Antibody data
- Antibody Data
- Antigen structure
- References [10]
- Comments [0]
- Validations
- Immunocytochemistry [1]
- Other assay [13]
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- Product number
- 51-1900 - Provider product page
- Provider
- Invitrogen Antibodies
- Product name
- SKP2 Polyclonal Antibody
- Antibody type
- Polyclonal
- Antigen
- Recombinant full-length protein
- Description
- Description: This 7A6 monoclonal antibody recognizes human VEGFR1 (vascular endothelial growth factor receptor 1, fms-like tyrosine kinase 1, FLT1). It is directed against the extracellular domain and can recognize both membrane-bound and soluble forms of VEGFR1, with approximate molecular weights of 180 kDa and 90 kDa, respectively. Mice lacking expression of VEGFR1 have disorganized vasculature and die in utero, however angiogenesis does not require the tyrosine kinase activity of VEGFR1 as expression of a membrane-bound form lacking the tyrosine kinase domain allows normal development. Although fertile and viable, mice lacking the tyrosine kinase domain of VEGFR1 do have a defect in the migration of macrophages. The soluble form of VEGFR1 can be detected in the serum of normal patients, and elevated levels of soluble VEGFR1 in pregnant women is associated with preeclampsia. Several tumor cell lines have been reported to express membrane-bound VEGFR1, including malignancies of hematopoietic origin.
- Reactivity
- Human
- Host
- Rabbit
- Isotype
- IgG
- Vial size
- 100 µg
- Concentration
- 0.25 mg/mL
- Storage
- -20°C
Submitted references Notch Signaling Activates Stem Cell Properties of Müller Glia through Transcriptional Regulation and Skp2-mediated Degradation of p27Kip1.
The physiological significance of p27(KIP1) expression in detrusor function.
The human papillomavirus type 18 E2 protein is a cell cycle-dependent target of the SCFSkp2 ubiquitin ligase.
Mechanoregulation of proliferation.
Disrupting Skp2-cyclin A interaction with a blocking peptide induces selective cancer cell killing.
Skp2 contains a novel cyclin A binding domain that directly protects cyclin A from inhibition by p27Kip1.
Ubiquitination and proteolysis of cancer-derived Smad4 mutants by SCFSkp2.
Skp2 regulates Myc protein stability and activity.
Inhibition of F-Box protein p45(SKP2) expression and stabilization of cyclin-dependent kinase inhibitor p27(KIP1) in vitamin D analog-treated cancer cells.
The pRb-related protein p130 is regulated by phosphorylation-dependent proteolysis via the protein-ubiquitin ligase SCF(Skp2).
Del Debbio CB, Mir Q, Parameswaran S, Mathews S, Xia X, Zheng L, Neville AJ, Ahmad I
PloS one 2016;11(3):e0152025
PloS one 2016;11(3):e0152025
The physiological significance of p27(KIP1) expression in detrusor function.
Niederhoff RA, Manson SR, Tawfik A, Austin PF
The Journal of urology 2010 Oct;184(4 Suppl):1686-91
The Journal of urology 2010 Oct;184(4 Suppl):1686-91
The human papillomavirus type 18 E2 protein is a cell cycle-dependent target of the SCFSkp2 ubiquitin ligase.
Bellanger S, Tan CL, Nei W, He PP, Thierry F
Journal of virology 2010 Jan;84(1):437-44
Journal of virology 2010 Jan;84(1):437-44
Mechanoregulation of proliferation.
Jiang X, Austin PF, Niederhoff RA, Manson SR, Riehm JJ, Cook BL, Pengue G, Chitaley K, Nakayama K, Nakayama KI, Weintraub SJ
Molecular and cellular biology 2009 Sep;29(18):5104-14
Molecular and cellular biology 2009 Sep;29(18):5104-14
Disrupting Skp2-cyclin A interaction with a blocking peptide induces selective cancer cell killing.
Ji P, Sun D, Wang H, Bauzon F, Zhu L
Molecular cancer therapeutics 2007 Feb;6(2):684-91
Molecular cancer therapeutics 2007 Feb;6(2):684-91
Skp2 contains a novel cyclin A binding domain that directly protects cyclin A from inhibition by p27Kip1.
Ji P, Goldin L, Ren H, Sun D, Guardavaccaro D, Pagano M, Zhu L
The Journal of biological chemistry 2006 Aug 18;281(33):24058-69
The Journal of biological chemistry 2006 Aug 18;281(33):24058-69
Ubiquitination and proteolysis of cancer-derived Smad4 mutants by SCFSkp2.
Liang M, Liang YY, Wrighton K, Ungermannova D, Wang XP, Brunicardi FC, Liu X, Feng XH, Lin X
Molecular and cellular biology 2004 Sep;24(17):7524-37
Molecular and cellular biology 2004 Sep;24(17):7524-37
Skp2 regulates Myc protein stability and activity.
