Ignet

Gene Information

Gene symbol: PLCE1

Gene name: phospholipase C, epsilon 1

HGNC ID: 17175

Synonyms: KIAA1516, PLCE, NPHS3

Related Genes

#	Gene Symbol	Number of hits
1	ACTN4	1 hits
2	ACTR2	1 hits
3	AGT	1 hits
4	ARFRP1	1 hits
5	AVIL	1 hits
6	BRAF	1 hits
7	CD2	1 hits
8	CD2AP	1 hits
9	CDC42	1 hits
10	CDKN1A	1 hits
11	DAG1	1 hits
12	DDN	1 hits
13	EGF	1 hits
14	EHD3	1 hits
15	IQGAP1	1 hits
16	LMX1B	1 hits
17	MAGI1	1 hits
18	MYH9	1 hits
19	NCK2	1 hits
20	NES	1 hits
21	NPHS1	1 hits
22	NPHS2	1 hits
23	PDPN	1 hits
24	PLA2R1	1 hits
25	PLCB1	1 hits
26	PLCG1	1 hits
27	PLCL1	1 hits
28	PODXL	1 hits
29	PTPRO	1 hits
30	RAC1	1 hits
31	RHOA	1 hits
32	RHOD	1 hits
33	SYNPO	1 hits
34	TCF21	1 hits
35	TJP1	1 hits
36	TRPA1	1 hits
37	TRPC6	1 hits
38	WT1	1 hits

