anti pim1 monoclonal antibody (Santa Cruz Biotechnology)

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Santa Cruz Biotechnology anti pim1 monoclonal antibody

(A) Violin plots based on scRNA-seq show that <t>Pim1</t> mRNA was enriched and upregulated in plaque from Ldlr -null mice fed HFD. Each black dot represents an individual lesional Mφ. (B) Comparison of surface CD36 expression between vehicle-treated Mφs and AZD1208-treated Mφs. Examples of histograms of CD36 signals were shown. Flow cytometry data were quantified (n = 3 mice for each group). (C) Comparison of surface CD36 expression between peritoneal Mφs from Pim1 -/- mice and WT mice. Examples of histograms of CD36 signals were shown. Flow cytometry data were quantified (n = 3 mice for each group). (D) CD36 expression in WT and Pim1 -/- Mφ was evaluated by Western blot analysis. A representative blot image was shown on the left. Protein expressions were quantified by densitometry and shown in the bar graphs on the right (n = 3 mice for each group). (E) WT murine peritoneal Mφs were treated with increasing doses of oxLDL (0, 5, 20, and 50 µg/mL) for 24 hours and PIM1 protein expression was then evaluated using flow cytometry. Examples of histograms of PIM1 signals were shown. Mean fluorescence intensity (MFI) normalized to control is shown in the bar graph (n = 3 mice for each group).

Anti Pim1 Monoclonal Antibody, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 204 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+pim+1/Pim-1+Antibody/bio_rxiv__2025__10__31__685966-74-28-31
Average 93 stars, based on 204 article reviews

anti pim1 monoclonal antibody - by Bioz Stars, 2026-10

93/100 stars

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1) Product Images from "Macrophage PIM1 Drives Atherosclerosis by Enhancing Foam Cell Formation Via CD36"

Article Title: Macrophage PIM1 Drives Atherosclerosis by Enhancing Foam Cell Formation Via CD36

Journal: bioRxiv

doi: 10.1101/2025.10.31.685966

(A) Violin plots based on scRNA-seq show that Pim1 mRNA was enriched and upregulated in plaque from Ldlr -null mice fed HFD. Each black dot represents an individual lesional Mφ. (B) Comparison of surface CD36 expression between vehicle-treated Mφs and AZD1208-treated Mφs. Examples of histograms of CD36 signals were shown. Flow cytometry data were quantified (n = 3 mice for each group). (C) Comparison of surface CD36 expression between peritoneal Mφs from Pim1 -/- mice and WT mice. Examples of histograms of CD36 signals were shown. Flow cytometry data were quantified (n = 3 mice for each group). (D) CD36 expression in WT and Pim1 -/- Mφ was evaluated by Western blot analysis. A representative blot image was shown on the left. Protein expressions were quantified by densitometry and shown in the bar graphs on the right (n = 3 mice for each group). (E) WT murine peritoneal Mφs were treated with increasing doses of oxLDL (0, 5, 20, and 50 µg/mL) for 24 hours and PIM1 protein expression was then evaluated using flow cytometry. Examples of histograms of PIM1 signals were shown. Mean fluorescence intensity (MFI) normalized to control is shown in the bar graph (n = 3 mice for each group).

Figure Legend Snippet: (A) Violin plots based on scRNA-seq show that Pim1 mRNA was enriched and upregulated in plaque from Ldlr -null mice fed HFD. Each black dot represents an individual lesional Mφ. (B) Comparison of surface CD36 expression between vehicle-treated Mφs and AZD1208-treated Mφs. Examples of histograms of CD36 signals were shown. Flow cytometry data were quantified (n = 3 mice for each group). (C) Comparison of surface CD36 expression between peritoneal Mφs from Pim1 -/- mice and WT mice. Examples of histograms of CD36 signals were shown. Flow cytometry data were quantified (n = 3 mice for each group). (D) CD36 expression in WT and Pim1 -/- Mφ was evaluated by Western blot analysis. A representative blot image was shown on the left. Protein expressions were quantified by densitometry and shown in the bar graphs on the right (n = 3 mice for each group). (E) WT murine peritoneal Mφs were treated with increasing doses of oxLDL (0, 5, 20, and 50 µg/mL) for 24 hours and PIM1 protein expression was then evaluated using flow cytometry. Examples of histograms of PIM1 signals were shown. Mean fluorescence intensity (MFI) normalized to control is shown in the bar graph (n = 3 mice for each group).