Kim SY, Herbst A, Tworkowski KA, Salghetti SE, Tansey WP
Molecular cell 2003 May;11(5):1177-88
Molecular cell 2003 May;11(5):1177-88
Inhibition of F-Box protein p45(SKP2) expression and stabilization of cyclin-dependent kinase inhibitor p27(KIP1) in vitamin D analog-treated cancer cells.
Lin R, Wang TT, Miller WH Jr, White JH
Endocrinology 2003 Mar;144(3):749-53
Endocrinology 2003 Mar;144(3):749-53
The pRb-related protein p130 is regulated by phosphorylation-dependent proteolysis via the protein-ubiquitin ligase SCF(Skp2).
Tedesco D, Lukas J, Reed SI
Genes & development 2002 Nov 15;16(22):2946-57
Genes & development 2002 Nov 15;16(22):2946-57
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Supportive validation
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- Invitrogen Antibodies (provider)
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- Experimental details
- Immunofluorescence analysis of SKP2 was performed using 70% confluent log phase A549 cells. The cells were fixed with 4% paraformaldehyde for 10 minutes, permeabilized with 0.1% Triton™ X-100 for 10 minutes, and blocked with 1% BSA for 1 hour at room temperature. The cells were labeled with SKP2 Rabbit Polyclonal Antibody (Product # 51-1900) at 2 µg/mL in 0.1% BSA and incubated for 3 hours at room temperature and then labeled with Goat anti-Rabbit IgG (H+L) Superclonal™ Secondary Antibody, Alexa Fluor® 488 conjugate (Product # A27034) at a dilution of 1:2000 for 45 minutes at room temperature (Panel a: green). Nuclei (Panel b: blue) were stained with SlowFade® Gold Antifade Mountant with DAPI (Product # S36938). F-actin (Panel c: red) was stained with Alexa Fluor® 555 Rhodamine Phalloidin (Product # R415, 1:300). Panel d represents the merged image showing nuclear localization. Panel e shows the control without primary antibody. The images were captured at 60X magnification.
Supportive validation
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- Fig 7 Effects of Skp2 loss of function on MG activation in neurosphere assays. (A, B) Validation experiments for the Skp2 loss of function approach in C6 glioma revealed a significant decrease in Skp2 protein (a) and transcript (b) levels in cells transduced with Skp2 siRNA lentivirus, compared to controls. (C) MG transduced with Skp2 siRNA lentivirus and cultured in the presence of Jag1 displayed a significant decrease in Skp2 transcript levels, compared to controls (FGF2-treated controls). (D, E) Skp2 siRNA-transduced cells expressed higher levels of p27 kip1 protein (D) and generated significantly fewer neurospheres (E), compared to controls. (F) Additionally, MG generated fewer neurospheres in the presence of proteosome inhibitor, MG132, versus controls. (G) Hoechst dye efflux assay revealed roughly half the number of SP cells in MG-derived neurospheres transduced with Skp2 siRNA lentivirus, compared to controls. A similar decrease in SP cell number was observed in cells treated with MG132, compared to controls. **p
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- Invitrogen Antibodies (provider)
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- Fig 1 Expression of the Notch-dependent regulatory axes' components during late retinal histogenesis and in enriched MG. (A-C) Levels of transcripts (fold change with respect to those at E18) corresponding to Nestin/Hes1 and GS temporally decreased and increased, respectively, during the stages of late retinal histogenesis (E18-PN10) and beyond (PN15-PN20). (D-F) Levels of transcripts corresponding to p27 Kip1 , Sox9 , and Skp2 progressively decreased during late histogenesis, except that those of p27 Kip1 and Sox9 significantly increased at PN20, compared to levels at PN10. (G) Immunocytochemical analysis of enriched MG revealed that GS + cells co-expressed immunoreactivities corresponding to p27 Kip1 , Skp2, Hes1, and NICD (activated Notch1). *p
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- Fig 4 Post-translational influence of Notch signaling on p27 Kip1 and Skp2 expression. (A) Western analyses revealed robust levels of p27 Kip1 in enriched MG, which relatively decreased in FGF2/Jag-1 groups and increased in cells treated with DAPT. (B) In contrast, relative to that of p27 Kip1 , levels of Skp2 were less in MG but increased in cells treated with FGF2/Jag-1 and decreased in the DAPT group. (C) An increase and a decrease in protein levels of NICD were observed in the presence of FGF2/Jag1 and DAPT, respectively, indicating that Notch signaling was perturbed. Levels in graphs represent the arbitrary scanning units and all protein levels were normalized to GAPDH. (D, E) Quantitative Western analysis revealed a significant decrease and increase in levels of p27 Kip1 (d) and Skp2 (e) protein levels in Jag1-treated groups, respectively, versus controls (FGF2), confirming the qualitative analyses carried out on the pooled samples (seen in ""A""). *p
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