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hff 1  (ATCC)


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    ATCC hff 1
    Hff 1, supplied by ATCC, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    (A) Glucose levels in medium produced by Alb-Cre and SPT3-hKO primary hepatocytes after 6 h. * p < 0.05 by t test. n = 5 biological replicates. (B) Expression by real-time qPCR of gluconeogenic genes following treatment with 100 nM glucagon (GC) for 3 h. Expression was measured by ΔΔcq method with a reference gene panel consisting of β-actin, Hmbs1, and Tbp1. Significance was determined by ANOVA. ** p < 0.01, * p < 0.05. The dashed line indicates p < 0.01 for control versus GC for both Alb-Cre and SPT3-hKO. n = 3 biological replicates. (C) Western blot showing expression of <t>PCK1</t> protein with GC treatment. This blot is representative of triplicate measurements. (D) Western blot showing P-CREB (Ser-133) phosphorylation in response to a GC dose of 0, 5, 10, 25, 50, or 100 nM. This blot is representative of triplicate measurements. (E) Stable isotopic labeling of metabolites feeding gluconeogenesis via the TCA cycle. Hepatocytes isolated from Alb-Cre and SPT3-hKO mice were treated with 4 mM U 13 C-glutamine for 6 h in DMEM without glucose, glutamine, or phenol red. Universally labeled target metabolites were targeted for analysis to assess the first pass through the TCA cycle. Cellular metabolite levels are expressed relative to total protein. The p values were calculated by t test. * p < 0.05, n = 6 biological replicates. (F) Expression of amino acid transporters in primary mouse hepatocytes by ΔΔcq method with a reference gene panel consisting of β-actin, Hmbs1, and Tbp1. Significance was determined by t test. ** p < 0.01, n = 3 biological replicates. All graphical data are represented as mean ± SEM.
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    Image Search Results


    Journal: Cell Reports

    Article Title: A single amino acid in the Salmonella effector SarA/SteE triggers supraphysiological activation of STAT3 for anti-inflammatory gene expression

    doi: 10.1016/j.celrep.2025.115530

    Figure Lengend Snippet:

    Article Snippet: Anti-pTYR-1000 monoclonal pool , CST , Cat#8954; RRID: AB_2687925.

    Techniques: Virus, Recombinant, Mutagenesis, Enzyme-linked Immunosorbent Assay, cDNA Synthesis, Genome Wide, Mass Spectrometry, Cell Culture, Software

    (A) Glucose levels in medium produced by Alb-Cre and SPT3-hKO primary hepatocytes after 6 h. * p < 0.05 by t test. n = 5 biological replicates. (B) Expression by real-time qPCR of gluconeogenic genes following treatment with 100 nM glucagon (GC) for 3 h. Expression was measured by ΔΔcq method with a reference gene panel consisting of β-actin, Hmbs1, and Tbp1. Significance was determined by ANOVA. ** p < 0.01, * p < 0.05. The dashed line indicates p < 0.01 for control versus GC for both Alb-Cre and SPT3-hKO. n = 3 biological replicates. (C) Western blot showing expression of PCK1 protein with GC treatment. This blot is representative of triplicate measurements. (D) Western blot showing P-CREB (Ser-133) phosphorylation in response to a GC dose of 0, 5, 10, 25, 50, or 100 nM. This blot is representative of triplicate measurements. (E) Stable isotopic labeling of metabolites feeding gluconeogenesis via the TCA cycle. Hepatocytes isolated from Alb-Cre and SPT3-hKO mice were treated with 4 mM U 13 C-glutamine for 6 h in DMEM without glucose, glutamine, or phenol red. Universally labeled target metabolites were targeted for analysis to assess the first pass through the TCA cycle. Cellular metabolite levels are expressed relative to total protein. The p values were calculated by t test. * p < 0.05, n = 6 biological replicates. (F) Expression of amino acid transporters in primary mouse hepatocytes by ΔΔcq method with a reference gene panel consisting of β-actin, Hmbs1, and Tbp1. Significance was determined by t test. ** p < 0.01, n = 3 biological replicates. All graphical data are represented as mean ± SEM.

