Ignet

Gene Information

Gene symbol: PSMD9

Gene name: proteasome (prosome, macropain) 26S subunit, non-ATPase, 9

HGNC ID: 9567

Synonyms: p27, Rpn4

Related Genes

#	Gene Symbol	Number of hits
1	AGT	1 hits
2	BCL2	1 hits
3	CCNA2	1 hits
4	CCNB1	1 hits
5	CCND1	1 hits
6	CD79A	1 hits
7	CDK2	1 hits
8	CDKN1A	1 hits
9	CDKN1B	1 hits
10	CDKN1C	1 hits
11	CDKN2A	1 hits
12	CHKA	1 hits
13	COL1A1	1 hits
14	CORO1A	1 hits
15	CR1	1 hits
16	CREB1	1 hits
17	CXCL10	1 hits
18	CYR61	1 hits
19	DES	1 hits
20	E2F1	1 hits
21	EPO	1 hits
22	HRAS	1 hits
23	IFI44	1 hits
24	MAPK14	1 hits
25	MYC	1 hits
26	NES	1 hits
27	NPHS1	1 hits
28	NRP1	1 hits
29	PCNA	1 hits
30	PPP1R8	1 hits
31	PTH	1 hits
32	PTHLH	1 hits
33	RHOD	1 hits
34	SYNPO	1 hits
35	TGFB1	1 hits
36	UCHL1	1 hits

Related Sentences

#	PMID	Sentence
1	32333927	Experimental studies have documented that 12-lipoxygenase (12-LOX) and its metabolite 12(S)-hydroxyeicosatetraenoic acid (HETE) play an important role in the pathogenesis of diabetic nephropathy. 12(S)-HETE may work in association with angiotensin II and transforming growth factor- β (TGF-β) reciprocally to induce fibrotic changes in the diabetic kidneys.
2	32333927	Conversely, 12(S)-HETE may also enhance the actions of angiotensin II by upregulating the expression of AT₁ receptors on the glomerulus, mesangium, and podocytes. 12(S)-HETE may also cross-talk with TGF-β in a reciprocal manner to induce the fibrotic changes in the diabetic kidney. 12(S)-HETE-triggered signaling pathways may involve activation of p38 mitogen-activated protein (p38MAP) kinase, increase in cAMP-responsive element-binding protein (CREB) transcriptional activity, epigenetic changes involving histone methylation through an increase in histone methyltransferase activity along with an upregulation of cyclin-kinase inhibitors including, p16, p21, and p27.
3	31801948	The high expression levels of cell cycle inhibitory proteins, including p21, p27, and p57, play an important role in maintaining the low level of proliferation of mature podocytes.
4	31801948	Proliferating cell nuclear antigen (PCNA)-, cyclin-dependent kinase 4 (CDK4)-, and Cyclin D1-positive podocytes were found in mice with adriamycin-induced nephropathy.
5	31801948	CDK4 and cyclin D1 were significantly up-regulated after incubation with adriamycin.
6	31801948	Overexpression of YAP in podocytes promoted their entry into the cell cycle; up-regulated cyclin D1, desmin, and snail2 expression and down-regulated Wilms' tumour 1 (WT1) and nephrin production.
7	31801948	Recombinant murine FGF-basic induced podocytes to re-enter the cell cycle, inhibited WT1 and nephrin, and increased desmin and snail2 expression.
8	31801948	Pretreating podocytes with verteporfin, an inhibitor of YAP/ TEA domain transcription factor (TEAD), decreased the adriamycin-induced overexpression of cyclin D1 and reduced the ratio of S-phase podocytes.
9	31801948	In conclusion, adriamycin induced podocytes to re-enter the cell cycle via upregulation of CDK4 and cyclin D1 expression, which was at least partly mediated by YAP signalling.
10	25953318	We observed significant increases in the protein expression of p27, p21, phospho-eukaryotic elongation factor 4E-binding protein 1, and phospho-p70 S6 ribosomal protein kinase, in both cultured podocytes exposed to high-glucose (HG) medium, and streptozotocin-induced diabetes mellitus (DM) rat glomeruli.
11	25953318	Increased protein expression of cleaved caspase-3 and cleaved poly (ADP-ribose) polymerase, together with increased Bax/Bcl-2 ratios, were also observed in HG-stimulated podocytes and DM glomeruli.
12	24583340	The neuronal deubiquitinase ubiquitin C-terminal hydrolase L1 (UCH-L1) is expressed and activated in podocytes of human and rodent MGN.
13	24583340	The neuronal deubiquitinase ubiquitin C-terminal hydrolase L1 (UCH-L1) is expressed and activated in podocytes of human and rodent MGN.
14	24583340	The neuronal deubiquitinase ubiquitin C-terminal hydrolase L1 (UCH-L1) is expressed and activated in podocytes of human and rodent MGN.
