Recombinant Human Pim-1 Oncogene, GST-tagged, Active
Cat.No. : | PIM1-392H |
Product Overview : | Recombinant human full-length PIM1 was expressed by baculovirus inSf9 cells usingan N-terminal GST tag. MW=62 kDa. |
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Cat. No. : | PIM1-392H |
Description : | PIM1 is a proto-oncogene that belongs to a family of serine/threonine protein kinases that are highly conserved through evolution in multicellular organisms. Originally identified from Moloney murine leukemia virus induced T-cell lymphomas in mice, PIM1 is involved in the control of cytokine-mediated cell proliferation, differentiation and survival of lymphoid and myeloid cells as well as others. Expression of PIM1 can be stimulated by a variety of growth factors and is regulated at four different levels: transcriptional, post-transcriptional, translational and post-translational. Expression of PIM1 is mediated through activation of the JAK/STAT pathway. |
Source : | Sf9 insect cells using baculovirus. |
Sequence : | Full-length. |
Applications : | Kinase Assay, Western Blot. |
Storage And Stability : | Store product at –70°C. For optimal storage, aliquot target into smaller quantities after centrifugation and store at recommended temperature. For most favorable performance, avoid repeated handling and multiple freeze/thaw cycles. |
Gene Name : | PIM1 pim-1 oncogene [ Homo sapiens ] |
Synonyms : | PIM1; pim-1 oncogene; PIM; Proto-oncogene serine/threonine-protein kinase Pim-1; EC 2.7.11.1 |
Gene ID : | 5292 |
mRNA Refseq : | NM_002648 |
Protein Refseq : | NP_002639 |
UniProt ID : | P11309 |
Chromosome Location : | 6p21 |
MIM : | 164960 |
Pathway : | Acute myeloid leukemia; Jak-STAT signaling pathway |
Function : | ATP binding; nucleotide binding; transferase activity; manganese ion binding; protein serine/threonine kinase activity; metal ion binding; transcription factor binding |
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◆ Lysates | ||
PIM1-3181HCL | Recombinant Human PIM1 293 Cell Lysate | +Inquiry |
◆ Assay kits | ||
Kit-1619 | PIM1 Kinase Binding Assay Kit | +Inquiry |
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For Research Use Only. Not intended for any clinical use. No products from Creative BioMart may be resold, modified for resale or used to manufacture commercial products without prior written approval from Creative BioMart.
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Customer Reviews (3)
Write a reviewWith the combination of this protein reagent's instructions, I can easily accomplish experimental design and operation.
With consistent and reliable results, this protein reagent is ideal for research projects that require replicability.
Following the use of this protein reagent, the reproducibility of my experiments has significantly improved, and I am highly satisfied.
Q&As (7)
Ask a questionPIM1 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.
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.
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.
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.
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.
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.
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.
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