Ignet

Gene Information

Gene symbol: MKI67

Gene name: antigen identified by monoclonal antibody Ki-67

HGNC ID: 7107

Related Genes

#	Gene Symbol	Number of hits
1	ACTC1	1 hits
2	AURKB	1 hits
3	BAX	1 hits
4	BCL2	1 hits
5	CASP3	1 hits
6	CCNA2	1 hits
7	CCNB1	1 hits
8	CCND1	1 hits
9	CD38	1 hits
10	CD44	1 hits
11	CD68	1 hits
12	CDKN1A	1 hits
13	CDKN1B	1 hits
14	CHKA	1 hits
15	CLDN1	1 hits
16	CLDN7	1 hits
17	CORO1A	1 hits
18	DES	1 hits
19	EIF4EBP1	1 hits
20	FGF2	1 hits
21	GJA1	1 hits
22	HAVCR1	1 hits
23	KRT8	1 hits
24	LRP2	1 hits
25	NES	1 hits
26	NPHS1	1 hits
27	NUDT6	1 hits
28	PAX2	1 hits
29	PCNA	1 hits
30	S100A4	1 hits
31	SYNPO	1 hits
32	UMOD	1 hits
33	VEGFA	1 hits
34	VIM	1 hits
35	WT1	1 hits

Related Sentences

#	PMID	Sentence
1	34309730	Fibroblast growth factor 2 (FGF2) augments podocyte injury, which induces glomerulosclerosis, although the mechanisms remain obscure.
2	34309730	In this study, we investigated the effects of FGF2 on cultured podocytes with interdigitating cell processes in rats.
3	34309730	After 48 h incubation with FGF2 dynamic changes in the shape of primary processes and cell bodies of podocytes resulted in the loss of interdigitation, which was clearly shown by time-lapse photography.
4	34309730	FGF2 reduced the gene expressions of constituents of the slit diaphragm, inflections of intercellular junctions positive for nephrin, and the width of the intercellular space.
5	34309730	Immunostaining for the proliferation marker Ki-67 was rarely seen and weakly stained in the control without FGF2, whereas intensely stained cells were frequently found in the presence of FGF2.
6	34309730	An in vitro scratch assay revealed that FGF2 enhanced migration of podocytes.
7	34309730	These findings show that FGF2 makes podocytes to transition from the quiescent state into the cell cycle and change their morphology due to enhanced motility, and that the culture system in this study is useful for analyzing the pathological changes of podocytes in vivo.
8	33641441	For immunostaining, parietal epithelial cells facing the injured glomeruli of BXSB/MpJ-Yaa expressed CD44, an activated parietal epithelial cell marker, and CD44-positive parietal epithelial cells showed nuclear localization of the androgen receptor and proliferation marker Ki67.
9	33641441	CD44- or Ki67-positive parietal epithelial cells were significantly fewer in castrated group than in sham-operated BXSB/MpJ-Yaa at six months.
10	32982795	However, the treated group exhibited tubular calcium oxalate (CaOx) crystals excretion, followed by a decline in kidney function demonstrated along with glomerular injury, which was confirmed by increased plasma creatinine and urea concentrations, increased glomerular desmin immunostaining, nephrin mRNA expression and decreased WT1 immunofluorescence.
11	32982795	Furthermore, NaOx treatment resulted in tubulointerstitial injury, which was confirmed by tubular dilation, albuminuria, increased Kim-1 and Ki67 mRNA expression, decreased megalin and Tamm-Horsfall protein (THP) expression.
12	32982795	Finally, the treatment induced increases in CD68 protein staining, MCP-1, IL-1β, NFkappaB, and α-SMA mRNA expression, which are consistent with proinflammatory and profibrotic signaling, respectively.
13	30858353	Importantly, targeting 4E-BP1 activation by the RNA interference of 4E-BP1 or pharmacologic rapamycin (inhibitor of mTORC1, blocking mTORC1-dependent phosphorylation of its substrate 4E-BP1) treatment was able to inhibit the increases of PCNA, Ki67, and the S-phase fraction of cell cycle in primary podocyte during 2-6 h of adriamycin treatment, and also attenuated the following apoptotic cell death of podocyte detected from the 4th hour, suggesting that 4E-BP1 could be a regulator to manipulate the amount of cell cycle re-entry provided by differentiated podocyte, and thus regulate the degree of podocyte apoptosis, bringing us a new potential podocyte-protective substance that can be used for therapy.
14	29990736	Differential susceptibility of kidneys and livers to proliferative processes and transcriptional level of the genes encoding desmin, vimentin, connexin 43, and nestin in rats exposed to furan.