15	24583340	The neuronal deubiquitinase ubiquitin C-terminal hydrolase L1 (UCH-L1) is expressed and activated in podocytes of human and rodent MGN.
16	24583340	The neuronal deubiquitinase ubiquitin C-terminal hydrolase L1 (UCH-L1) is expressed and activated in podocytes of human and rodent MGN.
17	24583340	The neuronal deubiquitinase ubiquitin C-terminal hydrolase L1 (UCH-L1) is expressed and activated in podocytes of human and rodent MGN.
18	24583340	UCH-L1 regulates the mono-ubiquitin pool and induces accumulation of poly-ubiquitinated proteins in affected podocytes.
19	24583340	UCH-L1 regulates the mono-ubiquitin pool and induces accumulation of poly-ubiquitinated proteins in affected podocytes.
20	24583340	UCH-L1 regulates the mono-ubiquitin pool and induces accumulation of poly-ubiquitinated proteins in affected podocytes.
21	24583340	UCH-L1 regulates the mono-ubiquitin pool and induces accumulation of poly-ubiquitinated proteins in affected podocytes.
22	24583340	UCH-L1 regulates the mono-ubiquitin pool and induces accumulation of poly-ubiquitinated proteins in affected podocytes.
23	24583340	UCH-L1 regulates the mono-ubiquitin pool and induces accumulation of poly-ubiquitinated proteins in affected podocytes.
24	24583340	Here, we investigated the role of UCH-L1 in podocyte hypertrophy and in the homeostasis of the hypertrophy associated "model protein" p27(Kip1).
25	24583340	Here, we investigated the role of UCH-L1 in podocyte hypertrophy and in the homeostasis of the hypertrophy associated "model protein" p27(Kip1).
26	24583340	Here, we investigated the role of UCH-L1 in podocyte hypertrophy and in the homeostasis of the hypertrophy associated "model protein" p27(Kip1).
27	24583340	Here, we investigated the role of UCH-L1 in podocyte hypertrophy and in the homeostasis of the hypertrophy associated "model protein" p27(Kip1).
28	24583340	Here, we investigated the role of UCH-L1 in podocyte hypertrophy and in the homeostasis of the hypertrophy associated "model protein" p27(Kip1).
29	24583340	Here, we investigated the role of UCH-L1 in podocyte hypertrophy and in the homeostasis of the hypertrophy associated "model protein" p27(Kip1).
30	24583340	In human and rat MGN, hypertrophic podocytes exhibited a simultaneous up-regulation of UCH-L1 and of cytoplasmic p27(Kip1) content.
31	24583340	In human and rat MGN, hypertrophic podocytes exhibited a simultaneous up-regulation of UCH-L1 and of cytoplasmic p27(Kip1) content.
32	24583340	In human and rat MGN, hypertrophic podocytes exhibited a simultaneous up-regulation of UCH-L1 and of cytoplasmic p27(Kip1) content.
33	24583340	In human and rat MGN, hypertrophic podocytes exhibited a simultaneous up-regulation of UCH-L1 and of cytoplasmic p27(Kip1) content.
34	24583340	In human and rat MGN, hypertrophic podocytes exhibited a simultaneous up-regulation of UCH-L1 and of cytoplasmic p27(Kip1) content.
35	24583340	In human and rat MGN, hypertrophic podocytes exhibited a simultaneous up-regulation of UCH-L1 and of cytoplasmic p27(Kip1) content.
36	24583340	In contrast, UCH-L1 levels and activity increased podocyte hypertrophy and total protein content in culture, specifically of cytoplasmic p27(Kip1).
37	24583340	In contrast, UCH-L1 levels and activity increased podocyte hypertrophy and total protein content in culture, specifically of cytoplasmic p27(Kip1).
38	24583340	In contrast, UCH-L1 levels and activity increased podocyte hypertrophy and total protein content in culture, specifically of cytoplasmic p27(Kip1).
39	24583340	In contrast, UCH-L1 levels and activity increased podocyte hypertrophy and total protein content in culture, specifically of cytoplasmic p27(Kip1).
40	24583340	In contrast, UCH-L1 levels and activity increased podocyte hypertrophy and total protein content in culture, specifically of cytoplasmic p27(Kip1).
41	24583340	In contrast, UCH-L1 levels and activity increased podocyte hypertrophy and total protein content in culture, specifically of cytoplasmic p27(Kip1).
42	24583340	UCH-L1 enhanced cytoplasmic p27(Kip1) levels by nuclear export and decreased poly-ubiquitination and proteasomal degradation of p27(Kip1).
43	24583340	UCH-L1 enhanced cytoplasmic p27(Kip1) levels by nuclear export and decreased poly-ubiquitination and proteasomal degradation of p27(Kip1).
44	24583340	UCH-L1 enhanced cytoplasmic p27(Kip1) levels by nuclear export and decreased poly-ubiquitination and proteasomal degradation of p27(Kip1).
