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Emerging Roles for Ciz1 in Cell Cycle Regulation and as a Driver of Tumorigenesis

Emerging Roles for Ciz1 in Cell Cycle Regulation and as a Driver of Tumorigenesis

Ciz1 was discovered in a S. cerevisiae yeast two-hybrid screen that identified cyclin E-p21 binding partners, although Ciz1 could interact with p21 directly [47]. Ciz1 appears to be unique to vertebrates; it is conserved in mammals, with partial conservation in birds and fish. Ciz1 is a non-essential gene in mice, with Ciz1 null mice showing no severe developmental defects [48]. However, Ciz1 interacts with several proteins that contribute to regulation of cellular proliferation, including transcriptional regulators, cell cycle regulators including cyclin E, cyclin A, CDK2, p21 and proteins that are not directly related to DNA replication (Appendix A Table A1 and references therein). The only functional interactions sites within Ciz1 that have been identified thus far are the conserved cyclin-binding motifs that mediate direct interactions with cyclin A2 and cyclin E [42]. Mutation of the cyclin-binding motifs demonstrated that Ciz1 interactions with cyclin E and cyclin A-CDK2 are essential for its DNA replication function, as mutations within Ciz1 that prevent cyclin binding are inactive in cell-free DNA replication assays [42]. In addition, Ciz1 contributes to cell cycle regulation, spermatogenesis and possibly cancer biology through direct interactions with cyclin A1/A2 that correlate with Ciz1 function in DNA replication and DNA repair respectively [31,42].
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Pocket proteins and cell cycle regulation in inner ear development

Pocket proteins and cell cycle regulation in inner ear development

Among the group of E2F family members that interact with the pocket proteins (Figure 3), E2F1, E2F2 and E2F3a are consid- ered potent transcriptional activators, binding according to our current understanding, exclusively to RB1 and peaking in expres- sion during the G1-S transition (Dyson, 1998). Consequently, as expected, combined ablation of all three activator E2Fs results in severe deregulation of E2F-target gene expression, impairing the capacity of cell proliferation and highlighting the importance of the activator complexes in cell cycle progression (Wu et al., 2001). In contrast, repressor E2Fs are expressed in quiescent cells and appear to be involved with cell cycle exit and differentiation (Dimova and Dyson, 2005). Given the crucial role of the activator E2Fs in the cell cycle regulation and direct interaction with RB1, one would predict that, similar to the loss of Rb1 or any of the remaining pocket proteins (Table 1), specific loss of any of the activators should have devastating effects on development and organogenesis. However, the conditional deletion of the activator E2Fs have failed to demonstrate a unique requirement for any single E2F, suggesting that loss of individual E2Fs or specific combinations can be functionally compensated by other related family members (Wu et al., 2001). The only exception was observed in embryos lacking E2F3, which have reduced viability presumably because of a defect in proliferation in certain cell types, such as fibroblasts (Humbert et al., 2000, Saavedra et al., 2002). Another contradiction is that the majority of double null mice for both Rb1 and any of the activator E2Fs survive to birth (Table 1), especially the combination of Rb -/- E2F2 -/- seems to
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Cdks, cyclins and CKIs: roles beyond cell cycle regulation

Cdks, cyclins and CKIs: roles beyond cell cycle regulation

Cell cycle control and stem cell self-renewal are two closely related processes. It is well-established that pluripotent embryonic stem cells (ESCs) possess a distinctive mode of cell cycle regulation characterized by rapidly alternating rounds of S and M phases that are interspersed by short gap phases (Becker et al., 2006; Burdon et al., 2002; Singh and Dalton, 2009). This property enables them to undergo the massive expansions in cell number necessary in early embryogenesis. As development proceeds, a gradual decline in the overall rate of cell cycle progression (which is mainly attributed to a lengthening of G1) accompanies the acquisition of more restricted cell fates in committed progenitors, ultimately culminating in complete cell cycle withdrawal as post-mitotic cells are generated. Considering the correlation between cell cycle kinetics and stem cell identity, it was perhaps not too surprising when it was first reported that cell cycle regulators actively participate in the specification of cell fate. This is particularly well studied in the context of neurodevelopment, in which an increase in G1 duration caused by chemical inhibition of Cdk kinase activity (Calegari and Huttner, 2003) or germline loss of G1 kinases (Lim and Kaldis, 2012) was sufficient to trigger premature neuron formation in neural stem cells (NSCs). As such, G1 lengthening was purported as a cause, rather than a consequence, of neuronal differentiation. There is now substantial evidence supporting a direct involvement of cell cycle regulators in the determination of division outcome, i.e. proliferation versus differentiation. However, it remains unclear how prolonging G1 induces differentiation mechanistically, other than the hypothesis that because G1 is the period of the cell cycle in which cells are exposed to extrinsic differentiating stimuli, spending more time in G1 should arguably lead to an accumulation of cell fate determinants to levels sufficient for them to exert an effect (Dehay and Kennedy, 2007; Götz and Huttner, 2005). Although this has been a compelling explanation thus far, recent studies are beginning to shed light on how changes in Cdk activity can modify intrinsic cell factors to influence cell fate.
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HE4 overexpression decreases pancreatic cancer Capan-1 cell sensitivity to paclitaxel via cell cycle regulation

