Ignet

Gene Information

Gene symbol: PKD2

Gene name: polycystic kidney disease 2 (autosomal dominant)

HGNC ID: 9009

Synonyms: PKD4, PC2, Pc-2, TRPP2

Related Genes

#	Gene Symbol	Number of hits
1	BTG2	1 hits
2	CTNNB1	1 hits
3	ENPP1	1 hits
4	IL1B	1 hits
5	INS	1 hits
6	JUP	1 hits
7	NOS2A	1 hits
8	PCSK1	1 hits
9	PKD1	1 hits
10	PKHD1	1 hits
11	PRKD1	1 hits
12	SOCS3	1 hits
13	UMOD	1 hits

Related Sentences

#	PMID	Sentence
1	7657031	Processing of proinsulin by furin, PC2, and PC3 in (co) transfected COS (monkey kidney) cells.
2	7657031	The enzymology of proinsulin conversion was studied in COS cells by cotransfection of three species of proinsulin and each of three conversion endoproteases (furin, PC2, and PC3).
3	7657031	PC2, by contrast, failed to cleave human proinsulin but was able to cleave both human proinsulin Arg62 and rat proinsulin II.
4	7657031	Cleavage by PC2 of these proinsulins was predominantly at the C-peptide-A-chain junction, generating the conversion intermediate des-64,65-split proinsulin as the major product and only very small amounts of insulin itself.
5	7657031	Processing of proinsulin by furin, PC2, and PC3 in (co) transfected COS (monkey kidney) cells.
6	7657031	The enzymology of proinsulin conversion was studied in COS cells by cotransfection of three species of proinsulin and each of three conversion endoproteases (furin, PC2, and PC3).
7	7657031	PC2, by contrast, failed to cleave human proinsulin but was able to cleave both human proinsulin Arg62 and rat proinsulin II.
8	7657031	Cleavage by PC2 of these proinsulins was predominantly at the C-peptide-A-chain junction, generating the conversion intermediate des-64,65-split proinsulin as the major product and only very small amounts of insulin itself.
9	7657031	Processing of proinsulin by furin, PC2, and PC3 in (co) transfected COS (monkey kidney) cells.
10	7657031	The enzymology of proinsulin conversion was studied in COS cells by cotransfection of three species of proinsulin and each of three conversion endoproteases (furin, PC2, and PC3).
11	7657031	PC2, by contrast, failed to cleave human proinsulin but was able to cleave both human proinsulin Arg62 and rat proinsulin II.
12	7657031	Cleavage by PC2 of these proinsulins was predominantly at the C-peptide-A-chain junction, generating the conversion intermediate des-64,65-split proinsulin as the major product and only very small amounts of insulin itself.
13	7657031	Processing of proinsulin by furin, PC2, and PC3 in (co) transfected COS (monkey kidney) cells.
14	7657031	The enzymology of proinsulin conversion was studied in COS cells by cotransfection of three species of proinsulin and each of three conversion endoproteases (furin, PC2, and PC3).
15	7657031	PC2, by contrast, failed to cleave human proinsulin but was able to cleave both human proinsulin Arg62 and rat proinsulin II.
16	7657031	Cleavage by PC2 of these proinsulins was predominantly at the C-peptide-A-chain junction, generating the conversion intermediate des-64,65-split proinsulin as the major product and only very small amounts of insulin itself.
17	14671193	Two principal components, PC1 and PC2 (55% of the variance), were used as metabolic syndrome phenotypes.
18	14671193	ANOVA was used to quantify the familial aggregation of PC1 and PC2.
19	14671193	Two principal components, PC1 and PC2 (55% of the variance), were used as metabolic syndrome phenotypes.
20	14671193	ANOVA was used to quantify the familial aggregation of PC1 and PC2.
21	15226261	Here we show that in orpk mice, a model system for PKD that harbors a mutation in the gene that encodes the polaris protein, pancreatic defects start to occur at the end of gestation, with an initial expansion of the developing pancreatic ducts.
22	15226261	Expression of polycystin-2, a protein involved in PKD, is mislocalized in orpk mice.
23	15226261	Furthermore, the cellular localization of beta-catenin, a protein involved in cell adhesion and Wnt signaling, is altered.
24	16801329	Renal histology and immunohistochemistry analyses of mutant fetuses revealed cysts derived from all nephron segments with multilayered epithelia and dysplastic regions, accompanied by a marked increase in the expression of beta-catenin and E-cadherin.
25	16801329	A significant proportion of cysts still expressed the cystic renal disease proteins, polycystin-1, polycystin-2, fibrocystin and uromodulin, implying that cyst formation may result from a deregulation of cell-cell adhesion and/or the Wnt/beta-catenin signaling pathway.
26	16801329	Both fetuses exhibited a severe pancreatic hypoplasia with underdeveloped and disorganized acini, together with an absence of ventral pancreatic-derived tissue. beta-catenin and E-cadherin were strongly downregulated in the exocrine and endocrine compartments, and the islets lacked the transporter essential for glucose-sensing GLUT2, indicating a beta-cell maturation defect.
27	17269447	In rodent islets, exposure to IL-1beta alone or combined with IFN-gamma induces expression of inducible nitric oxide synthase (iNOS).
28	17269447	In the removed grafts iNOS-/- islet tissue contained higher mRNA levels of insulin, proinsulin convertases (PC-1 and PC-2), and IL-1beta compared to transplanted wt islets.
29	17269447	The assessments of insulin, PC-1 and PC-2 mRNAs of the grafts suggest that the iNOS-/- islets may be more resistant to destruction in the transplantation model used; however, this was not sufficient to prolong the period of normoglycemia posttransplantation.
30	17269447	In rodent islets, exposure to IL-1beta alone or combined with IFN-gamma induces expression of inducible nitric oxide synthase (iNOS).
31	17269447	In the removed grafts iNOS-/- islet tissue contained higher mRNA levels of insulin, proinsulin convertases (PC-1 and PC-2), and IL-1beta compared to transplanted wt islets.
32	17269447	The assessments of insulin, PC-1 and PC-2 mRNAs of the grafts suggest that the iNOS-/- islets may be more resistant to destruction in the transplantation model used; however, this was not sufficient to prolong the period of normoglycemia posttransplantation.
33	22641569	HNF-1β mutation affects PKD2 and SOCS3 expression causing renal cysts and diabetes in MODY5 kindred.
34	23209428	Autosomal Dominant Polycystic Kidney Disease (ADPKD; MIM ID's 173900, 601313, 613095) leads to end-stage kidney disease, caused by mutations in PKD1 or PKD2.