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CCND1 — PCNA

Pathways - manually collected, often from reviews:

• BioCarta p53 signaling pathway: RB/E2F-1 complex (E2F1-RB1) → CDK4/CYCLIN D1/PCNA complex (CDK4-CCND1-PCNA) (modification, collaborate)
  
• BioCarta p53 signaling pathway: CDK4/CYCLIN D1/PCNA complex (CDK4-CCND1-PCNA) → p21 (CDKN1A) (modification, activates)
• BioCarta p53 signaling pathway: CDK4/CYCLIN D1/PCNA complex (CDK4-CCND1-PCNA) → RB (RB1) (modification, activates)
• BioCarta p53 signaling pathway: CDK4/CYCLIN D1/PCNA complex (CDK4-CCND1-PCNA) → PCNA (modification, collaborate)
• BioCarta p53 signaling pathway: CDK4/CYCLIN D1/PCNA complex (CDK4-CCND1-PCNA) → CYCLIN D1 (CCND1) (modification, collaborate)
• BioCarta p53 signaling pathway: CDK4/CYCLIN D1/PCNA complex (CDK4-CCND1-PCNA) → CDK4 (modification, collaborate)
• BioCarta p53 signaling pathway: PCNA → CYCLIN D1 (CCND1) (modification, collaborate)
• BioCarta il-2 receptor beta chain in t cell activation: cyclins (CCNE1/CCND2/CCND1/CCNH/CCND3/CCNB1/CCNA1) → PCNA (cell proliferation, activates)
• KEGG Cell cycle: PCNA → Complex of CCND1-CCND2-CCND3-CDK4-CDK6 (protein-protein, inhibition)
  

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: PCNA — CCND1 (direct interaction, pull down) Matsuoka et al., J Biol Chem 1994*
• IRef Biogrid Interaction: PCNA — CCND1 (physical association, affinity chromatography technology) Xiong et al., Genes Dev 1993*
• IRef Biogrid Interaction: PCNA — CCND1 (physical association, affinity chromatography technology) Zhang et al., Mol Biol Cell 1993
• MIPS CORUM Cell cycle kinase complex CDC2: Cell cycle kinase complex CDC2 complex (CCNB1-CCNB2-CCND1-CDK1-CDKN1A-PCNA) Zhang et al., Mol Biol Cell 1993
• MIPS CORUM Cell cycle kinase complex CDK2: Cell cycle kinase complex CDK2 complex (CCND1-CDK2-CDKN1A-PCNA) Zhang et al., Mol Biol Cell 1993
• MIPS CORUM Cell cycle kinase complex CDK4: Cell cycle kinase complex CDK4 complex (CCND1-CDK4-CDKN1A-PCNA) Zhang et al., Mol Biol Cell 1993
• MIPS CORUM Cell cycle kinase complex CDK5: Cell cycle kinase complex CDK5 complex (CCND1-CCND3-CDK5-CDKN1A-PCNA) Zhang et al., Mol Biol Cell 1993
• IRef Corum Interaction: Complex of PCNA-CCND1-CDK2-CDKN1A (association, anti bait coimmunoprecipitation) Zhang et al., Mol Biol Cell 1993
• IRef Corum Interaction: Complex of PCNA-CDK4-CDKN1A-CCND1 (association, anti bait coimmunoprecipitation) Zhang et al., Mol Biol Cell 1993
• IRef Corum Interaction: Complex of CCNB2-CDKN1A-CCNB1-PCNA-CDK1-CCND1 (association, anti bait coimmunoprecipitation) Zhang et al., Mol Biol Cell 1993
• IRef Corum Interaction: Complex of CCND1-PCNA-CCND3-CDK5-CDKN1A (association, anti bait coimmunoprecipitation) Zhang et al., Mol Biol Cell 1993
• IRef Hprd Interaction: Complex of 17 proteins (in vivo) Xiong et al., Genes Dev 1993*
• IRef Hprd Interaction: PCNA — CCND1 (in vitro) Matsuoka et al., J Biol Chem 1994*
• IRef Ophid Interaction: PCNA — CCND1 (aggregation, interologs mapping) Brown et al., Bioinformatics 2005
• IRef Ophid Interaction: PCNA — CCND1 (aggregation, confirmational text mining) Matsuoka et al., J Biol Chem 1994*