HE4 overexpression decreases pancreatic cancer Capan-1 cell sensitivity to paclitaxel via cell cycle regulation

the ovarian cancer cell line SKOV3 [37]. The common involvement of WAP domain factors in drug sensitivity points to the possibility that these effects could be medi- ated by the protease inhibitor activity. In this study, we observed that while HE4 overexpression could counter- act the paclitaxel-caused inhibition of cell proliferation, HE4 knockdown enhanced the drug effects. Moreover, HE4 appeared to affect drug sensitivity through modu- lation of cell cycle regulators such as PCNA and p21 in both Capan-1 and Suit-2 PDAC cell lines. As illustrated in Fig. 10, it is possible that HE4 directly inhibited a pro- tease responsible for the degradation of PCNA and/or other cell cycle regulators to promote DNA synthesis. Alternatively, the HE4 protease inhibitor activity could affect other factors up- or down-stream of DNA synthe- sis. For example, Paclitaxel was known to impede the cell cycle progression by stabilizing the microtubule. HE4 could affect the function of a factor(s) involved in micro- tubule assembly to directly counteract the effect of Pac. In any case, the HE4 effects would converge with those of paclitaxel on the level of cell cycle regulation. Further studies are required to determine the exact mechanism of HE4-mediated changes in paclitaxel sensitivity.
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miRNA involvement in cell cycle regulation in colorectal cancer cases

miRNA involvement in cell cycle regulation in colorectal cancer cases

metaphase checkpoints, are the predominant mechanisms of cell cycle regulation [4]. Uncontrolled growth is the hallmark of cancer, and as such perturbations in the cell cycle that downregulate cell cycle inhibitors, such as Rb, or upregulate cell cycle promoters, such as CDK activators, contribute to carcinogenesis [2]. MiRNAs, small, non-coding regulatory molecules, have been long established as post-transcriptional regulators of mRNA expression [5, 6]. MiRNAs have further been identified as a means of cell cycle control, through their involvement in the regulation of checkpoints as well as DNA repair [4, 7], and through the downregulation of cyclins, CDKs, cyclin-dependent kinase inhibitors (CKIs) and Rb [7]. In this way, miRNAs can act as oncogenes as well as tumor suppressors. Transcription Factors (TFs), including MYC and members of the E2F family, and miRNAs, such as the miR-17~92 and miR-106b~25 clusters, form feed-forward, feedback, and autoregulatory loops, further complicating the regulation of the cell cycle [4, 7, 8].
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Role of Cks85A in cell cycle regulation

Role of Cks85A in cell cycle regulation

Cdks are a highly conserved family of protein kinase. They were first identified in budding yeast Saccharomyces cerevisiae (Nurse and Bissett, 1981) and called Cdc28 and in fission yeast Schizosaccharomyces pombe (Beach et al., 1982) and called Cdc2. In higher eukaryotes there are several different Cdks which have roles in different stages of the cell cycle. There are several different Cdks in Drosophila melanogaster but Cdk1 (Cdc2), Cdk2 (Cdc2c) and Cdk4 are the critical ones in the Drosophila cell cycle (Lee and Orr-Weaver, 2003). Cell cycle regulation is not the only role of the Cdk/Cyclin complexes; they have other functions that include regulation of transcription, DNA repair, differentiation and apoptosis. Cdk7/Cyclin H is one such example, and has a role in basal transcription (Larochelle et al., 1998).
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CtrA Is Nonessential for Cell Cycle Regulation in Rhodobacter sphaeroides

