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Validated All-in-One™ qPCR Primer for SKP2(NM_005983.3) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
This gene encodes a member of the F-box protein family which is characterized by an approximately 40 amino acid motif, the F-box. The F-box proteins constitute one of the four subunits of ubiquitin protein ligase complex called SCFs (SKP1-cullin-F-box), which function in phosphorylation-dependent ubiquitination. The F-box proteins are divided into 3 classes: Fbws containing WD-40 domains, Fbls containing leucine-rich repeats, and Fbxs containing either different protein-protein interaction modules or no recognizable motifs. The protein encoded by this gene belongs to the Fbls class; in addition to an F-box, this protein contains 10 tandem leucine-rich repeats. This protein is an essential element of the cyclin A-CDK2 S-phase kinase. It specifically recognizes phosphorylated cyclin-dependent kinase inhibitor 1B (CDKN1B, also referred to as p27 or KIP1) predominantly in S phase and interacts with S-phase kinase-associated protein 1 (SKP1 or p19). In addition, this gene is established as a protooncogene causally involved in the pathogenesis of lymphomas. Alternative splicing of this gene generates 2 transcript variants encoding different isoforms. [provided by RefSeq].
Gene References into function
- crystal structure of the Cul1-Rbx1-Skp1-F boxSkp2 SCF complex
- The lower Cyclin A gene expression would predict drug resistance for acute leukemia patients.
- SKP2 is a major determinant of p27 levels in prostate cancer cells; overexpression of SKP2 may be one of the mechanisms that allow prostate cancer cells to escape growth control mediated by p27.
- role of Skp2 in breast cancer
- expressed in lymphoma: correlation with p27(Kip1) and proliferation index
- induction of Skp2 may be causally linked with decreased levels of p27 in prostate cancer and implicate PTEN in the regulation of Skp2 expression
- The activity of the ubiquitin ligase complex Skp1-Cul1/Cdc53-F-box protein Skp2 (SCF(Skp2)) and the proteasome were necessary for p130 degradation.
- S-phase kinase-associated protein 2 overexpression is associated with laryngeal squamous cell carcinomas
- Skp2 mRNA expression level was high in squamous cell carcinomas of the lung and was inversely related with the p27(Kip1) protein level
- Skp2 overexpression is associated with ovarian adenocarcinoma
- negatively charged amino acid is required for Skp2-Cks1 interaction and ubiquitination of p27Kip1
- SKP2's role does not include regulation of CDK9 expression
- hepatocyte growth factor suppresses HepG2 cell proliferation by directly increasing p27 expression and indirectly decreasing Skp2 expression, and beta 1-integrin modulates responsiveness of hepatoma cells by increasing Skp2.
- skp2 has a role in the downregulation of p27Kip1 by estrogens in breast cancer cells
- SCFSkp2 complex plays an important role in cell-cycle progression by determining the abundance of p57Kip2 and that of the related CDK inhibitor p27Kip1.
- increased p27 degradation through the ubiquitin-proteasome pathway could be regulated in pituitary tumors by changes in Skp2 expression
- Skp2 may be involved in Merkel cell tumorigenesis, but other factors may also influence cell proliferation in these tumors.
- Overexpression of Skp2 and Jab1 is associated with the reduction of p27(KIP1) expression, and may have a role in the progression of Oral Squamous Cell Carcinoma.
- induction of Skp2 and Cks1 degradation in G1 represents a principal mechanism by which APC/C(Cdh1) prevents the unscheduled degradation of SCF(Skp2-Cks1) substrates and maintains the G1 state
- F-box protein Skp2 is polyubiquitinated, and hence earmarked for destruction, by APC(CDH1)
- Skp2 protein expression is a significant independent poor prognostic marler in non-small cell lung carcinoma.
- the Skp2-p27kip1 pathway and the G1/S transition are regulated by RhoA, mDia, and ROCK
- down-regulation of Skp2 induces tumor cell-cycle arrest with a fatty acid synthase blockade
- Overexpression is associated with colorectal carcinogenesis and late metastasis to lymph nodes, whereas relative reduction of Skp2 is correlated with local invasion of primary carcinoma.
- Amplification and overexpression of SKP2 are associated with metastasis of non-small-cell lung cancers to lymph nodes.
- expression of p27, Skp2 & Ki67 was similar in normal secretory endometrium & endometrium from ovarian hyperstimulation; p27 is significantly lower while Skp2 and Ki67 are higher in endometrial carcinoma and endometrium from the proliferative phase
- S-phase kinase-associated protein 2 may have a role in progression of acute myelogenous leukemia
- SCFSkp2 is involved in controlling UBP43 protein levels and may play an important role in modulating type 1 IFN signaling
- SCFSkp2 mediates regulation of p27 stability and is regulated by tuberin
- Skp2 overexpression is closely associated with the suppression of p27 and the aggressiveness in NSCLC.
