphorylation of AKT, FOXO1, SIRT1 activity and p53 degradation.
44	25724269	Interestingly, selective inhibition of PP2A, by Okadaic acid at 5 nM, restored insulin induced phosphorylation of AKT, FOXO1, SIRT1 activity and p53 degradation.
45	25724269	On the other hand, partial inhibition of mTORc1, by low dose of Rapamycin (1 nM) also restored phosphorylation of AKT and SIRT1 activity, whereas no significant changes were observed in insulin induced phosphorylation of PP2A after mTORc1 inhibition.
46	25724269	On the other hand, partial inhibition of mTORc1, by low dose of Rapamycin (1 nM) also restored phosphorylation of AKT and SIRT1 activity, whereas no significant changes were observed in insulin induced phosphorylation of PP2A after mTORc1 inhibition.
47	25724269	On the other hand, partial inhibition of mTORc1, by low dose of Rapamycin (1 nM) also restored phosphorylation of AKT and SIRT1 activity, whereas no significant changes were observed in insulin induced phosphorylation of PP2A after mTORc1 inhibition.
48	25724269	On the other hand, partial inhibition of mTORc1, by low dose of Rapamycin (1 nM) also restored phosphorylation of AKT and SIRT1 activity, whereas no significant changes were observed in insulin induced phosphorylation of PP2A after mTORc1 inhibition.
49	25724269	On the other hand, partial inhibition of mTORc1, by low dose of Rapamycin (1 nM) also restored phosphorylation of AKT and SIRT1 activity, whereas no significant changes were observed in insulin induced phosphorylation of PP2A after mTORc1 inhibition.
50	25724269	To the best of our knowledge this is the first report suggesting independent role of PP2A and mTORc1 in palmitate induced IR and associated podocyte death.
51	25724269	To the best of our knowledge this is the first report suggesting independent role of PP2A and mTORc1 in palmitate induced IR and associated podocyte death.
52	25724269	To the best of our knowledge this is the first report suggesting independent role of PP2A and mTORc1 in palmitate induced IR and associated podocyte death.
53	25724269	To the best of our knowledge this is the first report suggesting independent role of PP2A and mTORc1 in palmitate induced IR and associated podocyte death.
54	25724269	To the best of our knowledge this is the first report suggesting independent role of PP2A and mTORc1 in palmitate induced IR and associated podocyte death.
55	25724269	Therefore, the best therapeutic approach for treatment of diabetic kidney disease should involve manipulating phosphorylation of both PP2A and mTORc1.
56	25724269	Therefore, the best therapeutic approach for treatment of diabetic kidney disease should involve manipulating phosphorylation of both PP2A and mTORc1.
57	25724269	Therefore, the best therapeutic approach for treatment of diabetic kidney disease should involve manipulating phosphorylation of both PP2A and mTORc1.
58	25724269	Therefore, the best therapeutic approach for treatment of diabetic kidney disease should involve manipulating phosphorylation of both PP2A and mTORc1.
59	25724269	Therefore, the best therapeutic approach for treatment of diabetic kidney disease should involve manipulating phosphorylation of both PP2A and mTORc1.
60	12012387	There has been an accumulation of data showing common cell biological features of the podocyte and the neuron: 1) Both cells possess long and short cell processes equipped with highly organized cytoskeletal systems; 2) Both show cytoskeletal segregation; microtubules (MTs) and intermediate filaments (IFs) in podocyte primary processes and in neurites, while actin filaments (AFs) are abundant in podocyte foot processes in neuronal synaptic regions; 3) In both cells, process formation is mechanically dependent on MTs, whose assembly is regulated by various microtubule- associated proteins (MAPs); 4) In both cells, process formation is positively regulated by PP2A, a Ser/Thr protein phosphatase; 5) In both cells, process formation is accelerated by laminin, an extracellular matrix protein.
61	12012387	In addition, recent data from our and other laboratories have shown that podocyte processes share many features with neuronal dendrites: 1) Podocyte processes and neuronal dendrites possess MTs with mixed polarity, namely, plus-end-distal and minus-end-distal MTs coexist in these processes; 2) To establish the mixed polarity of MTs, both express CHO1/MKLP1, a kinesin-related motor protein, and when its expression is inhibited formation of both podocyte processes and neuronal dendrites is abolished; 3) The elongation of both podocyte processes and neuronal dendrites is supported by rab8-regulated basolateral-type membrane transport; 4) Both podocyte processes and neuronal dendrites express synaptopodin, an actin-associated protein, in a development-dependent manner; interestingly, in both cells, synaptopodin is localized not in the main shaft of processes but in thin short projections from the main shaft.
62	11326753	Process formation of podocytes: morphogenetic activity of microtubules and regulation by protein serine/threonine phosphatase PP2A.
63	11326753	Process formation of podocytes: morphogenetic activity of microtubules and regulation by protein serine/threonine phosphatase PP2A.
64	11326753	Suppression of MT elongation by nanomolar vinblastine or inhibition of serine/threonine phosphatase PP2A with okadaic acid abolished process formation.
65	11326753	Suppression of MT elongation by nanomolar vinblastine or inhibition of serine/threonine phosphatase PP2A with okadaic acid abolished process formation.