CtrA Is Nonessential for Cell Cycle Regulation in Rhodobacter sphaeroides

Like in C. crescentus , CtrA homologs have been shown to play essential or important roles in cell viability and cell cycle regulation in Sinorhizobium meli- loti [4], Brucella abortus [9] [10], Agrobacterium tumefaciens [4], and Rickettsia prowazekii [4] [11]. However, CtrA was shown to be nonessential in both Rho- dobacter capsulatus [12] [13] and Ruegeria sp . TM 1040 [14]. Both microarray and proteomic expression analysis of a ctrA mutant in R. capsulatus revealed that CtrA is not essential for its cell cycle effects but it is an important regulator that controls over 225 genes, including those involved in motility, gene ex- change, gas vesicle formation, and synthesis of transcriptional regulators and signal transduction proteins [12] [15]. While R. capsulatus and Rugeria sp. TM1040 divide symmetrically, other species like A. tumefaciens , B. abortus , C. crescentus , and S. meliloti divide asymmetrically. These findings could sug- gest that CtrA does not possess as essential a role in cell cycle regulation in Rhodobacterales as it does in other orders such as Caulobacterales and Rhizo- biales .
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Yeast ASF1 Protein Is Required for Cell Cycle Regulation of Histone Gene Transcription

Yeast ASF1 Protein Is Required for Cell Cycle Regulation of Histone Gene Transcription

ASF1, which lacks this acidic region. The truncated Because HIR1 and HIR2 are required for the cell LexA-ASF1 protein showed an even stronger interaction cycle repression of HHT1-HHF1 and HHT2-HHF2 as with GAD-HIR1 in a two-hybrid assay (Table 2). This well as HTA1-HTB1 (Osley and Lycan 1987), we used shows that the HIR1-ASF1 interaction was not mediated Northern analysis to determine the effect of mutation via the acidic stretch of ASF1. of ASF1 on HHF2 transcription. The results (Figure 1, In a separate search, we used the truncated lexA-ASF1 C and D) show that, like hir1 mutants, asf1 mutants clone as bait and again obtained only one interacting also fail to repress HHF2 transcription in response to plasmid. This plasmid encoded a fusion of the carboxy- hydroxyurea treatment. HTA2-HTB2 transcription is terminal half of SAS4 to GAD. SAS4 (something about also under cell cycle control and is repressed in response silencing) was originally identified because sas4 muta- to hydroxyurea. However, this repression is indepen- tions restore silencing in strains containing a mutated dent of HIR1 and HIR2 (Osley and Lycan 1987; Figure HMR locus (Xu 1999). Identification of a silencing pro- 1, E and F). Repression of HTA2-HTB2 is similarly unaf- tein, SAS4, in a two-hybrid search with ASF1, which is fected by mutation of asf1 (Figure 1, E and F). This also implicated in silencing, was gratifying. The in vivo analysis shows that the pattern of transcriptional repres- significance of this interaction is under investigation. sion of the histone gene pairs is similar in asf1 and hir1 asf1 mutants have a Hir ⫺ phenotype: In wild-type cells, mutants. Both mutants are defective in repression of the four histone gene loci (HTA1-HTB1, HTA2-HTB2, transcription of HTA1-HTB1 and HHT2-HHF2, and nei- HHT1-HHF1, and HHT2-HHF2) are only transcribed ther is defective in repression of HTA2-HTB2.
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Reovirus-Induced Alterations in Gene Expression Related to Cell Cycle Regulation

Reovirus-Induced Alterations in Gene Expression Related to Cell Cycle Regulation

GAC ATC AAC AT-3⬘; reverse primer, 5⬘-TCC CGG CAA AAA CAA ATA AG-3⬘), and ␤-actin (BC004251) (forward primer, 5⬘-GAA ACT ACC TTC AAC TCC ATC-3⬘; reverse primer, 5⬘-CGA GGC CAG GAT GGA GCC GCC-3⬘), yielding product sizes of 495, 506, 200, and 219 bp, respectively. PCR cycle conditions were 94°C for 30 s, 55°C for 30 s, and 72°C for 1 min for 25 cycles. Dilutions of cDNA were performed to determine the linear range for each primer pair. PCR products were resolved on a 2% agarose gel containing ethidium bromide and were visualized with UV light. Densitometric analysis was performed using a FluorS MultiImager System and Quantity One software (Bio- Rad, Hercules, Calif.).
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The role of CDC25C in cell cycle regulation and clinical cancer therapy: a systematic review