15	29990736	Differential susceptibility of kidneys and livers to proliferative processes and transcriptional level of the genes encoding desmin, vimentin, connexin 43, and nestin in rats exposed to furan.
16	29990736	The transcriptional levels of intermediate filament proteins (desmin, vimentin, nestin, and connexin 43) were assessed by using quantitative real-time polymerase chain reaction (PCR), and the cell proliferation markers (proliferating cell nuclear antigen [PCNA] and proliferation-associated nuclear antigen [Ki-67]) were recognized by immunohistochemical analysis.
17	29990736	The transcriptional levels of intermediate filament proteins (desmin, vimentin, nestin, and connexin 43) were assessed by using quantitative real-time polymerase chain reaction (PCR), and the cell proliferation markers (proliferating cell nuclear antigen [PCNA] and proliferation-associated nuclear antigen [Ki-67]) were recognized by immunohistochemical analysis.
18	29990736	Moreover, furan enhances the expression of PCNA and Ki-67 in the liver tissues but not in the kidney tissues.
19	29990736	Moreover, furan enhances the expression of PCNA and Ki-67 in the liver tissues but not in the kidney tissues.
20	29307170	Immunohistochemical staining for PAX-2, Ki-67, and synaptopodin was performed to evaluate cell proliferation in the kidney tissues.Results: After 4 weeks of treatment, islet transplantation significantly alleviated damage to the podocytes and increased the number of glomerular transition cells compared to the DN and IN groups, which were defined as cells that double-stained for PAX-2 and synaptopodin in membranous nephropathy.
21	28643424	MDM2 is implicated in high-glucose-induced podocyte mitotic catastrophe via Notch1 signalling.
22	28643424	HG exposure forced podocytes to enter into S phase and bypass G2/M checkpoint with enhanced expression of Ki67, cyclin B1, Aurora B and p-H3.
23	28643424	Interestingly, knocking down MDM2 or MDM2 overexpression showed inhibition or activation of Notch1 signalling, respectively.
24	28643424	Notch1 signalling is an essential downstream pathway of MDM2 in mediating HG-induced MC in podocytes.
25	26376129	Markers of podocytes (WT-1, p57), parietal epithelial cells (PECs) (claudin-1), and cell proliferation (Ki-67) were identified by immunohistochemistry.
26	25888464	Main topics have been the definition of renal autoimmune components in human lupus biopsies; methods were laser capture of glomeruli and/or of single cells (CD38+ or Ki-67+) from tubulointerstitial areas as starting step followed by elution and characterization of renal antibodies by proteomics.
27	22484642	These floating cells were immunohistologically identified as podocytes, by the expression of podocalyxin, vimentin, Wilms' tumor 1, synaptopodin and nephrin with positivities of 100%, 88.4%, 80.4%, 74.7% and 22.6%, respectively.
28	22484642	Immunostaining of both detached and capillary-attached podocytes for Bax, Bcl-2, desmin, fibroblast-specific protein-1, α-smooth muscle actin and Ki-67 was negative, as were TUNEL assays.
29	22129965	Single and double immunostaining were performed with antibodies to the PEC protein paired box gene 2 (PAX2) and tight junction protein claudin-1, the podocyte-specific protein Wilms' tumor 1 (WT-1), and the proliferating cell protein (Ki-67).
30	22129965	Single and double immunostaining were performed with antibodies to the PEC protein paired box gene 2 (PAX2) and tight junction protein claudin-1, the podocyte-specific protein Wilms' tumor 1 (WT-1), and the proliferating cell protein (Ki-67).
31	22129965	The increase in PEC number was due to proliferation (increase in PAX2/Ki-67 double-positive cells).
32	22129965	The increase in PEC number was due to proliferation (increase in PAX2/Ki-67 double-positive cells).
33	22129965	Aging was accompanied by a progressive increase in the number of glomerular cells double staining for PAX2 and WT-1.
34	22129965	Aging was accompanied by a progressive increase in the number of glomerular cells double staining for PAX2 and WT-1.