Techniques Used: Comparison, Expressing, Flow Cytometry, Western Blot, Fluorescence, Control

WT peritoneal Mφ were treated with 10µM of AZD1208 or vehicle for 72 hours. (A) DiI-oxLDL-binding and -uptake assays by Mφ were evaluated by flow cytometry, respectively. Examples of histograms of DiI signals were shown. Flow cytometry data were quantified (n = 3 mice for each group). (B) Mφ from WT or Pim1 -/- cells were either treated with PBS or with 50µg/ml oxLDL for 24 hours. Oil Red O (ORO) staining was performed and representative images after staining were shown. (C) Foam cell rates were quantified (n = 3 mice for each group). More than 300 cells were counted for each condition. (D) Cholesterol was measured in peritoneal Mφs from WT and Pim1 -/- mice treated with PBS or oxLDL. Cholesterol concentrations were adjusted with protein content. Data in the bar graph were combined from three independent experiments.

Figure Legend Snippet: WT peritoneal Mφ were treated with 10µM of AZD1208 or vehicle for 72 hours. (A) DiI-oxLDL-binding and -uptake assays by Mφ were evaluated by flow cytometry, respectively. Examples of histograms of DiI signals were shown. Flow cytometry data were quantified (n = 3 mice for each group). (B) Mφ from WT or Pim1 -/- cells were either treated with PBS or with 50µg/ml oxLDL for 24 hours. Oil Red O (ORO) staining was performed and representative images after staining were shown. (C) Foam cell rates were quantified (n = 3 mice for each group). More than 300 cells were counted for each condition. (D) Cholesterol was measured in peritoneal Mφs from WT and Pim1 -/- mice treated with PBS or oxLDL. Cholesterol concentrations were adjusted with protein content. Data in the bar graph were combined from three independent experiments.

Techniques Used: Binding Assay, Flow Cytometry, Staining

Mφ from WT or Pim1 -/- mice were injected intraperitoneally into Apoe -/- mice fed on a HFD for 6 weeks to induce hyperlipidemia and a proatherogenic environment. (A) Schematic diagram showing the experimental design. (B) ORO staining was performed on peritoneal Mφs from HFD-treated Apoe -/- mice transplanted with WT mice-or Pim1 -/- mice-derived Mφs. Foam cell formation was quantified using ORO staining (n = 6 mice for each group). More than 300 cells were counted for each condition. (C) Cholesterol was measured from cells in (B). Cholesterol concentrations were adjusted to protein content. Data in the bar graph were combined from four independent experiments. (D) Apoe -/- mice on HFD for 6 weeks were injected with WT Mφ along with oral gavage of 30mg/g body weight of PIM inhibitor (AZD1208) or just vehicle. A schematic diagram showing the experimental design. (E) ORO staining was performed on peritoneal Mφs isolated from HFD-treated Apoe -/- mice intraperitoneally injected with or without AZD1208. Foam cell formation was quantified by ORO staining (n = 11 mice for each group). More than 300 cells were counted for each condition. (F) Cholesterol was measured from cells in (E). Cholesterol concentrations were adjusted to protein content. Data in the bar graph were combined from 10-12 independent experiments.

Figure Legend Snippet: Mφ from WT or Pim1 -/- mice were injected intraperitoneally into Apoe -/- mice fed on a HFD for 6 weeks to induce hyperlipidemia and a proatherogenic environment. (A) Schematic diagram showing the experimental design. (B) ORO staining was performed on peritoneal Mφs from HFD-treated Apoe -/- mice transplanted with WT mice-or Pim1 -/- mice-derived Mφs. Foam cell formation was quantified using ORO staining (n = 6 mice for each group). More than 300 cells were counted for each condition. (C) Cholesterol was measured from cells in (B). Cholesterol concentrations were adjusted to protein content. Data in the bar graph were combined from four independent experiments. (D) Apoe -/- mice on HFD for 6 weeks were injected with WT Mφ along with oral gavage of 30mg/g body weight of PIM inhibitor (AZD1208) or just vehicle. A schematic diagram showing the experimental design. (E) ORO staining was performed on peritoneal Mφs isolated from HFD-treated Apoe -/- mice intraperitoneally injected with or without AZD1208. Foam cell formation was quantified by ORO staining (n = 11 mice for each group). More than 300 cells were counted for each condition. (F) Cholesterol was measured from cells in (E). Cholesterol concentrations were adjusted to protein content. Data in the bar graph were combined from 10-12 independent experiments.