The role of CDC25C in cell cycle regulation and clinical cancer therapy: a systematic review

One of the most prominent features of tumor cells is uncontrolled cell proliferation caused by an abnormal cell cycle, and the abnormal expression of cell cycle-related proteins gives tumor cells their invasive, metastatic, drug-resistance, and anti-apoptotic abilities. Recently, an increasing number of cell cycle-associated proteins have become the candi- date biomarkers for early diagnosis of malignant tumors and potential targets for cancer therapies. As an important cell cycle regulatory protein, Cell Division Cycle 25C (CDC25C) participates in regulating G2/M progression and in mediating DNA damage repair. CDC25C is a cyclin of the specific phosphatase family that activates the cyclin B1/ CDK1 complex in cells for entering mitosis and regulates G2/M progression and plays an important role in checkpoint protein regulation in case of DNA damage, which can ensure accurate DNA information transmission to the daughter cells. The regulation of CDC25C in the cell cycle is affected by multiple signaling pathways, such as cyclin B1/CDK1, PLK1/Aurora A, ATR/CHK1, ATM/CHK2, CHK2/ERK, Wee1/Myt1, p53/Pin1, and ASK1/JNK-/38. Recently, it has evident that changes in the expression of CDC25C are closely related to tumorigenesis and tumor development and can be used as a potential target for cancer treatment. This review summarizes the role of CDC25C phosphatase in regulating cell cycle. Based on the role of CDC25 family proteins in the development of tumors, it will become a hot target for a new generation of cancer treatments.
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Gene Repression and Cell Cycle Regulation by PU.1 in Acute Myeloid Leukemia

Gene Repression and Cell Cycle Regulation by PU.1 in Acute Myeloid Leukemia

into S phase from G1 (126-127). As indicated above, E2F1 (when complexed with a DP) controls the transcription of genes essential for cell division; these include genes encoding cell cycle regulators (such as the cyclins indicated above), enzymes involved in nucleotide biosynthesis (such as thymidine kinase), and the main components of the DNA-replication machinery (126). The potency of E2F1 as a transcriptional activator has been shown through overexpression of the protein, which induces quiescent cells to re-enter the cell cycle (127-129). Furthermore, deregulation of E2F1 activity appears to be a characteristic of human cancers (125, 130). E2F1 is regulated via association with pRb; once pRb is phosphorylated by CDK-cyclin complexes, E2F1 is released. Thus, pRb restricts cell cycle progression by maintaining E2F1 and the disassociation of E2F1 from pRb drives proliferation (123). The idea that defects in regulation and inappropri- ate release of E2F1 might induce cancer, are illustrated by the fact that overexpression of E2F1 can induce transformation of primary cells (131-133). Moreover, Gibbs et al. have shown that deregulated expression of E2F1 blocks terminal myeloid differentiation, resulting in proliferation of immature myeloid cells (134). In addition to inducing prolif- eration, deregulated E2F1 activity can also trigger apoptosis (122, 126). This functional paradox of E2F1 has been investigated and the results demonstrate that E2F1 can have both oncogenic (through its role in cell cycle progression) and tumor-suppressive effects (through apoptosis induction) (130).
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The effective application of a discrete transition model to explore cell cycle regulation in yeast

The effective application of a discrete transition model to explore cell cycle regulation in yeast

The transient expression of Hcm1 is not required for the transient transcription of its target genes [13]. Because Hcm1 is subject to post-translational modification, it was suggested that this modification affects its activity during the cell cycle [13]. Since Hcm1 is a probable Cdk target [40] we examined if this regulation is mediated by either Cln3/Cdk, Cln1/Cdk1 or Clb5/Cdk (Figure 6). Simulations revealed that activation of Hcm1 by Cln3/ Cdk resulted in premature decline in the transcription of CLB2 in relation to S-phase (Figure 6B, upper panel). On the other hand, regulation by either Cln1/Cdk or Clb5/Cdk, showed the expected behavior (Figure 6B, middle and lower panels). In order to discriminate be- tween the latter two hypotheses, we examined the re- sponse of cells to pheromone treatment. Regulation by Clb5/Cdk showed an abnormal phenotype, namely some G1cells arrested after completion of S-phase (Figure 6C). Our simulations predict that Cln1/Cdk rather than Clb5/Cdk or Clb2/Cdk, is responsible for regulating the activity of Hcm1. All simulations in this report were done according to this prediction.
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Original Article Cullin-1 promotes cell proliferation via cell cycle regulation and is a novel in prostate cancer