Text-mined interactions from Literome

Paramio et al., Mol Cell Biol 1999 : The characteristics of this process indicate that K10 and K16 act on the retinoblastoma ( Rb ) pathway, as ( i ) K10 induced inhibition is hampered by cotransfection with viral oncoproteins which interfere with pRb but not with p53 ; ( ii ) K10 mediated cell growth arrest is rescued by the coexpression of specific cyclins, cyclin dependent kinases (CDKs), or cyclin-CDK complexes ; ( iii ) K10 induced inhibition does not take place in Rb-deficient cells but is restored in these cells by cotransfection with pRb or p107 but not p130 ; ( iv ) K16 efficiently rescues the cell growth arrest induced by pRb in HaCaT cells but not that induced by p107 or p130 ; and ( v ) pRb phosphorylation and cyclin D1 expression are reduced in K10 transfected cells and increased in K16 transfected cells
Sekiguchi et al., Oncogene 1999 : Expression of exogenous cyclin D1 , SV40 large T antigen or CCG1/TAF(II)250 increased cyclin A expression at 39.5 degrees C. Coexpression of HPV16 E7 and adenovirus E1b19K, which blocks apoptosis, rescued the proliferation of tsBN462 cells at 38.5 degrees C
Dierov et al., J Cell Biochem 1999 : This increased kinase activity was accompanied by an elevated level of cyclin D1 protein and increased G1 cyclin/cdk complex formation
Padmanabhan et al., J Neurosci 1999 : Analysis of the different cell cycle regulatory elements in this model revealed that apoptosis is preceded by an increase in the level of cyclin E protein, with elevated nuclear levels of cyclin D1 and with enhanced activity of the cyclin D1- and E- associated kinases
Sinibaldi et al., Oncogene 2000 (Cell Transformation, Neoplastic) : The kinase activities of cyclin D/CDK4, 6 and cyclin E/CDK2 complexes were only slightly elevated, consistent with the findings that coordinate increases in p21, cyclin D1 and cyclin E resulted in an increase in cyclin/CDK/p21 complexes
Teoh et al., Hepatology 2002 (Reperfusion Injury) : Preconditioning was associated with entry of hepatocytes into the cell cycle within 2 hours of subsequent IR, as indicated by proliferating cell nuclear antigen ( PCNA ) nuclear staining, induction of cyclin D1 and numerous mitotic figures ; in the absence of preconditioning, such changes were not seen until 24 hours
Calbó et al., J Biol Chem 2002 : Our data also demonstrate that ectopic overexpression of either cyclin is sufficient to induce mitogen independent growth in human T98G and Rat-1 cells, although the effects of cyclin D1 require downstream activation of cyclin E-CDK2 activity
Frederick et al., Mol Cell Neurosci 2004 : IGF-I enhanced FGF-2 induction of cyclin D1 , activation of G ( 1 ) cyclin-cyclin dependent kinase (cdk) complexes, and hyperphosphorylation of retinoblastoma protein ( pRb )
Zhao et al., J Cell Biochem 2004 (Breast Neoplasms) : In analyses of key cell-cycle regulating proteins, we observed that GFP-ER expression had no affect on the protein levels of cyclin D1 , cyclin E, or p27, a cyclin dependent kinase (Cdk) inhibitor
Reddy et al., Cancer Res 2005 (Cell Transformation, Neoplastic...) : Although cyclin D1 binds and activates cyclin dependent kinase 4 (Cdk4) , thereby mediating activation of a program of E2F dependent gene expression, it has been suggested that the oncogenic activities of cyclin D1 are independent of Cdk4