    Journal: Cell reports

    Article Title: SPTLC3 regulates plasma membrane sphingolipid composition to facilitate hepatic gluconeogenesis

    doi: 10.1016/j.celrep.2024.115054

    Figure Lengend Snippet: (A) Glucose levels in medium produced by Alb-Cre and SPT3-hKO primary hepatocytes after 6 h. * p < 0.05 by t test. n = 5 biological replicates. (B) Expression by real-time qPCR of gluconeogenic genes following treatment with 100 nM glucagon (GC) for 3 h. Expression was measured by ΔΔcq method with a reference gene panel consisting of β-actin, Hmbs1, and Tbp1. Significance was determined by ANOVA. ** p < 0.01, * p < 0.05. The dashed line indicates p < 0.01 for control versus GC for both Alb-Cre and SPT3-hKO. n = 3 biological replicates. (C) Western blot showing expression of PCK1 protein with GC treatment. This blot is representative of triplicate measurements. (D) Western blot showing P-CREB (Ser-133) phosphorylation in response to a GC dose of 0, 5, 10, 25, 50, or 100 nM. This blot is representative of triplicate measurements. (E) Stable isotopic labeling of metabolites feeding gluconeogenesis via the TCA cycle. Hepatocytes isolated from Alb-Cre and SPT3-hKO mice were treated with 4 mM U 13 C-glutamine for 6 h in DMEM without glucose, glutamine, or phenol red. Universally labeled target metabolites were targeted for analysis to assess the first pass through the TCA cycle. Cellular metabolite levels are expressed relative to total protein. The p values were calculated by t test. * p < 0.05, n = 6 biological replicates. (F) Expression of amino acid transporters in primary mouse hepatocytes by ΔΔcq method with a reference gene panel consisting of β-actin, Hmbs1, and Tbp1. Significance was determined by t test. ** p < 0.01, n = 3 biological replicates. All graphical data are represented as mean ± SEM.

    Article Snippet: PCK1 (D12F5) Rabbit mAb , Cell Signaling Technology , RRID:AB_2687968.

    Techniques: Produced, Expressing, Control, Western Blot, Isotopic Labeling, Isolation, Labeling

    Journal: Cell reports

    Article Title: SPTLC3 regulates plasma membrane sphingolipid composition to facilitate hepatic gluconeogenesis

    doi: 10.1016/j.celrep.2024.115054

    Figure Lengend Snippet:

    Article Snippet: PCK1 (D12F5) Rabbit mAb , Cell Signaling Technology , RRID:AB_2687968.

    Techniques: Recombinant, Enzyme-linked Immunosorbent Assay, Knock-Out

    TRPM2 expression in peripheral leukocytes correlates with blood lipids and IL-1β levels (A–D) Correlation of TRPM2 expression in peripheral leukocytes with total cholesterol (A), triglyceride (B), HDL (C), and LDL (D) levels in the plasma ( n = 66 human individuals). (E and F) TRPM2 expression ( n = 48, 11, 4, and 3 human individuals). (G) LDL-TRPM2 correlation in patients receiving low-moderate-intensity and high-intensity dosage statins ( n = 9 and 57 human individuals). (H) LDL-TRPM2 correlation in peripheral leukocytes in patients receiving ezetimibe or not ( n = 8 and 58 human individuals). (I–M) Correlation of plasma oxLDL level with total cholesterol (I), triglyceride (J), HDL (K), and LDL (L) levels in the plasma and TRPM2 expression in peripheral leukocytes (M) ( n = 66 human individuals). (N–Q) Correlation of plasma oxLDL level with total cholesterol (N), LDL (O), and oxLDL (P) levels in the plasma and TRPM2 expression in peripheral leukocytes (Q) ( n = 66 human individuals). Error bars: mean ± SEM; ns, no statistical significance, ∗∗, p < 0.01. See also <xref ref-type=Figures S1 and . " width="100%" height="100%">

    Journal: Cell Reports Medicine

    Article Title: TRPM2 overactivation drives hyperlipidemia-induced dysfunction of myeloid cells and neurovascular units

    doi: 10.1016/j.xcrm.2025.101998

    Figure Lengend Snippet: TRPM2 expression in peripheral leukocytes correlates with blood lipids and IL-1β levels (A–D) Correlation of TRPM2 expression in peripheral leukocytes with total cholesterol (A), triglyceride (B), HDL (C), and LDL (D) levels in the plasma ( n = 66 human individuals). (E and F) TRPM2 expression ( n = 48, 11, 4, and 3 human individuals). (G) LDL-TRPM2 correlation in patients receiving low-moderate-intensity and high-intensity dosage statins ( n = 9 and 57 human individuals). (H) LDL-TRPM2 correlation in peripheral leukocytes in patients receiving ezetimibe or not ( n = 8 and 58 human individuals). (I–M) Correlation of plasma oxLDL level with total cholesterol (I), triglyceride (J), HDL (K), and LDL (L) levels in the plasma and TRPM2 expression in peripheral leukocytes (M) ( n = 66 human individuals). (N–Q) Correlation of plasma oxLDL level with total cholesterol (N), LDL (O), and oxLDL (P) levels in the plasma and TRPM2 expression in peripheral leukocytes (Q) ( n = 66 human individuals). Error bars: mean ± SEM; ns, no statistical significance, ∗∗, p < 0.01. See also Figures S1 and .