45	24583340	UCH-L1 enhanced cytoplasmic p27(Kip1) levels by nuclear export and decreased poly-ubiquitination and proteasomal degradation of p27(Kip1).
46	24583340	UCH-L1 enhanced cytoplasmic p27(Kip1) levels by nuclear export and decreased poly-ubiquitination and proteasomal degradation of p27(Kip1).
47	24583340	UCH-L1 enhanced cytoplasmic p27(Kip1) levels by nuclear export and decreased poly-ubiquitination and proteasomal degradation of p27(Kip1).
48	24583340	In parallel, UCH-L1 increased podocyte turnover, migration and cytoskeletal rearrangement, which are associated with known oncogenic functions of cytoplasmic p27(Kip1) in cancer.
49	24583340	In parallel, UCH-L1 increased podocyte turnover, migration and cytoskeletal rearrangement, which are associated with known oncogenic functions of cytoplasmic p27(Kip1) in cancer.
50	24583340	In parallel, UCH-L1 increased podocyte turnover, migration and cytoskeletal rearrangement, which are associated with known oncogenic functions of cytoplasmic p27(Kip1) in cancer.
51	24583340	In parallel, UCH-L1 increased podocyte turnover, migration and cytoskeletal rearrangement, which are associated with known oncogenic functions of cytoplasmic p27(Kip1) in cancer.
52	24583340	In parallel, UCH-L1 increased podocyte turnover, migration and cytoskeletal rearrangement, which are associated with known oncogenic functions of cytoplasmic p27(Kip1) in cancer.
53	24583340	In parallel, UCH-L1 increased podocyte turnover, migration and cytoskeletal rearrangement, which are associated with known oncogenic functions of cytoplasmic p27(Kip1) in cancer.
54	24583340	We propose that UCH-L1 induces podocyte hypertrophy in MGN by increasing the total protein content through altered degradation and accumulation of proteins such as p27(Kip1) in the cytoplasm of podocytes.
55	24583340	We propose that UCH-L1 induces podocyte hypertrophy in MGN by increasing the total protein content through altered degradation and accumulation of proteins such as p27(Kip1) in the cytoplasm of podocytes.
56	24583340	We propose that UCH-L1 induces podocyte hypertrophy in MGN by increasing the total protein content through altered degradation and accumulation of proteins such as p27(Kip1) in the cytoplasm of podocytes.
57	24583340	We propose that UCH-L1 induces podocyte hypertrophy in MGN by increasing the total protein content through altered degradation and accumulation of proteins such as p27(Kip1) in the cytoplasm of podocytes.
58	24583340	We propose that UCH-L1 induces podocyte hypertrophy in MGN by increasing the total protein content through altered degradation and accumulation of proteins such as p27(Kip1) in the cytoplasm of podocytes.
59	24583340	We propose that UCH-L1 induces podocyte hypertrophy in MGN by increasing the total protein content through altered degradation and accumulation of proteins such as p27(Kip1) in the cytoplasm of podocytes.
60	24476693	Activation of the receptor for advanced glycation end products induces nuclear inhibitor of protein phosphatase-1 suppression.
61	24476693	Analysis of protein phosphatase-1 indicated that advanced glycation end products did not affect its expression, but increased its phosphatase activity.
62	24476693	Using differential display analysis we previously demonstrated that stimulation of RAGE in podocytes modulates the expression of numerous genes, among others nuclear inhibitor of protein phosphatase-1 (NIPP1).
63	24476693	Here we found that silencing of NIPP1 induced podocyte hypertrophy, cell cycle arrest, and significantly increased protein phosphatase-1 activity.
64	24476693	NIPP1 downregulation was associated with increased p27(Kip1) protein expression.
65	23825071	The pathophysiology of AGE-challenged podocytes, such as hypertrophy, apoptosis, and reduced cell migration, is closely related to the induction of the cell cycle inhibitor p27(Kip1) and to the inhibition of neuropilin 1 (NRP1).
66	23825071	The pathophysiology of AGE-challenged podocytes, such as hypertrophy, apoptosis, and reduced cell migration, is closely related to the induction of the cell cycle inhibitor p27(Kip1) and to the inhibition of neuropilin 1 (NRP1).
67	23825071	The pathophysiology of AGE-challenged podocytes, such as hypertrophy, apoptosis, and reduced cell migration, is closely related to the induction of the cell cycle inhibitor p27(Kip1) and to the inhibition of neuropilin 1 (NRP1).
68	23825071	We have previously demonstrated that treatment with erythropoietin is associated with protective effects for podocytes in vitro. db/db mice with overt DN aged 15-16 wk were treated with either placebo, epoetin-β, or continuous erythropoietin receptor activator (CERA) for 2 wk. db/db mice compared with nondiabetic db/m control mice revealed the expected increases in body weight, blood glucose, albumin-to-creatinine ratio, and AGE accumulation.