Srirangam et al., Clin Cancer Res 2006 (Breast Neoplasms...) : Ritonavir causes G1 arrest, depletes cyclin dependent kinases 2, 4, and 6 and cyclin D1 but not cyclin E, and depletes phosphorylated Rb and Ser473 Akt
Liu et al., J Neurosci 2006 : Our present study shows that c-Myc was significantly induced and that it inhibited p21 and induced proteins such as cyclin dependent kinases, cyclin D , and cyclin E, which are involved in the cell cycle process, along with phosphorylation of the retinoblastoma protein and Cdc2 ( cell division cycle 2 )
Sekine et al., Hepatology 2007 : Furthermore, cyclin D1 protein levels were not induced, and the expression of cyclins A, E, and proliferating cell nuclear antigen was delayed
Lee et al., Biol Pharm Bull 2007 (Lung Neoplasms) : PSC dose-dependently induced cyclin dependent kinase (CDK) inhibitor p21 expression, whereas the expression of cyclin D1 , cyclin A, CDK4, CDK2, and proliferating cell nuclear antigen ( PCNA ) were decreased by treatment with PSC
Takahashi-Yanaga et al., Cell Signal 2008 (Neoplasms) : Cyclin dependent kinases (CDKs) 4 and 6 are cyclin D1 binding partners, and activated cyclin D1/CDK4 and cyclin D1/CDK6 complex phosphorylate the retinoblastoma protein to induce the expression of target genes essential for S phase entry, resulting in facilitation of the progression from G1 to S phase
Lavine et al., Mol Endocrinol 2008 : Analysis of cyclin and cdk mRNA and protein abundance revealed that CCK overexpression increased cyclin A, cyclin B, cyclin E, cdk1, and cdk2 with no change in cyclin D1 , cyclin D2, cyclin D3, cdk4, or cdk6 in mouse and human islets
Santra et al., Nature 2009 (Melanoma) : Cyclin D1 degradation results from a direct interaction with FBXO31 and is dependent on the F-box motif of FBXO31 and phosphorylation of cyclin D1 at Thr 286, which is known to be required for cyclin D1 proteolysis
Meng et al., Cell cycle (Georgetown, Tex.) 2011 : In cyclin D1 ( -/- ) mouse embryonic fibroblasts ( MEFs ), cyclin D1a, but not cyclin D1b, reduced the cell spreading to a polarized morphology
Srirangam et al., J Thorac Oncol 2011 (Adenocarcinoma...) : Associated with G0/G1 arrest, ritonavir down-regulates cyclin dependent kinases, cyclin D1 , and retinoblastoma protein phosphorylation
Choi et al., Cancer Cell 2012 (Mammary Neoplasms, Experimental...) : Ubiquitous shutdown of cyclin D1 or inhibition of cyclin D-associated kinase activity in mice bearing ErbB2-driven mammary carcinomas triggered tumor cell senescence, without compromising the animals ' health
Schulze et al., Proc Natl Acad Sci U S A 1995 : Ectopic expression of cyclin D1 triggers premature activation of the cyclin A promoter by E2F, and this effect is blocked by the tumor suppressor protein p16INK4
Pagano et al., Genes Dev 1994 : Altogether, these results indicate that down-regulation of cyclin D1 is necessary for PCNA relocation and repair DNA synthesis as well as for the start of DNA replication
Schulze et al., Mol Cell Biol 1996 : Overexpression of cyclin D1 restores cyclin A transcription in suspended cells and rescues them from cell cycle arrest
Haas et al., Oncogene 1997 (Cell Transformation, Neoplastic) : We demonstrate that both cyclin D1 and CDK4 functionally depend on active Myc to exert their potential as oncogenes and vice versa that the transforming ability of Myc requires functional cyclin D/CDK complexes