- Cytoplasmic expression of Skp2 defines a subset of aggressive melanomas and could represent another pathway of deregulation of the cell cycle.
- Downregulation of both Skp2 and p27 increased apoptosis synergistically, Skp2 in tumor cells suppresses apoptosis through Bcl-2 expression
- Data suggest that p107, in addition to its interaction with E2F, inhibits cell proliferation through the control of Skp2 expression and the resulting stabilization of p27.
- COX-2 contributes to the expression of Skp2 and poor survival in human gastric carcinomas
- SKP2 plays an oncogenic role in lung cancer and that SKP2 silencing may be useful in the treatment of lung cancer
- expression of Skp2, p27KIP1 and Ki-67 in 10 naevi, 15 superficial spreading melanomas, 10 nodular melanomas and 14 melanoma metastases
- Skp2 expression might play an important role in the development and progression in non-small cell lung cancer
- Skp2 siRNA inhibits the cell proliferation of oral squamous cell carcinoma cells
- BCR-ABL cells show transcriptional up-regulation of Skp2. Expression of a p27(Kip1) mutant unable of being recognized by Skp2 results in inhibition of proliferation of BCR-ABL cells.
- Skp2 is not required for the degradation of Cdt1 in S phase- this degradation is necessary for the optimum progression of cells through S phase
- Skp2-SCF provides an unexpected and direct mechanistic link between DNA recombination and the cell cycle.
- N-Ras(L61) transformed cells lack a G0-G1 arrest upon TGF-beta treatment due to absence of p27. which is degraded through an SKP2-dependent pathwawy.
- study demonstrated the existence of a subtype of high-grade, negative estrogen receptor breast carcinomas with high S-phase kinase-associated protein Skp2 and low cdk-inhibitor p27 levels
- overexpression of Skp2 through gene amplification may contribute to the pathogenesis of GBM, and overabundance of the protein might be a useful prognostic tool in patients with this disease
- MKP-1 proteolysis can be achieved via ERK and SCF(Skp2) cooperation, thereby sustaining ERK activation
- Data show that hepatitis B virus X protein blocks the ubiquitination of c-myc through a direct interaction with the F box region of Skp2 and destabilization of the SCF(Skp2) complex.
- In PC3 and DU145 cells, Skp2 is the main determinant in the PI3K/Akt-dependent regulation of p27(kip1)
- Data suggest that PTEN may regulate the expression of p27 by negatively regulating S phase kinase-associated protein 2 expression.
- Skp2 overexpression is highly representative of intrinsic biological aggressiveness and is associated with myxofibrosarcomas
- Results suggest that Skp2 may play an important role particularly in young breast cancer, and it is also considered to have strong independent prognostic potential and thus may prove to be a useful target for the treatment of breast cancer.
- Results suggest that Skp2 expression was significantly associated with malignancy, and the Skp2 protein level may be a valuable prognostic factor for epithelial ovarian carcinomas.
- The F-box protein Skp2, in addition to utilizing Cul1-Skp1, utilizes Cul4A-DDB1 to induce proteolysis of p27Kip1.
- High expression for Skp2 is associated with breast cancer
- These data demonstrate a critical role for FAK in the regulation of cyclin-dependent kinase inhibitors (CDKIs) through two independent mechanisms: Skp2 dependent and Skp2 independent.
- phosphatidylinositol 3-kinase-dependent up-regulation of Skp2 which directly associates with BRCA2, leading to BRCA2 degradation in the proteasome and vigorous cell proliferation in prostate cancer
- Skp2-cyclin A interaction serves to directly protect cyclin A-cyclin-dependent kinase (Cdk)2 from inhibition by p27 through competitive binding.
- UV induces p21 degradation through an Skp2 and ubiquitin-independent pathway
- Expression of AR protein in PC3-Lenti-AR cells resulted in transactivation of p21 and growth inhibition in culture and in mouse xenografts. Such inhibition was due to induced G1 arrest as documented by expression changes in p27 and p45(SKP2) proteins.
- Results describe the regulation of neddylation and deneddylation of cullin1 by Nedd8 in SCFSkp2 ubiquitin ligase by F-box protein and substrate.
- These results suggest that 1,25-dihydroxyvitamin D3 induces the formation of VDR/Sp1 complex and acts via a Sp1- and HDAC1-depedent pathway to inhibit p45Skp2 transcription.
- IKKalpha regulates growth pathway involving the p52/RelB-dependent transcriptional regulation of the skp2 gene.
- Skp2 is required for downregulation of p27Kip1 levels in melanoma cells; Skp2 expression level regulates melanoma cell growth, most likely through effects on cell proliferation.
- cyclin D1 expression is suppressed in Skp2 knockdown HeLa cells.
- Results show that complex formation between Cks1 and Skp2 causes conformational changes in both proteins in regions distant from the respective binding sites.
- Skp2 is rapidly degraded following cellular stimulation by the cytokine transforming growth factor beta (TGF-beta) and that this degradation stabilizes the cell cycle arrest protein p27.
