ANTIBODIES
Contributor Information
- Institute University of Illinois Chicago
Tool Details
- Tool name: Anti-BARA/LIN-9 [mAb#1]
- Alternate names: BARA, BARPsv, Lin-9, TGS, TGS1, TGS2 or lin-9 DREAM MuvB core complex component
- Tool type: Antibodies
- Class: Monoclonal
- Conjugate: Unconjugated
- Reactivity: Rat ; Human ; Mouse
- Host: Mouse
- Application: FACS ; IP ; WB
- Description: LIN-9 regulates cell transformation and proliferation in mammalian cells by inhibiting DNA synthesis. LIN-9 is inhibited by the regulatory subunit of CDK4, cyclin D. Deletion of the first 84 amino acids of Mip/LIN-9 (Mip/LIN-9âÂÂ84) corrects the CDK4 null phenotype. Therefore, Mip/LIN-9, like the pocket proteins pRB, p107 and p130, is negatively regulated by CDK4. Moreover, the correction of the CDK4 null phenotype is accompanied by a restoration of the expression of genes such as E2F1, E2F3, and cyclin E suggesting that Mip/LIN-9 participates in the regulation of E2F target genes required for the G1/S transition.
- Immunogen: full-length GST-BARA/LIN9-L fusion protein
- Research area: Cell Cycle; Epigenetics & Nuclear Signalling
- For Research Use Only
Target Details
- Target: b-Chain Associated Regulator of Apoptosis
- Target background: LIN-9 regulates cell transformation and proliferation in mammalian cells by inhibiting DNA synthesis. LIN-9 is inhibited by the regulatory subunit of CDK4, cyclin D. Deletion of the first 84 amino acids of Mip/LIN-9 (Mip/LIN-9âÂÂ84) corrects the CDK4 null phenotype. Therefore, Mip/LIN-9, like the pocket proteins pRB, p107 and p130, is negatively regulated by CDK4. Moreover, the correction of the CDK4 null phenotype is accompanied by a restoration of the expression of genes such as E2F1, E2F3, and cyclin E suggesting that Mip/LIN-9 participates in the regulation of E2F target genes required for the G1/S transition.
Application Details
- Application: FACS ; IP ; WB
Handling
- Format: Liquid
- Storage buffer:
- Storage conditions:
- Shipping conditions: Shipping at 4°C
Documentation
- Available on request
References
- • Sandoval et al. 2006. Exp Cell Res. 312(13):2465-75. PMID: 16730350.
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