69	23825071	We have previously demonstrated that treatment with erythropoietin is associated with protective effects for podocytes in vitro. db/db mice with overt DN aged 15-16 wk were treated with either placebo, epoetin-β, or continuous erythropoietin receptor activator (CERA) for 2 wk. db/db mice compared with nondiabetic db/m control mice revealed the expected increases in body weight, blood glucose, albumin-to-creatinine ratio, and AGE accumulation.
70	23825071	We have previously demonstrated that treatment with erythropoietin is associated with protective effects for podocytes in vitro. db/db mice with overt DN aged 15-16 wk were treated with either placebo, epoetin-β, or continuous erythropoietin receptor activator (CERA) for 2 wk. db/db mice compared with nondiabetic db/m control mice revealed the expected increases in body weight, blood glucose, albumin-to-creatinine ratio, and AGE accumulation.
71	23825071	However, the albumin-to-creatinine ratio was significantly lower in db/db mice treated with epoetin-β or CERA.
72	23825071	However, the albumin-to-creatinine ratio was significantly lower in db/db mice treated with epoetin-β or CERA.
73	23825071	However, the albumin-to-creatinine ratio was significantly lower in db/db mice treated with epoetin-β or CERA.
74	23825071	Induction of p27(Kip1) and suppression of NRP1 were significantly reduced in the epoetin-β treatment group versus the CERA treatment group.
75	23825071	Induction of p27(Kip1) and suppression of NRP1 were significantly reduced in the epoetin-β treatment group versus the CERA treatment group.
76	23825071	Induction of p27(Kip1) and suppression of NRP1 were significantly reduced in the epoetin-β treatment group versus the CERA treatment group.
77	23825071	Together, independently from hematopoetic effects, epoetin-β or CERA treatment was associated with protective changes in DN, especially that NRP1 and p27(Kip1) expressions as well as numbers of podocytes returned to normal levels.
78	23825071	Together, independently from hematopoetic effects, epoetin-β or CERA treatment was associated with protective changes in DN, especially that NRP1 and p27(Kip1) expressions as well as numbers of podocytes returned to normal levels.
79	23825071	Together, independently from hematopoetic effects, epoetin-β or CERA treatment was associated with protective changes in DN, especially that NRP1 and p27(Kip1) expressions as well as numbers of podocytes returned to normal levels.
80	20495534	Immunohistochemistry was applied to detect the expression of nestin, cell-cycle regulatory protein p27, as well as complement C5b-9 and complement receptor 1 (CR1).
81	20495534	Immunohistochemistry was applied to detect the expression of nestin, cell-cycle regulatory protein p27, as well as complement C5b-9 and complement receptor 1 (CR1).
82	20495534	Compared with the Control, IgAN glomeruli had reduced podocyte expression of p27 and nestin along with decreased podocyte number.
83	20495534	Compared with the Control, IgAN glomeruli had reduced podocyte expression of p27 and nestin along with decreased podocyte number.
84	20200004	Parathyroid hormone-related protein induces hypertrophy in podocytes via TGF-beta(1) and p27(Kip1): implications for diabetic nephropathy.
85	20037814	The expression of Rho-kinase mRNA and P27 mRNA in kidney were detected by RT-PCR.
86	20037814	The expression of Rho-kinase mRNA and P27 mRNA in kidney were detected by RT-PCR.
87	20037814	But in the treatment group, the fasudil alleviated glomerular injury, with proliferating cell nuclear antigen (PCNA)-positive cell infiltration ameliorated and the expression of P27 increased.
88	20037814	But in the treatment group, the fasudil alleviated glomerular injury, with proliferating cell nuclear antigen (PCNA)-positive cell infiltration ameliorated and the expression of P27 increased.
89	17699553	Podocyte CCN1 expression was decreased in IgA nephropathy, diabetic nephropathy, and membranous nephropathy, whereas it remained unchanged in minimal change disease and focal segmental glomerulosclerosis.
90	17699553	In cultured podocytes, CCN1 markedly induced the expression of cyclin-dependent kinase inhibitor p27(Kip1) as well as synaptopodin in a dose-dependent manner and suppressed podocyte migration.
91	17457378	The PPAR-gamma agonist significantly restored expression of the cyclin-dependent kinase inhibitor p27 and the antiapoptotic molecule Bcl-xL while significantly decreasing proapoptotic caspase-3 activity.
92	17457378	We postulate that this protective effect may be mediated in part by effects on p27 and TGF-beta expression.
93	16775597	Forty-two kidney biopsies, MCD (14), FSGS (12), CGN (4), and normal (CON) (12), were evaluated by immunohistochemistry using dual staining for expression of p27, p21, and p57, and cyclins D and A, in podocytes of children with CGN.
94	16775597	On light microscopy, all podocytes expressed p27, whereas p21 and p57 expression was seen in a portion of podocytes in normal kidney biopsies.