Techniques Used: Injection, Staining, Derivative Assay, Isolation

(A) A schematic diagram showing the experimental design. (B) The levels of plasma cholesterol (n = 7-10 mice for each group). (C) The levels of plasma MCP-1 (n = 7-10 mice for each group). (D) Aortic arches from four mice with Apoe -/- Pim1 fl/fl and Apoe -/- Lyz2 Cre/+ Pim1 fl/fl fed a HFD for 12 weeks were dissected, pinned open, and stained en-face for lipid-rich plaque with ORO. The yellow arrow indicates plaque. Representative images from four mice in each group are shown. Percent of plaque area was shown at bottom left corner in each image. (E) Left panels show ORO staining of histological sections obtained at the level of the aortic sinus from these mice with. Immunofluorescence images with antibodies to PPARψ, and CD68 are shown in the 3 panels to the right. (F-G) The quantifications of positive ORO, PPARψ, CD68, and αSMA areas in the aortic sinus were measured (n = 7-10 mice for each group).

Figure Legend Snippet: (A) A schematic diagram showing the experimental design. (B) The levels of plasma cholesterol (n = 7-10 mice for each group). (C) The levels of plasma MCP-1 (n = 7-10 mice for each group). (D) Aortic arches from four mice with Apoe -/- Pim1 fl/fl and Apoe -/- Lyz2 Cre/+ Pim1 fl/fl fed a HFD for 12 weeks were dissected, pinned open, and stained en-face for lipid-rich plaque with ORO. The yellow arrow indicates plaque. Representative images from four mice in each group are shown. Percent of plaque area was shown at bottom left corner in each image. (E) Left panels show ORO staining of histological sections obtained at the level of the aortic sinus from these mice with. Immunofluorescence images with antibodies to PPARψ, and CD68 are shown in the 3 panels to the right. (F-G) The quantifications of positive ORO, PPARψ, CD68, and αSMA areas in the aortic sinus were measured (n = 7-10 mice for each group).

Techniques Used: Clinical Proteomics, Staining, Immunofluorescence

Peritoneal Mφs from WT and Pim1 -/- mice were isolated and cultured in vitro . Their RNA was then extracted and analyzed by bulk RNA sequencing. (A) A heatmap presents differentially expressed genes related to lipids, atherosclerosis, and PPAR signaling between WT and Pim1 -/- Mφ (n = 3 mice for each group). (B) Expression of PIM1, PPARγ, and CD36 in WT and Pim1 -/- Mφ were evaluated by Western blots. Representative blot images were shown (n = 3 mice for each group). (C) The effect of si Pim1 on the expression of PIM1, PPARγ, and CD36 in Mφs was assessed by Western blots. Representative blot images were shown (n = 4 mice for each group). (D) The effect of rosiglitazone (a PPARγ agonist) on CD36 expression in Mφ was assessed by Western blots. Representative blot images were shown (n = 3 mice for each group).

Figure Legend Snippet: Peritoneal Mφs from WT and Pim1 -/- mice were isolated and cultured in vitro . Their RNA was then extracted and analyzed by bulk RNA sequencing. (A) A heatmap presents differentially expressed genes related to lipids, atherosclerosis, and PPAR signaling between WT and Pim1 -/- Mφ (n = 3 mice for each group). (B) Expression of PIM1, PPARγ, and CD36 in WT and Pim1 -/- Mφ were evaluated by Western blots. Representative blot images were shown (n = 3 mice for each group). (C) The effect of si Pim1 on the expression of PIM1, PPARγ, and CD36 in Mφs was assessed by Western blots. Representative blot images were shown (n = 4 mice for each group). (D) The effect of rosiglitazone (a PPARγ agonist) on CD36 expression in Mφ was assessed by Western blots. Representative blot images were shown (n = 3 mice for each group).

Techniques Used: Isolation, Cell Culture, In Vitro, RNA Sequencing, Expressing, Western Blot

other:

Article Title: eIF4B Phosphorylation by Pim Kinases Plays a Critical Role in Cellular Transformation by Abl Oncogenes
Article Snippet: The following antibodies were used in this study: anti-FLAG (Sigma F1804M2); anti-Pim-1 (Santa Cruz sc-13513 12H8); antic-Myc (Santa Cruz sc-40 9E10); anti-Bcr (Santa Cruz sc-885 N20); anti-Bcl-xL (Cell Signaling 2764 54H6); anti-eIF4B (Cell Signaling 3592); anti-phospho-eIF4B (Ser406; Cell Signaling 5399); anti-phospho-eIF4B (Ser422; Cell Signaling 3591); antiBcl-2 (Cell Signaling 2870 50E3); anti-c-Abl (Merck Millipore OP19 19–110); anti-p70 S6K, and anti-phospho-p70S6K [Thr389] (Cell Signaling 9202 and 9205).