    Article Snippet: IL-1β (D3U3E) Rabbit mAb , Cell Signaling Technology , Cat#12703; RRID: AB_2687927.

    Techniques: Expressing

    Global TRPM2 knockout abolishes the exacerbation of ischemic brain injury by hyperlipidemia (A) The presence of atherosclerotic plaque (indicated by black arrows) at the bifurcation of common carotid artery (CCA) and in the internal carotid artery (ICA) (scale bar size: 2 mm). (B–E) Triphenyl tetrazolium chloride (TTC) staining 24 h after MCAO (60-min) and neurological deficit score in WT, Apoe −/− mice, and Apoe −/− gM2KO mice (B and C) and in Trpm2 fl/fl mice, Apoe −/− Trpm2 fl/fl cre − mice, and Apoe −/− Trpm2 fl/fl cre + mice (D and E) fed with or without HFD ( n = 12–20 mice per group) (scale bar size: 5 mm). (F and G) TRPM2 expression in brains from WT mice fed with or without HFD ( n = 5 and 5 mice). (H and I) TRPM2 and CD36 expression in primary neurons, CECs, BMDMs, and peripheral leukocytes isolated from WT mice ( n = 5, 5, 5, and 5 dishes of cells isolated from at least 5 mice). (J and K) TRPM2 expression in peripheral leukocytes isolated from WT mice fed with HFD for 0, 1, 2, 3, and 4 months ( n = 5, 5, 5, 5, and 5 dishes of cells isolated from at least 5 mice). (L) ELISA measurement of TRPM2 levels in lysates from B cells, T cells, monocytes, and neutrophils after cell sorting of peripheral leukocytes from WT mice with or without HFD treatment. (M and N) ELISA measurement of plasma oxLDL and IL-1β levels in WT mice fed with HFD for 0, 1, 2, 3, and 4 months ( n = 5, 5, 5, 5, and 5 plasma samples from different mice). (O and P) Correlation of plasma IL-1β level with plasma oxLDL level (O) and TRPM2 expression (P) in peripheral leukocytes ( n = 5 mice). (Q) Correlation of plasma oxLDL level with TRPM2 expression in peripheral leukocytes ( n = 5 mice). Error bars: mean ± SEM; ns, no statistical significance, ∗, p < 0.05, ∗∗, p < 0.01, ∗∗∗, p < 0.001. See also <xref ref-type=Figure S2 and Table S1 . " width="100%" height="100%">

    Journal: Cell Reports Medicine

    Article Title: TRPM2 overactivation drives hyperlipidemia-induced dysfunction of myeloid cells and neurovascular units

    doi: 10.1016/j.xcrm.2025.101998

    Figure Lengend Snippet: Global TRPM2 knockout abolishes the exacerbation of ischemic brain injury by hyperlipidemia (A) The presence of atherosclerotic plaque (indicated by black arrows) at the bifurcation of common carotid artery (CCA) and in the internal carotid artery (ICA) (scale bar size: 2 mm). (B–E) Triphenyl tetrazolium chloride (TTC) staining 24 h after MCAO (60-min) and neurological deficit score in WT, Apoe −/− mice, and Apoe −/− gM2KO mice (B and C) and in Trpm2 fl/fl mice, Apoe −/− Trpm2 fl/fl cre − mice, and Apoe −/− Trpm2 fl/fl cre + mice (D and E) fed with or without HFD ( n = 12–20 mice per group) (scale bar size: 5 mm). (F and G) TRPM2 expression in brains from WT mice fed with or without HFD ( n = 5 and 5 mice). (H and I) TRPM2 and CD36 expression in primary neurons, CECs, BMDMs, and peripheral leukocytes isolated from WT mice ( n = 5, 5, 5, and 5 dishes of cells isolated from at least 5 mice). (J and K) TRPM2 expression in peripheral leukocytes isolated from WT mice fed with HFD for 0, 1, 2, 3, and 4 months ( n = 5, 5, 5, 5, and 5 dishes of cells isolated from at least 5 mice). (L) ELISA measurement of TRPM2 levels in lysates from B cells, T cells, monocytes, and neutrophils after cell sorting of peripheral leukocytes from WT mice with or without HFD treatment. (M and N) ELISA measurement of plasma oxLDL and IL-1β levels in WT mice fed with HFD for 0, 1, 2, 3, and 4 months ( n = 5, 5, 5, 5, and 5 plasma samples from different mice). (O and P) Correlation of plasma IL-1β level with plasma oxLDL level (O) and TRPM2 expression (P) in peripheral leukocytes ( n = 5 mice). (Q) Correlation of plasma oxLDL level with TRPM2 expression in peripheral leukocytes ( n = 5 mice). Error bars: mean ± SEM; ns, no statistical significance, ∗, p < 0.05, ∗∗, p < 0.01, ∗∗∗, p < 0.001. See also Figure S2 and Table S1 .