Original Article Cullin-1 promotes cell proliferation via cell cycle regulation and is a novel in prostate cancer

A total of 142 pairs of human primary PCa tis- sues and their adjacent NCTs were collected between 2006 and 2009 at Huashan Hospital, Fudan University. These tissue samples were immediately snap-frozen in liquid nitrogen. All of the human materials were obtained with informed consent. The clinical information for the PCa patients is included in the Table 1. Two human PCa cell lines (PC-3, DU-145) and HEK- 293T cell line were purchased from the American Type Culture Collection (ATCC). DU- 145 and PC-3 cells were cultured in Ham’s F-12 media (Invitrogen, USA) with L-glutamine (300 mg/L, NaHCO3 1.5 g/L) and 10% FBS. HEK- 293T cells were cultured in DMEM. Cells were incubated with 5% CO 2 at 37°C.
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Original Article CDC5L contributes to malignant cell proliferation in human osteosarcoma via cell cycle regulation

Original Article CDC5L contributes to malignant cell proliferation in human osteosarcoma via cell cycle regulation

ing an effective and widely accepted approach for cancer therapy [12, 13]. CDC5L, as key reg- ulator for cell division cycle, has been shown to be overexpressed in OS, but its function signifi- cance remains unclear in OS cells. Thus, we conducted loss-of-function assay in OS cell lines Saos-2 and U2OS cells using siRNA trans- fection. Our results indicated that CDC5L silencing remarkably suppressed cell viability and colony formation in two OS cell lines. Furthermore, we found the inhibited cell prolif- eration is ascribed to G2/M phase arrest induced by CDC5L silencing, as confirmed by downregulation of CDK1, Cyclin B and PCNA expression.
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The Role of the Integrated Stress Response Kinase Gcn2 in Cell Cycle Regulation and Tumorigenesis

The Role of the Integrated Stress Response Kinase Gcn2 in Cell Cycle Regulation and Tumorigenesis

Next, we wanted to determine if p21 contributes to cell survival under amino acid deprivation. To do so, the shNT and shp21 MEF clones were cultured in complete media or media lacking leucine. After 72 hours, the viable cells were re-plated at low density in complete media. Virtually all shNT cells were able to recover from nutrient stress and form colonies. However, clonogenic survival was significantly reduced by approximately 40-50% in the two shp21 MEF clones after leucine deprivation (Figures II-6H). These results demonstrate that p21 is dispensable for cell growth under nutrient replete conditions but is critical for cell survival during the recovery from amino acid starvation. Furthermore, these results are consistent with another study which showed that p21 promotes cell survival under the combined stresses of complete amino acid and serum starvation independently of p53 88 .
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Morphogenesis signaling components influence cell cycle regulation by cyclin dependent kinase

Morphogenesis signaling components influence cell cycle regulation by cyclin dependent kinase

These results supported the Ras2-activated PKA pathway via Flo8 to be an important regulator of Cdc28. Previous genetic evidence by La Valle and Wittenberg suggested that Swe1 regulation of Cdc28 may be an effector of PKA [18]. Therefore, we directly tested if Swe1 function is mod- ulated by the PKA pathway. We found that deletions of RAS2, FLO8, or the filamentous-growth specific PKA cata- lytic subunit TPK2 [47] in otherwise wild-type cells each diminished Cdc28 Tyr19 phosphorylation, placing the PKA signaling upstream of Swe1 and Cdc28 (Figure 5A). Given the relationship between PKA and Swe1, we also tested if cdc28-E217V is modulated by SWE1. Strikingly, deletion of SWE1 conferred suppression of both growth and morphology defects of cdc28-E217V (Fig. 5B, C). Again, we asked if these effects were specific to Swe1 or if the absence of any negative regulator of CDK function would improve cdc28-E217V defects. Toward examining this question, we observed that deletion of the Cdc28 sto- ichiometic inhibitor SIC1 had only subtle effects on growth of cdc28-E217V cells [48].
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Aberrant Cell Cycle Regulation in Cervical Carcinoma