- CKS1B influences myeloma cell growth and survival through SKP2- and p27(Kip1)-dependent and -independent mechanisms
- Skp2 overexpression is highly representative of biological aggressiveness of gallbladder carcinoma and is independently associated with poor overall survival.
- integrin beta1 has a role in inhibiting cell proliferation by preventing the Skp2-dependent degradation of p27(Kip1) via PI3K pathway
- Skp2 may play an important role in salivary adenoid cystic carcinoma development through the down-regulation of p27.
- Overexpression of Skp2 is associated with neuroendocrine lung tumors
- Results suggest that SKP2 has a major role in the regulation of p27 degradtion in human urothelial carcinoma.
- of Skp2 is a critical step for the suppression of cell proliferation by Tubocapsanolide A because ectoexpression of Skp2 effectively reversed Tubocapsanolide A-induced p27 up-regulation and growth inhibition in human lung cancer cells
- Data suggest that the aberrantly high Notch1 signaling in T-ALL maintains SKP2 at a high level and reduces p27Kip1, leading to more rapid cell cycle progression.
- High Skp2 protein expression is correlated with large tumor size, depth of invasion in squamous lesions, and high stage in ur=terine cerival neoplasms but not with patient survival.
- Skp2 plays an important role for the development of thyroid cancer.
- Skp2 protein expression was inversely correlated with expression of p27, the primary target of the SCF(Skp2) E3-ligase, in neuroblastoma tumors suggesting that Skp2 may have a key role in the progression of neuroblastomas.
- Results describe a self-amplifying feedback loop that autoinduces Skp2 during G1 phase progression.
- SKP2 variant Skp2B interacts with the repressor of estrogen receptor activity (REA) and that overexpression of Skp2B leads to a reduction in REA levels.
- SCF(Skp2) and APC(Cdc20) mark MLL for degradation at S phase and late M phase, respectively.
- Notch-induced Tal1/SCL degradation not only required Skp2 and lso CHIP protein.
- downregulation of SKP2 was critical for FOXP3-mediated growth inhibition in breast cancer cells that do not overexpress ERBB2/HER2.
- We showed that Skp2 siRNA transfection decreased Skp2 protein and induced the accumulation of p27 protein in MCF-7 cells. Skp2 siRNA inhibited the cell proliferation both in vitro and in vivo.
- Skp2-mediated degradation of RASSF1A plays an important role in cell proliferation and survival.
- pro-IL-16 forms a complex with GABPbeta1 and HDAC3 in suppressing the transcription of Skp2.
- In this review, Skp2 is described as part of an autoinduction loop that may act with other regulatory controls on the restriction point of the cell cycle.
- serum starvation induces G1 arrest through suppression of Skp2-dependent CDK2 activity and Skp2-independent CDK4 activity in human SK-OV-3 ovarian cancer cells
- that Skp2 controls p300-p53 signaling pathways in cancer cells, making Skp2 a potential molecular target for cancer therapy.
- a correlation between Skp2 and APC(Cdh1) in breast cancer
- SKP2 and the ubiquitin-proteasome pathway may be potential targets for therapeutic intervention for treatment of colorectal cancer.
- The expression of Skp2 and p27 proteins in 48 cases of Extranodal nasal-type natural killer cell lymphoma was studied and their correlations with Epstein-Barr virus status and clinical outcomes, was evaluated.
- Skp2 promotes S-phase progression in myxofibrosarcomas
- independent prognosticator of LCR. CONCLUSIONS: The results of our study have shown that Skp2 expression is frequent in NPC and has a wide range of distribution in H-score.
- The combination of high cyclin E and Skp2 expression predicts for poor prognosis in breast cancer in univariate analysis only, it is associated with high risk features, and it is associated with the basal phenotype.
- skp2 small interfering RNA inhibited growth in Tca8113 cells (derived from primary carcinoma of human tongue squamous cells) in vitro and suppressed tumor proliferation in vivo.
- the identification of an androgen-receptor -Skp2 pathway in prostate-cancer cells that depend on the AR for proliferation.
- High levels of Skp2 is associated with invasive head and neck squamous cell carcinoma.
- These data indicate that elevated Skp2 expression may overcome p53-dependent cell cycle checkpoints in melanoma cells and highlight Skp2 actions that are independent of p27(Kip1) degradation.
- Skp2 expression correlates with tumor dedifferentiation and may contribute to biological aggression in Hepatocellular carcinoma .
- Low Skp2 expression were correlated with larger tumor size and higher stage, as well as tumor necrosis in renal cell carcinoma
- SKP2 is amplified and overexpressed in esophageal squamous cell carcinoma, which protects cells from anoikis.
- Mechanisms of WIF1-induced G(1) arrest include (a) SKP2 down-regulation leading to p27/Kip1 accumulation and (b) c-myc down-regulation releasing p21/WAF1 transcription.