Related Sentences

#	PMID	Sentence
1	17086182	Using positional cloning, we identified mutations in the phospholipase C epsilon gene (PLCE1) as causing early-onset nephrotic syndrome with end-stage kidney disease.
2	17530296	Renin-angiotensin axis blockade reduces proteinuria in presymptomatic patients with familial FSGS.
3	17530296	Familial and genetic forms of focal segmental glomerulosclerosis (FSGS) are associated with six different mutations in genes affecting the podocyte (NPHS2, ACTN4, CD2AP, WT1, TRPC6, and PLCE1).
4	17530296	We describe three children from two different families with familial FSGS in whom partial to complete remission of proteinuria was attained through early blockade of the renin-angiotensin axis.
5	17530296	We speculate that presymptomatic patients with normal renal function who have genetic or familial FSGS may benefit from early blockade of the renin-angiotensin axis and that this may also prevent progressive renal disease.
6	17942568	Recently, we identified recessive mutations in the phospholipase C epsilon 1 gene (PLCE1) as a new cause of early-onset nephrotic syndrome and demonstrated interaction of PLCepsilon1 with IQGAP1.
7	17942568	It relates the PLCE1 ortholog (plc-1) to the C. elegans ortholog (lin-45) of human BRAF (v-raf murine sarcoma viral oncogene homolog B1).
8	17942568	Recently, we identified recessive mutations in the phospholipase C epsilon 1 gene (PLCE1) as a new cause of early-onset nephrotic syndrome and demonstrated interaction of PLCepsilon1 with IQGAP1.
9	17942568	It relates the PLCE1 ortholog (plc-1) to the C. elegans ortholog (lin-45) of human BRAF (v-raf murine sarcoma viral oncogene homolog B1).
10	18364721	Candidate genes so far identified in renal disease include those encoding the podocyte proteins nephrin and podocin, the transcription factor WT1, the calcium channel TRPC6 and the enzyme phospholipase C-epsilon-1 (in congenital nephrotic syndrome and focal segmental glomerulosclerosis), and carnosinase (in diabetic nephropathy).
11	19956976	Analysis of recessive CD2AP and ACTN4 mutations in steroid-resistant nephrotic syndrome.
12	19956976	Based on the phenotype of Actn4 and Cd2ap null mice, we aimed to define the role of recessive CD2AP and ACTN4 mutations in a cohort of children with SRNS for which NPHS1, NPHS2, and PLCE1 mutations had been previously excluded.
13	19956976	CD2AP and ACTN4 mutational analysis was performed in 42 children from 35 unrelated families.
14	19956976	Recessive CD2AP and ACTN4 mutations are rare in children with SRNS.
15	20634963	CDKN1, DAG1, DDN, EHD3, MYH9, NES, NPHS1, NPHS2, PDPN, PLA2R1, PLCE1, PODXL, PTPRO, SYNPO, TCF21, TJP1, WT1).
16	20634963	This finding was further validated by assessing the expression of the axon guidance molecules neuritin (NRN1) and roundabout receptor ROBO1 and -2.
17	22693670	The close relationships of slit diaphragm (SD) molecules such as nephrin, podocin, CD2-associated protein (CD2AP), a-actinin-4, transient receptor potential cation channel 6 (TRPC6), Densin and membrane-associated guanylate kinase inverted 1 (MAGI-1), α3β1 integrin, WT1, phospholipase C epsilon-1 (PLCE1), Lmx1b, and MYH9, and mitochondrial disorders and circulating factors in the pathogenesis of glomerular proteinuria were also gradually discovered.
18	27885584	WT1 and NPHS2 gene mutation analysis and clinical management of steroid-resistant nephrotic syndrome.
19	27885584	Non-responsiveness of these children would be a risk with the possibility of mutational changes in podocyte genes (NPHS1, NPHS2, WT1, PLCE1).
20	27885584	NPHS1, NPHS2, and WT1 genes are identified/directly linked to SRNS.
21	27885584	The present study is a surveillance on the mutation analysis of WT1 (exons 8 and 9) and NPHS2 (exons 1-8) gene in SRNS followed by clinical management.
22	29058690	Advillin acts upstream of phospholipase C ϵ1 in steroid-resistant nephrotic syndrome.
23	29058690	Additionally, AVIL colocalized and interacted with the phospholipase enzyme PLCE1 and with the ARP2/3 actin-modulating complex.
24	29058690	Knockdown of AVIL in human podocytes reduced actin stress fibers at the cell periphery, prevented recruitment of PLCE1 to the ARP3-rich lamellipodia, blocked EGF-induced generation of diacylglycerol (DAG) by PLCE1, and attenuated the podocyte migration rate (PMR).
25	29058690	The PMR was increased by overexpression of WT Avil or PLCE1, or by EGF stimulation; however, this increased PMR was ameliorated by inhibition of the ARP2/3 complex, indicating that ARP-dependent lamellipodia formation occurs downstream of AVIL and PLCE1 function.
26	29058690	Together, these results delineate a comprehensive pathogenic axis of SRNS that integrates loss of AVIL function with alterations in the action of PLCE1, an established SRNS protein.
27	29058690	Advillin acts upstream of phospholipase C ϵ1 in steroid-resistant nephrotic syndrome.
28	29058690	Additionally, AVIL colocalized and interacted with the phospholipase enzyme PLCE1 and with the ARP2/3 actin-modulating complex.
29	29058690	Knockdown of AVIL in human podocytes reduced actin stress fibers at the cell periphery, prevented recruitment of PLCE1 to the ARP3-rich lamellipodia, blocked EGF-induced generation of diacylglycerol (DAG) by PLCE1, and attenuated the podocyte migration rate (PMR).
30	29058690	The PMR was increased by overexpression of WT Avil or PLCE1, or by EGF stimulation; however, this increased PMR was ameliorated by inhibition of the ARP2/3 complex, indicating that ARP-dependent lamellipodia formation occurs downstream of AVIL and PLCE1 function.
