Cloning and characterization of human IC53-2, a novel CDK5 activator binding protein

Xie, Yihu; He, Xiang; Tang, Yingjie; Li, Jinjun; Pan, Zhi Mei; Qin, Wen; Wan, Da Fang; Gu, Jiafeng

doi:10.1038/sj.cr.7290153

Cited by 10 publications

(11 citation statements)

References 15 publications

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“…However, a similar NF-kBsuppressive effect of CDK5RAP3 was not observed in our study using HCC cells, and this could probably be attributed to some tissue-specific effects. In contrast, overexpression of the CDK5RAP3 isoform has been reported to promote cell proliferation of HCC cells (7). Recently, CDK5RAP3 has been shown to be overexpressed in lung adenocarcinoma (16).…”

Section: Discussionmentioning

confidence: 99%

“…More recently, CDK5RAP3 has been found to be underexpressed in head and neck cancers, and forced expression of CDK5RAP3 can negatively regulate NF-kB activity (5), which suggests that CDK5RAP3 may function as a tumor suppressor. On the contrary, stable overexpression of the CDK5RAP3 isoform has been shown to promote hepatocellular carcinoma (HCC) and cardiac cell proliferation (6,7), which indicates, furthermore, that CDK5RAP3 may enhance cell growth.…”

Section: Introductionmentioning

confidence: 99%

“…The expression of the human CDK5RAP3 isoform (IC53-2) has previously been shown to promote the proliferation of HCC cells (7). To study the effect of the full-length (FL) form of CDK5RAP3 on growth properties of HCC cells, we conducted a colony formation assay in human HCC cell lines with transient overexpression and knockdown of CDK5RAP3.…”

Section: Cdk5rap3 Enhanced Cell Proliferation and Tumorigenicity Of Hmentioning

confidence: 99%

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Overexpression of a Novel Activator of PAK4, the CDK5 Kinase–Associated Protein CDK5RAP3, Promotes Hepatocellular Carcinoma Metastasis

et al. 2011

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The CDK5 kinase regulatory subunit-associated protein 3 (CDK5RAP3 or C53/LZAP) regulates apoptosis induced by genotoxic stress. Although CDK5RAP3 has been implicated in cancer progression, its exact role in carcinogenesis is not well established. In this article, we report that CDK5RAP3 has an important prometastatic function in hepatocarcinogenesis. An examination of human hepatocellular carcinoma (HCC) samples revealed at least twofold overexpression of CDK5RAP3 transcripts in 58% (39/67) of HCC specimens when compared with corresponding nontumorous livers. CDK5RAP3 overexpression was associated with more aggressive biological behavior. In HCC cell lines, stable overexpression of CDK5RAP3 promoted, and small interfering RNA-mediated knockdown inhibited, tumorigenic activity and metastatic potential. We found that overexpression of CDK5RAP3 and p21-activated protein kinase 4 (PAK4) correlated in human HCCs, and that CDK5RAP3 was a novel binding partner of PAK4, and this binding enhanced PAK4 activity. siRNA-mediated knockdown of PAK4 in CDK5RAP3-expressing HCC cells reversed the enhanced cell invasiveness mediated by CDK5RAP3 overexpression, implying that PAK4 is essential for CDK5RAP3 function. Taken together, our findings reveal that CDK5RAP3 is widely overexpressed in HCC and that overexpression of CDK5RAP3 promotes HCC metastasis through PAK4 activation. Cancer Res; 71(8); 2949-58. Ó2011 AACR.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Cdk5rap3 Enhanced Cell Proliferation and Tumorigenicity Of Hmentioning

confidence: 99%

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Overexpression of a Novel Activator of PAK4, the CDK5 Kinase–Associated Protein CDK5RAP3, Promotes Hepatocellular Carcinoma Metastasis

et al. 2011

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“…Cyclin dependent kinase Cdk5 is a serine/threonine kinase which dimerizes with activator subunits of either 35 or 39 kDa (Ching et al, 2002;Wang et al, 2006). This complex is reported to inhibit neuronal apoptosis by up-regulating Bcl-2 , control postsynaptic density 95 and NMDA receptor clustering at synapses (Morabito et al, 2004), modulate GTP-dependent secretion by neutrophils (Rosales et al, 2004) and stimulate cell growth (Xie et al, 2003). cDNAs for Cdk5 activator binding proteins designated C42, C48, and C53 were cloned and C42 inhibits Cdk5 activation (Ching et al, 2002).…”

