Recombinant Mouse Pim1 Protein, Myc/DDK-tagged

• Cat.No.: Pim1-4868M
• Product Overview: Purified recombinant protein of mouse full-length proviral integration site 1 (Pim1), with C-terminal MYC/DDK tag, expressed in HEK293T cells.

Specification

• Description: Proto-oncogene with serine/threonine kinase activity involved in cell survival and cell proliferation and thus providing a selective advantage in tumorigenesis. Exerts its oncogenic activity through: the regulation of MYC transcriptional activity, the regulation of cell cycle progression and by phosphorylation and inhibition of proapoptotic proteins (BAD, MAP3K5, FOXO3). Phosphorylation of MYC leads to an increase of MYC protein stability and thereby an increase of transcriptional activity. The stabilization of MYC exerted by PIM1 might explain partly the strong synergism between these two oncogenes in tumorigenesis. Mediates survival signaling through phosphorylation of BAD, which induces release of the anti-apoptotic protein Bcl-X(L)/BCL2L1. Phosphorylation of MAP3K5, another proapoptotic protein, by PIM1, significantly decreases MAP3K5 kinase activity and inhibits MAP3K5-mediated phosphorylation of JNK and JNK/p38MAPK subsequently reducing caspase-3 activation and cell apoptosis. Stimulates cell cycle progression at the G1-S and G2-M transitions by phosphorylation of CDC25A and CDC25C. Phosphorylation of CDKN1A, a regulator of cell cycle progression at G1, results in the relocation of CDKN1A to the cytoplasm and enhanced CDKN1A protein stability. Promotes cell cycle progression and tumorigenesis by down-regulating expression of a regulator of cell cycle progression, CDKN1B, at both transcriptional and post-translational levels. Phosphorylation of CDKN1B, induces 14-3-3 binding, nuclear export and proteasome-dependent degradation. May affect the structure or silencing of chromatin by phosphorylating HP1 gamma/CBX3. Acts also as a regulator of homing and migration of bone marrow cells involving functional interaction with the CXCL12-CXCR4 signaling axis. Also phosphorylates and activates the ATP-binding cassette transporter ABCG2, allowing resistance to drugs through their excretion from cells. Promotes brown adipocyte differentiation
• Source: HEK293T
• Species: Mouse
• Tag: Myc&DDK
• Molecular Mass: 35.9 kDa
• Purity: > 80% as determined by SDS-PAGE and Coomassie blue staining
• Stability: Stable for 12 months from the date of receipt of the product under proper storage and handling conditions. Avoid repeated freeze-thaw cycles.
• Storage: Store at -80 centigrade after receiving vials.
• Concentration: >50 μg/mL as determined by microplate BCA method
• Storage Buffer: 25 mM Tris.HCl, pH 7.3, 100 mM glycine, 10% glycerol.

Gene Information

• Gene Name: Pim1 proviral integration site 1 [ Mus musculus (house mouse) ]
• Official Symbol: Pim1
• Synonyms: PIM1; proviral integration site 1; serine/threonine-protein kinase pim-1; pim-1 oncogene; proto-oncogene serine/threonine-protein kinase pim-1; Pim-1
• Gene ID: 18712
• mRNA Refseq: NM_008842
• Protein Refseq: NP_032868
• UniProt ID: Q8CFN8

Reviews

01/30/2022

With the combination of this protein reagent's instructions, I can easily accomplish experimental design and operation.

04/29/2020

With consistent and reliable results, this protein reagent is ideal for research projects that require replicability.

01/02/2020

Following the use of this protein reagent, the reproducibility of my experiments has significantly improved, and I am highly satisfied.

Q&As

What are the main substrates of PIM1 and how does their interaction affect cellular processes?

PIM1 phosphorylates a variety of substrates, including BAD, c-Myc, and eIF4B. Phosphorylation of BAD inhibits its pro-apoptotic function, while phosphorylation of c-Myc and eIF4B enhances their transcriptional and translational activities, promoting cell survival and protein synthesis, respectively.

How is PIM1 activity regulated by signaling pathways?

PIM1 activity is regulated by several signaling pathways, including the PI3K/AKT and JAK/STAT pathways. Activation of these pathways leads to the phosphorylation and activation of PIM1, while inhibition of these pathways can result in reduced PIM1 activity.

What is the potential of PIM1 as a prognostic marker or therapeutic target in different cancer types?

Further research is needed to assess the potential of PIM1 as a prognostic marker and therapeutic target in different cancer types. Understanding the specific roles of PIM1 in various cancers and its interactions with other signaling pathways will help determine its clinical relevance and potential utility in personalized cancer treatment strategies.

What role does PIM1 play in cancer development?

PIM1 has been implicated in promoting cell proliferation, survival, and resistance to apoptosis, contributing to cancer development. Its overexpression has been observed in various cancer types and is associated with poor prognosis. PIM1 also interacts with oncogenic signaling pathways, further promoting tumor growth and progression.

Are there any potential therapeutic strategies targeting PIM1?

Several small molecule inhibitors targeting PIM1 kinase activity have been developed and show promise as potential therapeutics. These inhibitors can selectively inhibit PIM1 activity and have demonstrated anti-tumor effects in preclinical studies. Combination therapy with PIM1 inhibitors and other targeted drugs may also be a viable approach for treating PIM1-driven cancers.

How does PIM1 regulate cell cycle progression and proliferation?

PIM1 regulates cell cycle progression and proliferation by phosphorylating key substrates, such as p27 and CDC25A, which control the activity of cyclin-dependent kinases (CDKs). This phosphorylation promotes the degradation of p27 and stabilizes CDC25A, leading to enhanced CDK activity and cell cycle progression.

How is PIM1 expression regulated at the transcriptional level?

PIM1 expression can be regulated by various factors, including cytokines, growth factors, and oncogenic signals. These factors can activate specific transcription factors, such as STAT3 and NF-κB, which bind to the PIM1 promoter and enhance its transcriptional activity, resulting in increased PIM1 expression.