31	29058690	Together, these results delineate a comprehensive pathogenic axis of SRNS that integrates loss of AVIL function with alterations in the action of PLCE1, an established SRNS protein.
32	29058690	Advillin acts upstream of phospholipase C ϵ1 in steroid-resistant nephrotic syndrome.
33	29058690	Additionally, AVIL colocalized and interacted with the phospholipase enzyme PLCE1 and with the ARP2/3 actin-modulating complex.
34	29058690	Knockdown of AVIL in human podocytes reduced actin stress fibers at the cell periphery, prevented recruitment of PLCE1 to the ARP3-rich lamellipodia, blocked EGF-induced generation of diacylglycerol (DAG) by PLCE1, and attenuated the podocyte migration rate (PMR).
35	29058690	The PMR was increased by overexpression of WT Avil or PLCE1, or by EGF stimulation; however, this increased PMR was ameliorated by inhibition of the ARP2/3 complex, indicating that ARP-dependent lamellipodia formation occurs downstream of AVIL and PLCE1 function.
36	29058690	Together, these results delineate a comprehensive pathogenic axis of SRNS that integrates loss of AVIL function with alterations in the action of PLCE1, an established SRNS protein.
37	29058690	Advillin acts upstream of phospholipase C ϵ1 in steroid-resistant nephrotic syndrome.
38	29058690	Additionally, AVIL colocalized and interacted with the phospholipase enzyme PLCE1 and with the ARP2/3 actin-modulating complex.
39	29058690	Knockdown of AVIL in human podocytes reduced actin stress fibers at the cell periphery, prevented recruitment of PLCE1 to the ARP3-rich lamellipodia, blocked EGF-induced generation of diacylglycerol (DAG) by PLCE1, and attenuated the podocyte migration rate (PMR).
40	29058690	The PMR was increased by overexpression of WT Avil or PLCE1, or by EGF stimulation; however, this increased PMR was ameliorated by inhibition of the ARP2/3 complex, indicating that ARP-dependent lamellipodia formation occurs downstream of AVIL and PLCE1 function.
41	29058690	Together, these results delineate a comprehensive pathogenic axis of SRNS that integrates loss of AVIL function with alterations in the action of PLCE1, an established SRNS protein.
42	32223311	Loss-of-function mutations in phospholipase C-ε1 (PLCE1) have been detected in patients with nephrotic syndrome, but other family members with the same mutation were asymptomatic, suggesting additional stressor are required to cause the full phenotype.
43	32223311	Therefore, we tested whether ANG II enhances glomerular damage in Plce1-deficient mice.
44	32223311	ANG II increased blood pressure equally in Plce1-deficient and wild-type littermates.
45	32223311	Loss-of-function mutations in phospholipase C-ε1 (PLCE1) have been detected in patients with nephrotic syndrome, but other family members with the same mutation were asymptomatic, suggesting additional stressor are required to cause the full phenotype.
46	32223311	Therefore, we tested whether ANG II enhances glomerular damage in Plce1-deficient mice.
47	32223311	ANG II increased blood pressure equally in Plce1-deficient and wild-type littermates.
48	32223311	Loss-of-function mutations in phospholipase C-ε1 (PLCE1) have been detected in patients with nephrotic syndrome, but other family members with the same mutation were asymptomatic, suggesting additional stressor are required to cause the full phenotype.
49	32223311	Therefore, we tested whether ANG II enhances glomerular damage in Plce1-deficient mice.
50	32223311	ANG II increased blood pressure equally in Plce1-deficient and wild-type littermates.
51	32238860	PLCE1 encodes phospholipase C epsilon, and its mutations cause recessive nephrotic syndrome.
52	32238860	PLCE1 colocalized with Rho GTPases in glomeruli.
53	32238860	Knockdown or knockout of PLCE1 in podocytes resulted in decreased levels of GTP-bound Rac1 and Cdc42, but not those of RhoA, and caused a reduction in cell migration.
54	32238860	Similar to the PLCE1 knockout, NCK2 knockout resulted in decreased podocyte migration.
55	32238860	Knockout of PLCE1 reduced the EGF-induced activation of ERK and cell proliferation in podocytes, whereas knockout of NCK2 did not affect proliferation.
56	32238860	Further, the knockout of PLCE1 also resulted in decreased expression of podocyte markers, including NEPH1, NPHS1, WT1, and SYNPO, upon differentiation, but the knockout of NCK2 did not affect the expression of these markers.
57	32238860	Therefore, our findings demonstrate that PLCE1 regulates Rho GTPase activity and cell migration through interacting with NCK2 and that PLCE1 also plays a role in the proliferation and differentiation of podocytes, regardless of the presence of NCK2.
58	32238860	PLCE1 encodes phospholipase C epsilon, and its mutations cause recessive nephrotic syndrome.
59	32238860	PLCE1 colocalized with Rho GTPases in glomeruli.
60	32238860	Knockdown or knockout of PLCE1 in podocytes resulted in decreased levels of GTP-bound Rac1 and Cdc42, but not those of RhoA, and caused a reduction in cell migration.
61	32238860	Similar to the PLCE1 knockout, NCK2 knockout resulted in decreased podocyte migration.
62	32238860	Knockout of PLCE1 reduced the EGF-induced activation of ERK and cell proliferation in podocytes, whereas knockout of NCK2 did not affect proliferation.
63	32238860	Further, the knockout of PLCE1 also resulted in decreased expression of podocyte markers, including NEPH1, NPHS1, WT1, and SYNPO, upon differentiation, but the knockout of NCK2 did not affect the expression of these markers.
64	32238860	Therefore, our findings demonstrate that PLCE1 regulates Rho GTPase activity and cell migration through interacting with NCK2 and that PLCE1 also plays a role in the proliferation and differentiation of podocytes, regardless of the presence of NCK2.