Incubation:

Article Title: Phosphorylation of NFATC1 at PIM1 target sites is essential for its ability to promote prostate cancer cell migration and invasion
Article Snippet: Fluorescence was then measured with the Envision plate reader (Perkin Elmer) with an excitation wavelength of 320 nm and an emission wavelength of 405 nm. .. Cells were lysed in 2x LSB and heated at 95 °C for 5 min. Proteins were separated by SDS-PAGE, immobilized onto PVDF-membrane (EDM Millipore, Merck) and incubated overnight with anti-PIM-1 (1:500, 12H8; Santa Cruz Biotechnology, Santa Cruz, CA, USA), anti-PIM-2 (1:1000, D1D2; Cell Signaling Technology, Danvers, MA, USA), anti-PIM-3 (1:1000, D17C9; Cell Signaling Technology), anti-NFATC1 (1:500, Santa Cruz Biotechnology), anti-V5 (1:500, Invitrogen, Carlsbad, CA, USA), anti-Flag (1:500, F1804; Sigma-Aldrich), anti-ACTB (anti-β-actin; 1:1000, 13E5, #4970S, Cell signaling Technology), anti-GAPDH (1:50000, Sigma-Aldrich), anti-β Tubulin (1:40000, Sigma-Aldrich) or anti-Fibrillarin (1:1000, Cell Signaling Technology) antibodies. .. After incubations with secondary antibodies, chemiluminescence reactions were generated using either AmershamTM ECL Plus or ECL Prime reagents (GE Healthcare).

Article Title: Pim-1 Kinase Phosphorylates and Stabilizes 130 kDa FLT3 and Promotes Aberrant STAT5 Signaling in Acute Myeloid Leukemia with FLT3 Internal Tandem Duplication
Article Snippet: .. Briefly, blots were incubated with primary antibodies, including 1∶400 dilution of monoclonal (Santa Cruz) and polyclonal (Cell Signaling Technology, Danvers, MA) anti-Pim-1, 1∶400 dilution of polyclonal anti-FLT3 (Santa Cruz), 1∶200 dilution of polyclonal anti-phospho-BAD at serine 112 (Cell Signaling Technology), 1∶1,000 dilution of polyclonal anti-BAD, monoclonal anti-phospho-c-Jun, monoclonal anti-c-jun, monoclonal phospho-Akt or monoclonal Akt (Cell Signaling Technology), 1∶2,000 dilution of monoclonal anti-glyceraldehyde 3-phosphate dehydrogenase (GAPDH) (Calbiochem, San Diego, CA), 1∶1,000 dilution of monoclonal anti-HSP90 (Santa Cruz), 1∶200 dilution of monoclonal anti-calnexin (Santa Cruz), 1∶100 dilution of monoclonal anti-phosphoserine (16B4, Calbiochem, San Diego, CA), 1∶1,000 dilution of monoclonal anti-phosphotyrosine (pY) (4G10, Millipore Co., Billerica, MA), 1∶200 dilution of monoclonal anti-ubiquitin (Santa Cruz), 1∶200 dilution of polyclonal anti-phospho-Y591 (Cell Signaling Technology) and 1∶500 dilution of anti-STAT5 and anti-phospho-STAT5 (Cell Signaling Technology), for 1 hour at room temperature or overnight at 4°C, followed by detection with horseradish peroxidase-conjugated secondary antibody. .. Densitometric scanning was performed with the Biospectrum AC imaging system (UVP, Upland, CA).