95	16775597	The staining for p27 decreased significantly, in order, from normal (100%) to MCD (45.8%) to CGN (24.2%) to FSGS (16.6%). p21 staining was significantly decreased from normal (69.8%) to CGN (15.5%) to MCD (2.2%) to FSGS (0.6%), and the difference between CGN and MCD and FSGS was also significant.
96	16775597	Cyclin D staining was significantly increased in CGN (26.8%) compared to normal (7.2%), MCD (1.6%), and FSGS (0.0%), and the difference between CGN and MCD and FSGS was also significant.
97	16775597	Thus, p27 and p21 but not p57 was decreased in CGN, as in FSGS when compared to normal.
98	16731829	Thiazolidinediones are ligands for peroxisome proliferator-activated receptor (PPAR)-gamma, widely used as insulin sensitizer in type 2 diabetic patients and implicated in apoptosis, cell proliferation, and cell cycle regulation.
99	16731829	Thiazolidinediones are ligands for peroxisome proliferator-activated receptor (PPAR)-gamma, widely used as insulin sensitizer in type 2 diabetic patients and implicated in apoptosis, cell proliferation, and cell cycle regulation.
100	16731829	Although similar HbA(1c) levels were observed in both groups, pioglitazone significantly inhibited glomerular hypertrophy and mesangial matrix expansion and reduced urinary albumin excretion compared with the insulin-treated group.
101	16731829	Although similar HbA(1c) levels were observed in both groups, pioglitazone significantly inhibited glomerular hypertrophy and mesangial matrix expansion and reduced urinary albumin excretion compared with the insulin-treated group.
102	16731829	In addition, pioglitazone significantly reduced the number of glomerular p27(Kip1)-positive cells.
103	16731829	In addition, pioglitazone significantly reduced the number of glomerular p27(Kip1)-positive cells.
104	16731829	Pioglitazone suppressed high glucose-induced phosphorylation of p44/42 mitogen-activated protein kinase and reduced Bcl-2 and p27(Kip1) protein levels.
105	16731829	Pioglitazone suppressed high glucose-induced phosphorylation of p44/42 mitogen-activated protein kinase and reduced Bcl-2 and p27(Kip1) protein levels.
106	16382022	IFN-inducible protein-10 (IP-10/CXCL10) is a potent chemoattractant for activated T lymphocytes and was reported recently to have several additional biologic activities.
107	16382022	IFN-inducible protein-10 (IP-10/CXCL10) is a potent chemoattractant for activated T lymphocytes and was reported recently to have several additional biologic activities.
108	16382022	In cultured podocytes subjected to recombinant IP-10 treatment, the expression of slit-diaphragm (SD) components nephrin and podocin clearly was heightened.
109	16382022	In cultured podocytes subjected to recombinant IP-10 treatment, the expression of slit-diaphragm (SD) components nephrin and podocin clearly was heightened.
110	16382022	Rats that had puromycin aminonucleoside nephropathy and anti-nephrin antibody-induced nephropathy and were subjected to anti-IP-10 function-blocking antibody (anti-IP-10 mAb) treatment displayed a decrease in the protein level of SD components, as well as exacerbated proteinuria.
111	16382022	Rats that had puromycin aminonucleoside nephropathy and anti-nephrin antibody-induced nephropathy and were subjected to anti-IP-10 function-blocking antibody (anti-IP-10 mAb) treatment displayed a decrease in the protein level of SD components, as well as exacerbated proteinuria.
112	16382022	Cultured podocytes subjected to recombinant IP-10 treatment displayed an increase in the protein level of p27(Kip1), whereas the levels of cyclins E and A decreased.
113	16382022	Cultured podocytes subjected to recombinant IP-10 treatment displayed an increase in the protein level of p27(Kip1), whereas the levels of cyclins E and A decreased.
114	16382022	The expression of IP-10 and SD components was heightened by the treatment of siRNA of cyclin A, whereas these expressions were lowered by the treatment of siRNA of p27(Kip1).
115	16382022	The expression of IP-10 and SD components was heightened by the treatment of siRNA of cyclin A, whereas these expressions were lowered by the treatment of siRNA of p27(Kip1).
116	16382022	Proteinuric rats subjected to anti-IP-10 mAb treatment displayed a heightened expression of cyclin A from the early phase of the disease, which indicates that the anti-IP-10 mAb treatment exacerbates podocyte injury by disturbing the cell-cycle balance.
117	16382022	Proteinuric rats subjected to anti-IP-10 mAb treatment displayed a heightened expression of cyclin A from the early phase of the disease, which indicates that the anti-IP-10 mAb treatment exacerbates podocyte injury by disturbing the cell-cycle balance.
118	16177004	Galectin-9 (Gal-9) was identified previously and demonstrated to have apoptotic potential to thymocytes in mice and activated CD8(+) T cells in nephrotoxic serum nephritis model.