Section: Metabolismmentioning

confidence: 99%

Gene expression in diapause-destined embryos of the crustacean, Artemia franciscana

Qiu

Tsoi

MacRae

2007

Mechanisms of Development

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Diapause-destined embryos of the crustacean Artemia franciscana cease development as gastrulae, encyst, and enter a resting stage characterized by greatly reduced metabolic activity and extreme stress resistance. To better understand diapause induction and maintenance in Artemia embryos gene expression was analyzed by subtractive hybridization at two days post-fertilization, a time early in this developmental process. Eighty-five of 264 cDNA clones sequenced matched GenBank entries and they fell into categories designated as environmental information processing, cellular processes, genetic information processing and metabolism. Semi-quantitative RT-PCR of cDNAs populating the subtractive library identified seventeen up-regulated and four down-regulated transcripts, the former including those encoding a human transcription cofactor homologue, three small heat shock proteins, putative cell growth suppressor proteins and several enzymes. As examples, p8 may modulate gene expression during diapause in Artemia embryos. BRCA1 associated protein-1 (BAP1) and other functionally related proteins may influence cell growth and division during transition into diapause, a time when these processes are inhibited, whereas small heat shock proteins protect embryos from stress. This study represents the first systematic molecular characterization of diapause in crustaceans. Several differentially expressed genes were identified, expanding the repertoire of proteins potentially modified during diapause and suggesting mechanistic pathways indigenous to the initiation and maintenance of this physiological state.

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“…Relative quantification of cytokine mRNAs (IFN-b, IFNc, IL-12, TNF-a, IL-6, IL-17, or IL-10) (2,5,12,20) in comparison to transcripts of the b-actin gene (endogenous control) (19) was performed in real-time polymerase chain reaction (PCR) using a SuperScript Ò SYBR Ò Green III Platinum One-Step qRT-PCR kit (Invitrogen).…”

Section: Relative Quantification Of Cytokine Mrnasmentioning

confidence: 99%

Human Papillomavirus Vaccine-Induced Cytokine Messenger RNA Expression in Vaccinated Women

et al. 2015

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The objective of this work was to evaluate the influence of human papillomavirus (HPV) vaccination on peripheral blood mononuclear cell (PBMC) proliferation and cytokine gene transcription. PBMCs isolated after HPV immunization were incubated with HPV vaccine, phytohemagglutinin, or buffer. Cell proliferation was assessed by MTT reduction assay. RNA was extracted from PBMCs, and the relative concentration of cytokine messenger RNA (mRNA) transcripts (IFN-β, IFN-γ, IL-12, TNF-α, IL-6, IL-17, or IL-10) relative to transcription of the β-actin gene was determined by real-time polymerase chain reaction. PBMC proliferation in response to HPV vaccine and PHA were greater than that observed in unstimulated cells (p<0.001). Cytokine mRNAs were upregulated in stimulated PBMC cultures. The median increase in vaccine-stimulated cultures was: IFN-β=334.4-fold; IL-12=46.33-fold; IFN-γ=12.64-fold; IL-6=9.07-fold; IL-17=7.33-fold; IL-10=6.47-fold; and TNF-α=2.36-fold. The IFN-β expression was significantly higher (p<0.05). Proliferative PBMC responses and multiple cytokine gene expression were detected in women who received the HPV vaccine.

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Cloning and characterization of human IC53-2, a novel CDK5 activator binding protein

Cited by 10 publications

References 15 publications

Overexpression of a Novel Activator of PAK4, the CDK5 Kinase–Associated Protein CDK5RAP3, Promotes Hepatocellular Carcinoma Metastasis

Overexpression of a Novel Activator of PAK4, the CDK5 Kinase–Associated Protein CDK5RAP3, Promotes Hepatocellular Carcinoma Metastasis

Gene expression in diapause-destined embryos of the crustacean, Artemia franciscana

Human Papillomavirus Vaccine-Induced Cytokine Messenger RNA Expression in Vaccinated Women

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