Ignet

Gene Information

Gene symbol: KCNIP2

Gene name: Kv channel interacting protein 2

HGNC ID: 15522

Synonyms: KCHIP2

Related Genes

#	Gene Symbol	Number of hits
1	CACNA1C	1 hits
2	CACNA1H	1 hits
3	CACNA2D1	1 hits
4	CACNB1	1 hits
5	KCNA2	1 hits
6	KCNA3	1 hits
7	KCNA4	1 hits
8	KCNA5	1 hits
9	KCNAB1	1 hits
10	KCNB1	1 hits
11	KCND1	1 hits
12	KCND2	1 hits
13	KCND3	1 hits
14	KCNE1	1 hits
15	KCNG2	1 hits
16	KCNH2	1 hits
17	KCNJ2	1 hits
18	KCNJ3	1 hits
19	KCNK3	1 hits
20	KCNN2	1 hits
21	KCNQ1	1 hits
22	SCN1B	1 hits
23	SCN5A	1 hits

Related Sentences

#	PMID	Sentence
1	18482733	Western blot analyses revealed that expression of the Kv accessory protein, KChIP2, is also reduced in MHC-PPARalpha ventricles in parallel with the decrease in Kv4.2.
2	18482733	Although the properties of the endogenous and the "augmented" I(ss) suggest a role(s) for two pore domain K(+) channel (K2P) pore-forming subunits, the expression levels of KCNK2 (TREK1), KCNK3 (TASK1) and KCNK5 (TASK2) in MHC-PPARalpha and WT ventricles are not significantly different.
3	18599872	Fast transient outward K+ current (I(to,f)), slow delayed outward K+ current (I(K,slow)), and steady-state K+ current (I(SS)) were significantly decreased in p90RSK-Tg mouse ventricular myocytes. mRNA levels of Kv4.3, Kv4.2, Kv1.5, Kv2.1, and KChIP2 from ventricles between p90RSK-Tg and nontransgenic littermate control mice were similar, as assessed by quantitative reverse transcriptase-polymerase chain reaction, indicating that p90RSK regulates voltage-gated K+ channels through posttranslational modification.
4	18599872	Kv4.3- and Kv1.5- rather than Kv4.2- and Kv2.1-encoded channels in HEK 293 cells were inhibited by p90RSK.
5	18599872	In vitro phosphorylation analysis showed that Kv4.3 was phosphorylated by p90RSK at 2 conserved sites, Ser516 and Ser550. p90RSK expression significantly inhibited Kv4.3- and Kv4.3 and KChIP2-encoded channel activities in HEK 293 cells, whereas p90RSK's effects were blocked by amino acid mutation(s) at phosphorylation site(s) in Kv4.3.
6	18599872	Hydrogen peroxide, a mediator of induced cardiac p90RSK activation in ischemia/reperfusion injury and diabetes mellitus, had effects similar to those of p90RSK on Kv4.3- or Kv4.3- and KChIP2-encoded channels.
7	18599872	Fast transient outward K+ current (I(to,f)), slow delayed outward K+ current (I(K,slow)), and steady-state K+ current (I(SS)) were significantly decreased in p90RSK-Tg mouse ventricular myocytes. mRNA levels of Kv4.3, Kv4.2, Kv1.5, Kv2.1, and KChIP2 from ventricles between p90RSK-Tg and nontransgenic littermate control mice were similar, as assessed by quantitative reverse transcriptase-polymerase chain reaction, indicating that p90RSK regulates voltage-gated K+ channels through posttranslational modification.
8	18599872	Kv4.3- and Kv1.5- rather than Kv4.2- and Kv2.1-encoded channels in HEK 293 cells were inhibited by p90RSK.
9	18599872	In vitro phosphorylation analysis showed that Kv4.3 was phosphorylated by p90RSK at 2 conserved sites, Ser516 and Ser550. p90RSK expression significantly inhibited Kv4.3- and Kv4.3 and KChIP2-encoded channel activities in HEK 293 cells, whereas p90RSK's effects were blocked by amino acid mutation(s) at phosphorylation site(s) in Kv4.3.
10	18599872	Hydrogen peroxide, a mediator of induced cardiac p90RSK activation in ischemia/reperfusion injury and diabetes mellitus, had effects similar to those of p90RSK on Kv4.3- or Kv4.3- and KChIP2-encoded channels.
11	18599872	Fast transient outward K+ current (I(to,f)), slow delayed outward K+ current (I(K,slow)), and steady-state K+ current (I(SS)) were significantly decreased in p90RSK-Tg mouse ventricular myocytes. mRNA levels of Kv4.3, Kv4.2, Kv1.5, Kv2.1, and KChIP2 from ventricles between p90RSK-Tg and nontransgenic littermate control mice were similar, as assessed by quantitative reverse transcriptase-polymerase chain reaction, indicating that p90RSK regulates voltage-gated K+ channels through posttranslational modification.
12	18599872	Kv4.3- and Kv1.5- rather than Kv4.2- and Kv2.1-encoded channels in HEK 293 cells were inhibited by p90RSK.
13	18599872	In vitro phosphorylation analysis showed that Kv4.3 was phosphorylated by p90RSK at 2 conserved sites, Ser516 and Ser550. p90RSK expression significantly inhibited Kv4.3- and Kv4.3 and KChIP2-encoded channel activities in HEK 293 cells, whereas p90RSK's effects were blocked by amino acid mutation(s) at phosphorylation site(s) in Kv4.3.
14	18599872	Hydrogen peroxide, a mediator of induced cardiac p90RSK activation in ischemia/reperfusion injury and diabetes mellitus, had effects similar to those of p90RSK on Kv4.3- or Kv4.3- and KChIP2-encoded channels.
15	22581745	Expression of genes encoding cardiac muscle proteins (Myh6/7, Mybpc3, Myl1/3, Actc1, Tnni3, Tnn2, Tpm1/2/4 and Dbi) and intercellular proteins (Gja1/4/5/7, Dsp and Cav1/3) were unaltered in GK ventricle compared with control ventricle.
16	22581745	The expression of genes encoding some membrane pumps and exchange proteins was unaltered (Atp1a1/2, Atp1b1 and Slc8a1), whilst others were either upregulated (Atp1a3, relative expression 2.61 ± 0.69 versus 0.84 ± 0.23) or downregulated (Slc9a1, 0.62 ± 0.07 versus 1.08 ± 0.08) in GK ventricle compared with control ventricle.
17	22581745	The expression of genes encoding some calcium (Cacna1c/1g, Cacna2d1/2d2 and Cacnb1/b2), sodium (Scn5a) and potassium channels (Kcna3/5, Kcnj3/5/8/11/12, Kchip2, Kcnab1, Kcnb1, Kcnd1/2/3, Kcne1/4, Kcnq1, Kcng2, Kcnh2, Kcnk3 and Kcnn2) were unaltered, whilst others were either upregulated (Cacna1h, 0.95 ± 0.16 versus 0.47 ± 0.09; Scn1b, 1.84 ± 0.16 versus 1.11 ± 0.11; and Hcn2, 1.55 ± 0.15 versus 1.03 ± 0.08) or downregulated (Hcn4, 0.16 ± 0.03 versus 0.37 ± 0.08; Kcna2, 0.35 ± 0.03 versus 0.80 ± 0.11; Kcna4, 0.79 ± 0.25 versus 1.90 ± 0.26; and Kcnj2, 0.52 ± 0.07 versus 0.78 ± 0.08) in GK ventricle compared with control ventricle.