119	16177004	Galectin-9 (Gal-9) was identified previously and demonstrated to have apoptotic potential to thymocytes in mice and activated CD8(+) T cells in nephrotoxic serum nephritis model.
120	16177004	Gal-9 reduced glomerular expression of TGF-beta1 and the number of p27(Kip1)- and p21(Cip1)-positive cells in glomeruli.
121	16177004	Gal-9 reduced glomerular expression of TGF-beta1 and the number of p27(Kip1)- and p21(Cip1)-positive cells in glomeruli.
122	16177004	Double staining with nephrin and type IV collagen revealed that podocytes were mainly positive for p27(Kip1).
123	16177004	Double staining with nephrin and type IV collagen revealed that podocytes were mainly positive for p27(Kip1).
124	16177004	Gal-9 reversed the high-glucose-mediated upregulation of p27(Kip1) and p21(Cip1) and inhibited cell-cycle-dependent hypertrophy, i.e., reduced [(3)H]proline incorporation.
125	16177004	Gal-9 reversed the high-glucose-mediated upregulation of p27(Kip1) and p21(Cip1) and inhibited cell-cycle-dependent hypertrophy, i.e., reduced [(3)H]proline incorporation.
126	16164635	p27(Kip1) Knockout mice are protected from diabetic nephropathy: evidence for p27(Kip1) haplotype insufficiency.
127	15499562	Targets of Cux-1 repression include the cyclin kinase inhibitors p21 and p27.
128	15499562	To begin to determine whether Cux-1 regulation by the Notch signaling pathway is conserved in mammals, we compared the expression patterns of Cux-1, the murine Notch receptors (Notch 1-4), and the murine ligands (Jagged 1, Jagged 2, and Delta 1) during murine embryogenesis and kidney development.
129	15208647	To assess the cellular mechanisms underlying the mesangial cell proliferation and glomerulosclerosis in progressive human IgA nephropathy (IgAN), we examined the expression of E2F1, Rb, c-Myc, proliferating cell nuclear antigen (PCNA), cyclins (D1, E and A), cyclin-dependent kinase 2 (CDK2) and CDK inhibitors (p21(waf1), p27(kip1), 57(kip2) and p16(ink4a)) by immunohistochemistry in renal biopsy specimens.
130	15208647	To assess the cellular mechanisms underlying the mesangial cell proliferation and glomerulosclerosis in progressive human IgA nephropathy (IgAN), we examined the expression of E2F1, Rb, c-Myc, proliferating cell nuclear antigen (PCNA), cyclins (D1, E and A), cyclin-dependent kinase 2 (CDK2) and CDK inhibitors (p21(waf1), p27(kip1), 57(kip2) and p16(ink4a)) by immunohistochemistry in renal biopsy specimens.
131	15208647	To assess the cellular mechanisms underlying the mesangial cell proliferation and glomerulosclerosis in progressive human IgA nephropathy (IgAN), we examined the expression of E2F1, Rb, c-Myc, proliferating cell nuclear antigen (PCNA), cyclins (D1, E and A), cyclin-dependent kinase 2 (CDK2) and CDK inhibitors (p21(waf1), p27(kip1), 57(kip2) and p16(ink4a)) by immunohistochemistry in renal biopsy specimens.
132	15208647	High endogenous expression of p27(kip1) and p57(kip2) by podocytes in normal glomeruli and glomeruli with minor lesions was observed to decrease in proliferating and sclerosing glomeruli; this pattern displayed a strong inverse correlation with the mean glomerulosclerosis score and the index of glomerular lesion.
133	15208647	High endogenous expression of p27(kip1) and p57(kip2) by podocytes in normal glomeruli and glomeruli with minor lesions was observed to decrease in proliferating and sclerosing glomeruli; this pattern displayed a strong inverse correlation with the mean glomerulosclerosis score and the index of glomerular lesion.
134	15208647	High endogenous expression of p27(kip1) and p57(kip2) by podocytes in normal glomeruli and glomeruli with minor lesions was observed to decrease in proliferating and sclerosing glomeruli; this pattern displayed a strong inverse correlation with the mean glomerulosclerosis score and the index of glomerular lesion.
135	15208647	Increased apoptotic activity was identified in progressive glomerular lesions of advanced IgAN, which correlated with the proliferative activity in these lesions as assessed by total expression levels of PCNA and CDK2 in glomeruli, E2F1 expression levels in the mesangium, cyclin D1 expression levels in endothelium and the c-Myc glomerular staining score.
136	15208647	Increased apoptotic activity was identified in progressive glomerular lesions of advanced IgAN, which correlated with the proliferative activity in these lesions as assessed by total expression levels of PCNA and CDK2 in glomeruli, E2F1 expression levels in the mesangium, cyclin D1 expression levels in endothelium and the c-Myc glomerular staining score.
