Ignet

Gene Information

Gene symbol: CDKN2B

Gene name: cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4)

HGNC ID: 1788

Synonyms: P15, MTS2, INK4B, TP15, CDK4I, p15INK4b

Related Genes

#	Gene Symbol	Number of hits
1	CASP3	1 hits
2	MAPK14	1 hits
3	MYC	1 hits
4	SMAD3	1 hits
5	STAT3	1 hits
6	TAGLN	1 hits
7	TGFB1	1 hits
8	TGFB2	1 hits

Related Sentences

#	PMID	Sentence
1	16207831	Using a unique system of conditionally immortalized podocytes, it is demonstrated that autocrine TGF-beta2 induces G0/G1 arrest and differentiation under nonpermissive culture through Smad3-dependent induction of the cyclin-dependent kinase inhibitor p15(Ink4b) (Cdkn2b).
2	16207831	When exposed to recombinant TGF-beta1 (or TGF-beta2), nonpermissive culture podocytes switch to G2/M arrest and apoptosis, selectively at advanced TGF-beta concentrations and specifically in association with suppression of Cdkn2b and activation of proapoptotic p38 mitogen-activated protein kinase.
3	16207831	Autocrine TGF-beta2/Smad3/Cdkn2b signaling in podocytes specifies G0/G1 arrest associated with podocyte differentiation, whereas increasing TGF-beta concentrations beyond a critical threshold induces G2/M block and apoptosis associated with selective p38 mitogen-activated protein kinase activation and with suppression of Cdkn2b.
4	16207831	In summary, the results suggest a new functional requirement of TGF-beta2 in growth arrest and differentiation of murine podocytes in vitro and demonstrate that a critical TGF-beta concentration threshold may specify a molecular switch to proapoptotic signaling profiles and apoptosis.
5	16207831	Using a unique system of conditionally immortalized podocytes, it is demonstrated that autocrine TGF-beta2 induces G0/G1 arrest and differentiation under nonpermissive culture through Smad3-dependent induction of the cyclin-dependent kinase inhibitor p15(Ink4b) (Cdkn2b).
6	16207831	When exposed to recombinant TGF-beta1 (or TGF-beta2), nonpermissive culture podocytes switch to G2/M arrest and apoptosis, selectively at advanced TGF-beta concentrations and specifically in association with suppression of Cdkn2b and activation of proapoptotic p38 mitogen-activated protein kinase.
7	16207831	Autocrine TGF-beta2/Smad3/Cdkn2b signaling in podocytes specifies G0/G1 arrest associated with podocyte differentiation, whereas increasing TGF-beta concentrations beyond a critical threshold induces G2/M block and apoptosis associated with selective p38 mitogen-activated protein kinase activation and with suppression of Cdkn2b.
8	16207831	In summary, the results suggest a new functional requirement of TGF-beta2 in growth arrest and differentiation of murine podocytes in vitro and demonstrate that a critical TGF-beta concentration threshold may specify a molecular switch to proapoptotic signaling profiles and apoptosis.
9	16207831	Using a unique system of conditionally immortalized podocytes, it is demonstrated that autocrine TGF-beta2 induces G0/G1 arrest and differentiation under nonpermissive culture through Smad3-dependent induction of the cyclin-dependent kinase inhibitor p15(Ink4b) (Cdkn2b).
10	16207831	When exposed to recombinant TGF-beta1 (or TGF-beta2), nonpermissive culture podocytes switch to G2/M arrest and apoptosis, selectively at advanced TGF-beta concentrations and specifically in association with suppression of Cdkn2b and activation of proapoptotic p38 mitogen-activated protein kinase.
11	16207831	Autocrine TGF-beta2/Smad3/Cdkn2b signaling in podocytes specifies G0/G1 arrest associated with podocyte differentiation, whereas increasing TGF-beta concentrations beyond a critical threshold induces G2/M block and apoptosis associated with selective p38 mitogen-activated protein kinase activation and with suppression of Cdkn2b.
12	16207831	In summary, the results suggest a new functional requirement of TGF-beta2 in growth arrest and differentiation of murine podocytes in vitro and demonstrate that a critical TGF-beta concentration threshold may specify a molecular switch to proapoptotic signaling profiles and apoptosis.
13	32583562	Smad3 signaling and transgelin expression are often activated during puromycin aminonucleoside (PAN)-induced podocyte injury.
14	32583562	The effects of SIS3 on the expression of the podocyte cytoskeletal proteins transgelin, p15^INK4B , phosphor-smad3, phosphor-JAK/stat3, the apoptotic marker cleaved caspase 3, and c-myc were investigated using western blot.
15	32583562	Transgelin expression and Smad3 phosphorylation were increased in the MPC5 cell line with prolonged PAN treatment.
16	32583562	In addition, c-myc expression, p15^INK4B , and JAK phosphorylation were all increased after treatment with PAN.
17	32583562	Moreover, stimulating podocytes directly with TGFβ-1 also led to enhanced expression of transgelin or phosphor-JAK/stat3, and this could be inhibited by SIS3.
18	32583562	In conclusion, transgelin expression was induced through the Smad3 signaling pathway during PAN-induced podocyte injury, and the resulting abnormal distribution of F-actin and the enhanced expression of transgelin could be reversed by blockade of this pathway.
19	32583562	Smad3 signaling and transgelin expression are often activated during puromycin aminonucleoside (PAN)-induced podocyte injury.
20	32583562	The effects of SIS3 on the expression of the podocyte cytoskeletal proteins transgelin, p15^INK4B , phosphor-smad3, phosphor-JAK/stat3, the apoptotic marker cleaved caspase 3, and c-myc were investigated using western blot.
21	32583562	Transgelin expression and Smad3 phosphorylation were increased in the MPC5 cell line with prolonged PAN treatment.
22	32583562	In addition, c-myc expression, p15^INK4B , and JAK phosphorylation were all increased after treatment with PAN.
23	32583562	Moreover, stimulating podocytes directly with TGFβ-1 also led to enhanced expression of transgelin or phosphor-JAK/stat3, and this could be inhibited by SIS3.
24	32583562	In conclusion, transgelin expression was induced through the Smad3 signaling pathway during PAN-induced podocyte injury, and the resulting abnormal distribution of F-actin and the enhanced expression of transgelin could be reversed by blockade of this pathway.