65	32238860	PLCE1 encodes phospholipase C epsilon, and its mutations cause recessive nephrotic syndrome.
66	32238860	PLCE1 colocalized with Rho GTPases in glomeruli.
67	32238860	Knockdown or knockout of PLCE1 in podocytes resulted in decreased levels of GTP-bound Rac1 and Cdc42, but not those of RhoA, and caused a reduction in cell migration.
68	32238860	Similar to the PLCE1 knockout, NCK2 knockout resulted in decreased podocyte migration.
69	32238860	Knockout of PLCE1 reduced the EGF-induced activation of ERK and cell proliferation in podocytes, whereas knockout of NCK2 did not affect proliferation.
70	32238860	Further, the knockout of PLCE1 also resulted in decreased expression of podocyte markers, including NEPH1, NPHS1, WT1, and SYNPO, upon differentiation, but the knockout of NCK2 did not affect the expression of these markers.
71	32238860	Therefore, our findings demonstrate that PLCE1 regulates Rho GTPase activity and cell migration through interacting with NCK2 and that PLCE1 also plays a role in the proliferation and differentiation of podocytes, regardless of the presence of NCK2.
72	32238860	PLCE1 encodes phospholipase C epsilon, and its mutations cause recessive nephrotic syndrome.
73	32238860	PLCE1 colocalized with Rho GTPases in glomeruli.
74	32238860	Knockdown or knockout of PLCE1 in podocytes resulted in decreased levels of GTP-bound Rac1 and Cdc42, but not those of RhoA, and caused a reduction in cell migration.
75	32238860	Similar to the PLCE1 knockout, NCK2 knockout resulted in decreased podocyte migration.
76	32238860	Knockout of PLCE1 reduced the EGF-induced activation of ERK and cell proliferation in podocytes, whereas knockout of NCK2 did not affect proliferation.
77	32238860	Further, the knockout of PLCE1 also resulted in decreased expression of podocyte markers, including NEPH1, NPHS1, WT1, and SYNPO, upon differentiation, but the knockout of NCK2 did not affect the expression of these markers.
78	32238860	Therefore, our findings demonstrate that PLCE1 regulates Rho GTPase activity and cell migration through interacting with NCK2 and that PLCE1 also plays a role in the proliferation and differentiation of podocytes, regardless of the presence of NCK2.
79	32238860	PLCE1 encodes phospholipase C epsilon, and its mutations cause recessive nephrotic syndrome.
80	32238860	PLCE1 colocalized with Rho GTPases in glomeruli.
81	32238860	Knockdown or knockout of PLCE1 in podocytes resulted in decreased levels of GTP-bound Rac1 and Cdc42, but not those of RhoA, and caused a reduction in cell migration.
82	32238860	Similar to the PLCE1 knockout, NCK2 knockout resulted in decreased podocyte migration.
83	32238860	Knockout of PLCE1 reduced the EGF-induced activation of ERK and cell proliferation in podocytes, whereas knockout of NCK2 did not affect proliferation.
84	32238860	Further, the knockout of PLCE1 also resulted in decreased expression of podocyte markers, including NEPH1, NPHS1, WT1, and SYNPO, upon differentiation, but the knockout of NCK2 did not affect the expression of these markers.
85	32238860	Therefore, our findings demonstrate that PLCE1 regulates Rho GTPase activity and cell migration through interacting with NCK2 and that PLCE1 also plays a role in the proliferation and differentiation of podocytes, regardless of the presence of NCK2.
86	32238860	PLCE1 encodes phospholipase C epsilon, and its mutations cause recessive nephrotic syndrome.
87	32238860	PLCE1 colocalized with Rho GTPases in glomeruli.
88	32238860	Knockdown or knockout of PLCE1 in podocytes resulted in decreased levels of GTP-bound Rac1 and Cdc42, but not those of RhoA, and caused a reduction in cell migration.
89	32238860	Similar to the PLCE1 knockout, NCK2 knockout resulted in decreased podocyte migration.
90	32238860	Knockout of PLCE1 reduced the EGF-induced activation of ERK and cell proliferation in podocytes, whereas knockout of NCK2 did not affect proliferation.
91	32238860	Further, the knockout of PLCE1 also resulted in decreased expression of podocyte markers, including NEPH1, NPHS1, WT1, and SYNPO, upon differentiation, but the knockout of NCK2 did not affect the expression of these markers.
92	32238860	Therefore, our findings demonstrate that PLCE1 regulates Rho GTPase activity and cell migration through interacting with NCK2 and that PLCE1 also plays a role in the proliferation and differentiation of podocytes, regardless of the presence of NCK2.
93	32238860	PLCE1 encodes phospholipase C epsilon, and its mutations cause recessive nephrotic syndrome.
94	32238860	PLCE1 colocalized with Rho GTPases in glomeruli.
95	32238860	Knockdown or knockout of PLCE1 in podocytes resulted in decreased levels of GTP-bound Rac1 and Cdc42, but not those of RhoA, and caused a reduction in cell migration.
96	32238860	Similar to the PLCE1 knockout, NCK2 knockout resulted in decreased podocyte migration.
97	32238860	Knockout of PLCE1 reduced the EGF-induced activation of ERK and cell proliferation in podocytes, whereas knockout of NCK2 did not affect proliferation.
98	32238860	Further, the knockout of PLCE1 also resulted in decreased expression of podocyte markers, including NEPH1, NPHS1, WT1, and SYNPO, upon differentiation, but the knockout of NCK2 did not affect the expression of these markers.
99	32238860	Therefore, our findings demonstrate that PLCE1 regulates Rho GTPase activity and cell migration through interacting with NCK2 and that PLCE1 also plays a role in the proliferation and differentiation of podocytes, regardless of the presence of NCK2.