137	15208647	Increased apoptotic activity was identified in progressive glomerular lesions of advanced IgAN, which correlated with the proliferative activity in these lesions as assessed by total expression levels of PCNA and CDK2 in glomeruli, E2F1 expression levels in the mesangium, cyclin D1 expression levels in endothelium and the c-Myc glomerular staining score.
138	15208647	Our results suggest that the onset and magnitude of mesangial cell proliferation and glomerulosclerosis is associated with the upregulation of E2F1 by mesangial cells and the downregulation of p27(kip1) and p57(kip2) by glomerular epithelial cells.
139	15208647	Our results suggest that the onset and magnitude of mesangial cell proliferation and glomerulosclerosis is associated with the upregulation of E2F1 by mesangial cells and the downregulation of p27(kip1) and p57(kip2) by glomerular epithelial cells.
140	15208647	Our results suggest that the onset and magnitude of mesangial cell proliferation and glomerulosclerosis is associated with the upregulation of E2F1 by mesangial cells and the downregulation of p27(kip1) and p57(kip2) by glomerular epithelial cells.
141	14600034	The expression of proliferating cellular antigen (PCNA), cyclin-dependent kinase inhibitor p27, Wilms tumor gene (WT1), and desmin, a marker of early podocyte damage, was investigated by immunohistology.
142	14600034	In parallel, the increase in podocyte volume in SNX+solvent rats was abrogated by treatment with 1,25(OH)(2)D(3), and immunohistochemistry revealed less expression of desmin, PCNA, and p27, suggesting less podocyte injury and activation of the cyclin cascade.
143	12478365	Glomerular differentiation in p27 and p57 double-mutant metanephroi.
144	12478365	Glomerular differentiation in p27 and p57 double-mutant metanephroi.
145	12478365	Glomerular differentiation in p27 and p57 double-mutant metanephroi.
146	12478365	Glomerular differentiation in p27 and p57 double-mutant metanephroi.
147	12478365	Glomerular differentiation in p27 and p57 double-mutant metanephroi.
148	12478365	Glomerular differentiation in p27 and p57 double-mutant metanephroi.
149	12478365	The cell cycle inhibitors p27 and p57 are initially concurrently expressed at a critical point of glomerulogenesis and podocyte differentiation.
150	12478365	The cell cycle inhibitors p27 and p57 are initially concurrently expressed at a critical point of glomerulogenesis and podocyte differentiation.
151	12478365	The cell cycle inhibitors p27 and p57 are initially concurrently expressed at a critical point of glomerulogenesis and podocyte differentiation.
152	12478365	The cell cycle inhibitors p27 and p57 are initially concurrently expressed at a critical point of glomerulogenesis and podocyte differentiation.
153	12478365	The cell cycle inhibitors p27 and p57 are initially concurrently expressed at a critical point of glomerulogenesis and podocyte differentiation.
154	12478365	The cell cycle inhibitors p27 and p57 are initially concurrently expressed at a critical point of glomerulogenesis and podocyte differentiation.
155	12478365	The present study generated mice lacking both p27 and p57, in order to investigate the synergistic roles of these molecules in glomerular differentiation.
156	12478365	The present study generated mice lacking both p27 and p57, in order to investigate the synergistic roles of these molecules in glomerular differentiation.
157	12478365	The present study generated mice lacking both p27 and p57, in order to investigate the synergistic roles of these molecules in glomerular differentiation.
158	12478365	The present study generated mice lacking both p27 and p57, in order to investigate the synergistic roles of these molecules in glomerular differentiation.
159	12478365	The present study generated mice lacking both p27 and p57, in order to investigate the synergistic roles of these molecules in glomerular differentiation.
160	12478365	The present study generated mice lacking both p27 and p57, in order to investigate the synergistic roles of these molecules in glomerular differentiation.
161	12478365	It appeared that p27 and p57 double-mutant mice died between E16.5 and E18.5, before glomerular differentiation can take place.
162	12478365	It appeared that p27 and p57 double-mutant mice died between E16.5 and E18.5, before glomerular differentiation can take place.
163	12478365	It appeared that p27 and p57 double-mutant mice died between E16.5 and E18.5, before glomerular differentiation can take place.
164	12478365	It appeared that p27 and p57 double-mutant mice died between E16.5 and E18.5, before glomerular differentiation can take place.
165	12478365	It appeared that p27 and p57 double-mutant mice died between E16.5 and E18.5, before glomerular differentiation can take place.
166	12478365	It appeared that p27 and p57 double-mutant mice died between E16.5 and E18.5, before glomerular differentiation can take place.
167	12478365	Western blot analysis of metanephroi after 6 days in culture showed an up-regulation of p21 protein in p27 mutant and double-mutant, but not in p57 mutant metanephroi.
168	12478365	Western blot analysis of metanephroi after 6 days in culture showed an up-regulation of p21 protein in p27 mutant and double-mutant, but not in p57 mutant metanephroi.
