CAND1 Binds to Unneddylated CUL1 and Regulates the Formation of SCF Ubiquitin E3 Ligase Complex

Zheng, Jian‐Yu; Xiaoming, Yang; Harrell, Jennifer M.; Ryzhikov, Sophia; Shim, Eun Hee; Lykke-Andersen, Karin; Wei, Ning; Sun, Hong; Kobayashi, Ryûji; Zhang, Hui

doi:10.1016/s1097-2765(02)00784-0

Cited by 278 publications

(321 citation statements)

References 22 publications

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“…32 Interaction between Cul1 and p120 CAND1 is required for SCF function, 33 but p120 CAND1 binds only to unneddylated Cul1. 11,34 For this reason, proper levels of neddylation may be important for SCF function.…”

Section: Discussionmentioning

confidence: 99%

Drosophila homolog of APP-BP1 (dAPP-BP1) interacts antagonistically with APPL during Drosophila development

Kim

et al. 2006

Cell Death Differ

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b-Amyloid precursor protein binding protein 1 (APP-BP1) was previously identified based on its binding to the carboxyl terminal of b-amyloid precursor protein. In this report, we have discovered that a mutation of dAPP-BP1 (Drosophila ortholog of APP-BP1) hinders tissue development, causes apoptosis in imaginal disc cells, and blocks the NEDD8 conjugation pathway. We show that dAPP-BP1 specifically binds the intracellular domain of APP-like protein (APPL). The dAPP-BP1 mutation partially suppresses the abnormal macrochaete phenotype of Appl d , while overexpression of dAPP-BP1 causes abnormal macrochaetes. When APPL is overexpressed, the normal bristle pattern in the fly thorax is disturbed and apoptosis is induced in wing imaginal discs. APPL overexpression phenotypes are enhanced by reducing the level of dAPP-BP1. APPL overexpression is shown to inhibit the NEDD8 conjugation pathway. APPL-induced apoptosis is rescued by overexpression of dAPP-BP1. Our data suggest that APPL and dAPP-BP1 interact antagonistically during Drosophila development.

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Section: Discussionmentioning

confidence: 99%

Drosophila homolog of APP-BP1 (dAPP-BP1) interacts antagonistically with APPL during Drosophila development

Kim

et al. 2006

Cell Death Differ

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“…Deneddylated cullins can displace the Skp1 and F-box proteins. Once the Nedd8 is displaced, Cand1 comes and binds to the complex thereby rendering the SCF complex inactive (Zheng et al, 2002). Through the yeast hybrid system, it was found that the binding part of MIF was JAB1/CSN5 (Kleemann et al, 2000).…”

Section: Mif and Cell Cyclementioning

confidence: 99%

Macrophage Migration Inhibitory Factor: a Potential Marker for Cancer Diagnosis and Therapy

Babu¹,

Chetal²,

Kumar³

2012

Asian Pacific Journal of Cancer Prevention

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Macrophage migration inhibitory factor (MIF) is a pluripotent cytokine which plays roles in inflammation, immune responses and cancer development. It assists macrophages in carrying out functions like phagocytosis, adherence and motility. Of late, MIF is implicated in almost all stages of neoplasia and expression is a feature of most types of cancer. The presence of MIF in almost all tumors and all stages of cancer makes it an interesting candidate for cancer therapy. This review explores the roles of MIF in neoplasia.

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“…Cullin is a family of scaffold proteins that are involved in various E3 ubiquitin ligases such as the SCF (ROC1-SKP1-cullin1/Cdc53-F box protein) complex; it has been reported that CAND1 may function as a negative regulator of SCF complex assembly. 19,20 As cullin-based ubiquitin ligases have important physiological roles such as cell cycle regulation and cell proliferation, we hypothesized that CAND1 expression would be regulated by miR-148a and that this mechanism would facilitate prostate cancer progression. We investigated whether CAND1 mRNA levels would change by transfecting miR-148a precursor in LNCaP cells (Figure 3a).…”

Section: Mir-148a Regulates Cand1 Expression In Lncap Cellsmentioning

confidence: 99%

miR-148a is an androgen-responsive microRNA that promotes LNCaP prostate cell growth by repressing its target CAND1 expression

Murata

Takayama

Katayama

et al. 2010

Prostate Cancer Prostatic Dis

132

105

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Recent advances in cancer biology reveal that microRNAs (miRNAs) are involved in the regulation of cancer-related genes, or they function as tumor suppressors or oncogenes. In prostate cancer, evidence has accumulated for the contribution of the androgen-dependent gene network to tumor growth, although the precise functions of miRNAs in prostate cancer remain to be investigated. Here, we identified androgen-responsive miRNAs by the short RNA sequencing analysis in LNCaP prostate cancer cells. Among 10 miRNAs with known sequences, we have determined that miR148a reduces the expression of cullin-associated and neddylation-dissociated 1 (CAND1), a negative regulator of SKP1-Cullin1-F-box (SCF) ubiquitin ligases, by binding to the 3 0 -untranslated region of CAND1 mRNA. CAND1 knockdown by small interfering RNA promoted the proliferation of LNCaP cells. Our study indicates the potential contribution of miR-148a to the growth of human prostate cancer.

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CAND1 Binds to Unneddylated CUL1 and Regulates the Formation of SCF Ubiquitin E3 Ligase Complex

Cited by 278 publications

References 22 publications

Drosophila homolog of APP-BP1 (dAPP-BP1) interacts antagonistically with APPL during Drosophila development

Drosophila homolog of APP-BP1 (dAPP-BP1) interacts antagonistically with APPL during Drosophila development

Macrophage Migration Inhibitory Factor: a Potential Marker for Cancer Diagnosis and Therapy

miR-148a is an androgen-responsive microRNA that promotes LNCaP prostate cell growth by repressing its target CAND1 expression

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