    Article Snippet: IL-1β (D3U3E) Rabbit mAb , Cell Signaling Technology , Cat#12703; RRID: AB_2687927.

    Techniques: Knock-Out, Staining, Expressing, Isolation, Enzyme-linked Immunosorbent Assay, FACS

    Increase of TRPM2 expression by hyperlipidemia generates a pro-inflammatory macrophage phenotype (A–D) TRPM2 expression in human peripheral leukocytes treated with LDL (A and B) and oxLDL (C and D) for 0, 6, 12, 18, 24, and 48 h ( n = 5 human individuals). (E and F) TRPM2 expression in human peripheral leukocytes treated with oxLDL for 48 h ( n = 3, 3, and 2 human individuals). (G and H) TRPM2 expression in WT mouse peripheral leukocytes treated with oxLDL for 48 h with the co-treatment of DMSO, SSO, and scavengers Mn (III) TBAP and L-NMA ( n = 5 dishes of cells isolated from at least 5 mice). (I and J) TRPM2, pp65, caspase-1, and IL-1β (precursor and mature) expression in WT and M2KO mouse BMDMs primed with LPS and IFNγ for overnight, with or without the preincubation of oxLDL for 48 h ( n = 5 dishes of cells isolated from at least 5 mice). (K and L) Examination of macrophage IL-1β release ( n = 5 dishes of cells isolated from at least 5 mice). Proteins in supernatant were isolated using trichloroacetic acid (TCA) precipitation. Error bars: mean ± SEM; ns, no statistical significance, ∗, p < 0.05, ∗∗, p < 0.01, ∗∗∗, p < 0.001. See also <xref ref-type=Figure S2 . " width="100%" height="100%">

    Journal: Cell Reports Medicine

    Article Title: TRPM2 overactivation drives hyperlipidemia-induced dysfunction of myeloid cells and neurovascular units

    doi: 10.1016/j.xcrm.2025.101998

    Figure Lengend Snippet: Increase of TRPM2 expression by hyperlipidemia generates a pro-inflammatory macrophage phenotype (A–D) TRPM2 expression in human peripheral leukocytes treated with LDL (A and B) and oxLDL (C and D) for 0, 6, 12, 18, 24, and 48 h ( n = 5 human individuals). (E and F) TRPM2 expression in human peripheral leukocytes treated with oxLDL for 48 h ( n = 3, 3, and 2 human individuals). (G and H) TRPM2 expression in WT mouse peripheral leukocytes treated with oxLDL for 48 h with the co-treatment of DMSO, SSO, and scavengers Mn (III) TBAP and L-NMA ( n = 5 dishes of cells isolated from at least 5 mice). (I and J) TRPM2, pp65, caspase-1, and IL-1β (precursor and mature) expression in WT and M2KO mouse BMDMs primed with LPS and IFNγ for overnight, with or without the preincubation of oxLDL for 48 h ( n = 5 dishes of cells isolated from at least 5 mice). (K and L) Examination of macrophage IL-1β release ( n = 5 dishes of cells isolated from at least 5 mice). Proteins in supernatant were isolated using trichloroacetic acid (TCA) precipitation. Error bars: mean ± SEM; ns, no statistical significance, ∗, p < 0.05, ∗∗, p < 0.01, ∗∗∗, p < 0.001. See also Figure S2 .

    Article Snippet: IL-1β (D3U3E) Rabbit mAb , Cell Signaling Technology , Cat#12703; RRID: AB_2687927.

    Techniques: Expressing, Isolation, TCA Precipitation

    Journal: Cell Reports Medicine

    Article Title: TRPM2 overactivation drives hyperlipidemia-induced dysfunction of myeloid cells and neurovascular units

    doi: 10.1016/j.xcrm.2025.101998

    Figure Lengend Snippet:

    Article Snippet: IL-1β (D3U3E) Rabbit mAb , Cell Signaling Technology , Cat#12703; RRID: AB_2687927.

    Techniques: Recombinant, Sequencing, Enzyme-linked Immunosorbent Assay, Bicinchoninic Acid Protein Assay, Knock-Out, Generated, Software, Microscopy, Imaging

    Journal: Cell Reports Medicine

    Article Title: TRPM2 overactivation drives hyperlipidemia-induced dysfunction of myeloid cells and neurovascular units

    doi: 10.1016/j.xcrm.2025.101998

    Figure Lengend Snippet:

    Article Snippet: Caspase-3 (D3R6Y) Rabbit mAb , Cell Signaling Technology , Cat#14220; RRID: AB_2687927.

    Techniques: Recombinant, Sequencing, Enzyme-linked Immunosorbent Assay, Bicinchoninic Acid Protein Assay, Knock-Out, Generated, Software, Microscopy, Imaging