35	21289056	In addition, there was greater apoptosis (cleaved caspase-3 immunostaining), fewer podocytes (Wilms' tumor-1 immunostaining), and less proliferation (Ki-67 immunostaining) in diseased SM22α +/+ mice.
36	17229913	Nephrotic-range proteinuria was observed already at 2 wk, together with dedifferentiation and dysregulation of podocytes, indicated by decreased expression of nephrin, synaptopodin, and Wilms' tumor 1 protein and increased expression of Ki-67.
37	17229913	The acceleration of phenotypic changes of podocytes, proteinuria, and subsequent glomerulosclerosis by heminephrectomy was almost completely inhibited by angiotensin II type 1 receptor (AT1R) blocker olmesartan.
38	16761013	We used Synaptopodin, vascular endothelial growth factor, and CD10 as podocyte markers, CK8 and PAX2 as PEC markers and Ki-67 as marker of cell proliferation.
39	16761013	The proliferating PAX-2 and CK8 positive cells that covered the capillary tuft were always in continuity with PAX-2/CK8 positive cells lining Bowman's capsule.
40	16120817	Similar to Tg26 kidneys, podocytes in kd/kd kidneys showed de novo cyclin D1, Ki-67, and desmin expression with loss of synaptopodin and WT-1 expression.
41	15232745	The observation that podocytes express proliferation markers (Ki67, proliferating-cell nuclear antigen and topoisomerase IIalpha) in non-proliferative, mature-looking glomeruli suggests an initial pathogenic act to activate or to keep podocytes from quiescence.
42	15232745	The subsequent proliferation of podocytes is in keeping with downregulation of WT1 and cyclin kinase inhibitors of p16 and p21.
43	15232745	The final scene of evolving glomerulopathy displays apoptosis and expression of Fas-L and Bax in sclerotic mesangial lesions, which eventually end up with global sclerosis.
44	15034095	The authors studied FSGS lesions at days 1, 3, 6, 7, 10, 14, and 21, in relation to changes in the expression of specific markers for normal podocytes (WT-1, synaptopodin, ASD33, and the Thy-1.1 antigen), for mouse PEC (CD10), for activated podocytes (desmin), for macrophages (CD68), and for proliferation (Ki-67).
45	15034095	The composition of the extracellular matrix (ECM) that forms tuft adhesions or scars was studied using mAb against collagen IV alpha2 and alpha4 chains and antibodies directed against different heparan sulfate species.
46	12704573	Interestingly, the latter showed that expression of cyclin-dependent kinase inhibitors p21 and proliferation marker Ki-67 are the same in cellular FSGS, collapsing glomerulopathy, and human immunodeficiency virus-associated FSGS.
47	10879738	All of the cellular lesions expressed cytokeratin, frequently with Ki-67 (82.4%) and less frequently with cyclin A (17.7%), but were invariably negative for podocyte markers (PHM-5 and synaptopodin) and CKIs (p27kip1 and p57kip2).
48	10879738	In conclusion, proliferation of PEC, sustained by repression of CKIs in nature and simultaneous activation of cyclin A, is the actual molecular background to the cellular lesions in FGS.
49	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.
50	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.
51	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.
52	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.
53	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.
54	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.
55	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.
56	9811343	Among these cells), cyclin D1 and CKIs were markedly down-regulated.
57	9811343	Among these cells), cyclin D1 and CKIs were markedly down-regulated.
58	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.
59	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.
60	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.
61	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.
62	9811343	Furthermore, bcl-2 (an apoptosis inhibitory protein) showed a reciprocal expression pattern to that of CKI.
63	9811343	Furthermore, bcl-2 (an apoptosis inhibitory protein) showed a reciprocal expression pattern to that of CKI.