Article Title: Phosphorylation of NFATC1 at PIM1 target sites is essential for its ability to promote prostate cancer cell migration and invasion.
Article Snippet: Fluorescence was then measured with the Envision plate reader (Perkin Elmer) with an excitation wavelength of 320 nm and an emission wavelength of 405 nm. .. Cells were lysed in 2x LSB and heated at 95 °C for 5 min. Proteins were separated by SDS-PAGE, immobilized onto PVDF-membrane (EDM Millipore, Merck) and incubated overnight with anti-PIM-1 (1:500, 12H8; Santa Cruz Biotechnology, Santa Cruz, CA, USA), anti-PIM-2 (1:1000, D1D2; Cell Signaling Technology, Danvers, MA, USA), anti-PIM-3 (1:1000, D17C9; Cell Signaling Technology), anti-NFATC1 (1:500, Santa Cruz Biotechnology), anti-V5 (1:500, Invitrogen, Carlsbad, CA, USA), anti-Flag (1:500, F1804; Sigma-Aldrich), anti-ACTB (anti-β-actin; 1:1000, 13E5, #4970S, Cell signaling Technology), anti-GAPDH (1:50000, Sigma-Aldrich), anti-β Tubulin (1:40000, Sigma-Aldrich) or anti-Fibrillarin (1: 1000, Cell Signaling Technology) antibodies. .. After incubations with secondary antibodies, chemiluminescence reactions were generated using either AmershamTM ECL Plus or ECL Prime reagents (GE Healthcare).

Control:

Article Title: AZD1208, a Pan-Pim Kinase Inhibitor, Has Anti-Growth Effect on 93T449 Human Liposarcoma Cells via Control of the Expression and Phosphorylation of Pim-3, mTOR, 4EBP-1, S6, STAT-3 and AMPK.
Article Snippet: Anti-p-eIF-2α (S51) (ab32157) antibody was bought from Abcam (Cambridge, MA, USA). .. Anti-Pim-1 (sc-374116), anti-Pim-3 (sc-98959), anti-p-STAT-3 (Tyr(Y)705) (sc-8059), anti-STAT-3 (sc-8019), secondary goat anti-Rabbit and goat anti-Mouse IgG antibodies, control siRNA (sc-37007), AMPK siRNA (sc-45312), LKB-1 siRNA (sc-35816) and Pim-3 siRNA (sc-61353) were purchased from Santa Cruz Biotechnology (Delaware, CA, USA). z-VAD-fmk and AG490 were purchased from Calbiochem (Madison, WI, USA). .. Super SignalTM West Pico PLUS Enhanced chemiluminescence (ECL, #34080) was purchased from Thermo Scientific (Waltham, MA, USA).

Article Title: AZD1208, a Pan-Pim Kinase Inhibitor, Has Anti-Growth Effect on 93T449 Human Liposarcoma Cells via Control of the Expression and Phosphorylation of Pim-3, mTOR, 4EBP-1, S6, STAT-3 and AMPK
Article Snippet: Anti-p-eIF-2α (S51) (ab32157) antibody was bought from Abcam (Cambridge, MA, USA). .. Anti-Pim-1 (sc-374116), anti-Pim-3 (sc-98959), anti-p-STAT-3 (Tyr(Y)705) (sc-8059), anti-STAT-3 (sc-8019), secondary goat anti-Rabbit and goat anti-Mouse IgG antibodies, control siRNA (sc-37007), AMPK siRNA (sc-45312), LKB-1 siRNA (sc-35816) and Pim-3 siRNA (sc-61353) were purchased from Santa Cruz Biotechnology (Delaware, CA, USA). z-VAD-fmk and AG490 were purchased from Calbiochem (Madison, WI, USA). .. Super SignalTM West Pico PLUS Enhanced chemiluminescence (ECL, #34080) was purchased from Thermo Scientific (Waltham, MA, USA).

Western Blot:

Article Title: Specific recruitment of protein kinase A to the immunoglobulin locus regulates class-switch recombination
Article Snippet: Antibodies for flow cytometry were as follows: allophycocyanin–anti-IgG1 (X56), phycoerythrin-indotricarbocyanine–anti-B220 (RA3-6B2) and fluorescein isothiocyanate– anti-IgG3 (R40–82; all from BD Pharmingen). .. Antibodies for immunoblot analysis were as follows: anti-Xpress (R910-25; Invitrogen), anti-PKA-Cα (610981; BD Transduction), anti-PKA-RIα (610610; BD Transduction), anti-PKA-RIIα (612242; BD Transduction), anti-hemagglutinin (3F10; Roche), anti-α-tubulin (T9026; Sigma), anti-β-tubulin (sc-5274; Santa Cruz Biotechnology), anti-Flag (M2; Sigma), anti-GFP (33–2600; Zymed) and anti-Pim-1 (sc-28777; Santa Cruz Biotechnology). ..

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