Aberrant Cell Cycle Regulation in Cervical Carcinoma

whether alterations of p16 might be involved in HPV-positive cervical cancers, Yoshinouchi looked for gene alterations and changes in the ability of the p16 protein to interact with CDK4 in 5 cervical cancer cell lines. No alteration of this gene was detected, and the p16 and CDK4 pro- teins were normally expressed. Additionally, the ability of p16 to interact with CDK4 was not abrogated in these cell lines. These cell lines were HPV-positive and carried wild-type p53 genes. These findings suggest that phosphorylation of pRb by CDK4 is not critical in the carcinogenesis or in the establishment of HPV-positive cervical cancer cell lines, since the HPV viral-transforming proteins E6 or E7 inactivate p53 and pRb tumor suppressor protein function, resulting in deregu- lated progression of the cell cycle. 38 So far, re-
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Novel Cell Cycle Regulation in Breast Cancer Treatment Resistance

Novel Cell Cycle Regulation in Breast Cancer Treatment Resistance

Claudin-low breast cancer is a newly categorized subtype. Previously, patients under this subtype were classified as basal-like; however, after DNA microarray studies were performed, it was found that a subset of tumours presented with low levels of the claudin genes. Claudins are needed for epithelial cell tight-tight junctions (Prat et al., 2010). Tumours in this subtype, which make up 5% to 10% of all breast cancers, show low expression for claudins 3, 4, and 7, as well as E-cadherin, a protein required for cell- cell junction (Perou, 2010; Perou et al., 2000; Prat and Perou, 2011). Furthermore, they are normally ER/PR/Her2 negative (Sabatier et al., 2014). Claudin-low tumours have shown an increase in immune cell infiltration, stem cell features, and features representing epithelial-mesenchymal transition (EMT). Some researchers believe claudin- low breast cancers derive from the lobules, mainly because they are associated with high grade tumours, have little differentiation and are able to infiltrate the immune cells (Prat et al., 2010; Sabatier et al., 2014). Similar to basal-like breast cancers, claudin-low breast cancers also have a poor prognosis and cannot benefit from targeted therapy, and, therefore, only chemotherapy is used as a form of treatment (Perou et al., 2000).
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Cell cycle and cell growth regulation by the CUL4-DDB1-ROC1 ubiquitin ligases

Cell cycle and cell growth regulation by the CUL4-DDB1-ROC1 ubiquitin ligases

hypothesis is that one of the CUL4-DDB1 ubiquitin ligases targets p53 for ubiquitination, probably through COP1 or one of DWD proteins. COP1 is composed of a RING finger domain and a WD40 repeat, and its catalytic activity could be boosted by recruiting another RING finger protein, ROC1, through CUL4-DDB1-DET1 complex. These hypotheses are worth to be tested in the future and would strengthen our understanding on CUL4 function, cell cycle regulation and apoptosis. p21, on the other hand, is more likely to be an authentic substrate of CUL4-DDB1, because p21 is accumulated in both DDB1-/- and DDB1-/- p53-/- double null mice, suggesting that p21 up-regulation is not due to transcriptional enhancement. One way to find out which DWD protein recruits p21 to CUL4-DDB1 is to test the bindings between p21 and DWD proteins one by one. This method may look tedious, but could be very effective, and is definitely worth to try.
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Glucose Regulation of Saccharomyces cerevisiae Cell Cycle Genes

Glucose Regulation of Saccharomyces cerevisiae Cell Cycle Genes

starvation affects CLN3 transcription (19, 36) and Cln3 translation (16). Glucose also increases the transcription of CLN3 in a process that requires a set of repeated elements upstream of the CLN3 open reading frame that are binding sites for the Azf1 protein (33). Little is known about nutri- ent regulation of BCK2 and CDC28; however, we have shown that these transcripts are upregulated when glucose is added to post-log-phase cells (55). In this report we char- acterize the glucose induction of CLN3, BCK2, and CDC28 mRNA. Induction of these genes requires the transport and metabolism of glucose but does not require the cAMP-, Tor-, RGT2/SNF3-, or HXK2-mediated nutrient signaling pathways. Our results suggest that a pathway that monitors glucose metabolism regulates transcription of cell cycle reg- ulatory genes.
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