169	12478365	Western blot analysis of metanephroi after 6 days in culture showed an up-regulation of p21 protein in p27 mutant and double-mutant, but not in p57 mutant metanephroi.
170	12478365	Western blot analysis of metanephroi after 6 days in culture showed an up-regulation of p21 protein in p27 mutant and double-mutant, but not in p57 mutant metanephroi.
171	12478365	Western blot analysis of metanephroi after 6 days in culture showed an up-regulation of p21 protein in p27 mutant and double-mutant, but not in p57 mutant metanephroi.
172	12478365	Western blot analysis of metanephroi after 6 days in culture showed an up-regulation of p21 protein in p27 mutant and double-mutant, but not in p57 mutant metanephroi.
173	12478365	These findings suggest that p27 and p57 are synergistically involved, in part, to determine the number, but not the differentiation, in podocytes.
174	12478365	These findings suggest that p27 and p57 are synergistically involved, in part, to determine the number, but not the differentiation, in podocytes.
175	12478365	These findings suggest that p27 and p57 are synergistically involved, in part, to determine the number, but not the differentiation, in podocytes.
176	12478365	These findings suggest that p27 and p57 are synergistically involved, in part, to determine the number, but not the differentiation, in podocytes.
177	12478365	These findings suggest that p27 and p57 are synergistically involved, in part, to determine the number, but not the differentiation, in podocytes.
178	12478365	These findings suggest that p27 and p57 are synergistically involved, in part, to determine the number, but not the differentiation, in podocytes.
179	11856766	A conditionally immortalized human podocyte cell line demonstrating nephrin and podocin expression.
180	11856766	After transfer to the "nonpermissive" temperature (37 degrees C), they entered growth arrest and expressed markers of differentiated in vivo podocytes, including the novel podocyte proteins, nephrin, podocin, CD2AP, and synaptopodin, and known molecules of the slit diaphragm ZO-1, alpha-, beta-, and gamma-catenin and P-cadherin.
181	11856766	The differentiation was accompanied by a growth arrest and the upregulation of cyclin-dependent kinase inhibitors, p27 and p57, as well as cyclin D(1), whereas cyclin A was downregulated.
182	11796823	Renal fibronectin, collagen iv, and vascular endothelial growth factor mRNA levels were increased at 7 months.
183	11796823	In addition, glomeruli from the diabetic rats showed up-regulation of the cyclin kinase inhibitors, p21 and p27.
184	10526006	Additionally, serial section analysis revealed that Ki-67-positive cells in the crescents were frequently cyclin-A positive and Bcl-2 positive, but seldom cyclin-B(1) positive.
185	10526006	Additionally, serial section analysis revealed that Ki-67-positive cells in the crescents were frequently cyclin-A positive and Bcl-2 positive, but seldom cyclin-B(1) positive.
186	10526006	Moreover, the expression of cyclin-dependent kinase inhibitor p27(Kip1) was low in the cellular crescents, despite being exclusively positive in podocytes within the same section.
187	10526006	Moreover, the expression of cyclin-dependent kinase inhibitor p27(Kip1) was low in the cellular crescents, despite being exclusively positive in podocytes within the same section.
188	10526006	We concluded that the major component of the cellular crescents is made up of PECs and that apparent expression of cyclins and Bcl-2 and restrained expression of p27(Kip1) may be synergistically associated with the development of cellular crescents in human CRGN.
189	10526006	We concluded that the major component of the cellular crescents is made up of PECs and that apparent expression of cyclins and Bcl-2 and restrained expression of p27(Kip1) may be synergistically associated with the development of cellular crescents in human CRGN.
190	9811343	To determine the relationship between cell cycle regulation and differentiation, the spatiotemporal expression of cyclin A, cyclin B1, cyclin D1, the cyclin-dependent kinase inhibitors (CKIs) p27 and p57, and markers of differentiating podocytes in developing human kidneys was investigated by immunohistochemistry.
191	9811343	In S-shaped body stage, Ki-67, a cell proliferation marker that labels the G1/S/G2/M phase, was expressed in the majority (more than 80%) of presumptive podocytes, along with cyclin A (approximately 20% of the Ki-67-positive cells) and cyclin B1 (less than 5% of Ki-67-positive cells) expression.
192	9811343	Among these cells), cyclin D1 and CKIs were markedly down-regulated.
193	9811343	At the capillary-loop stage, by contrast, CKIs and cyclin D1 were intensely positive in podocytes, whereas no Ki-67, cyclin B1, or cyclin A expression was seen.
194	9811343	Moreover, double-immunolabeling and serial-section analysis provided evidence that CKIs and markers specific for differentiating podocytes, namely PHM-5 (podocalyxin-like protein in humans), synaptopodin (a foot process-related protein), and C3b receptor, were co-expressed at the capillary-loop stage.
195	9811343	Furthermore, bcl-2 (an apoptosis inhibitory protein) showed a reciprocal expression pattern to that of CKI.