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Rabbit Anti-Mouse Pim-1 Oncogene (PIM1) Polyclonal Antibody

Cat. No.VD1N22

Product TypeAnimal-targeted Antibodies

Size

Product Overview

BioVenic rabbit polyclonal antibody is specific for mouse pim-1 oncogene. It is affinity purified by protein A. It can be applied to WB, IHC, ICC and IP assays of mouse pim-1 oncogene.

Specifications

Application WB; IHC; ICC; IP
Clonality Polyclonal
Classification Primary Antibody
Clone A1N22
Host Rabbit
Target Species Mouse
Species Reactivity Mouse
Specificity Mouse Pim-1 Oncogene
Isotype IgG
Immunogen Recombinant protein of mouse Pim-1 oncogene
Purification Protein A Purified
Concentration 0.36 mg/mL
Conjugation Unconjugated
Preservative and Stabilizer 0.05% Proclin 300
Buffer 0.01M Phosphate Buffered Saline, pH 7.4, with 50% Glycerol
Physical State Liquid

Target Information

Mouse PIM1 is a serine/threonine kinase that plays a critical role in cell survival and proliferation. It regulates multiple cellular functions, including cell cycle progression and apoptosis. PIM1 promotes cell survival by phosphorylating and inactivating pro-apoptotic proteins such as BAD and MAP3K5, and it enhances cell proliferation by stabilizing MYC and regulating its transcriptional activity. Additionally, PIM1 is involved in mitochondrial integrity and has been implicated in drug resistance mechanisms.

Target Mouse Pim-1 Oncogene
Target Synonym Proto-Oncogene Serine/Threonine-Protein Kinase Pim-1
Gene ID 18712
UniProt ID P06803

Shipping and Storage

This product is shipped with wet ice packs. Store at -20°C on receipt (up to 2 years). Avoid repeated freezing and thawing as this may denature the antibody.

Documents

COA

To request a Certificate of Analysis, please enter the Lot No. in the search box. Note: Certificate of Analysis not available for kits.

The product is for research use only.
Not for commercial, prophylactic, diagnostic, or therapeutic applications.

References

  1. Hu, Xiu Feng, et al. "PIM-1-specific mAb suppresses human and mouse tumor growth by decreasing PIM-1 levels, reducing Akt phosphorylation, and activating apoptosis." The Journal of clinical investigation 119.2 (2009): 362-375.
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