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Downregulation of the Cx43‐interacting <t>protein</t> <t>SNAT2</t> leads to disorders of proline metabolism and disturbances in redox balance of Cx43‐KO iPSC‐CMs. (A) Bar graph to compare the mRNA expression of the proline transporters ( SLC36A1 , SLC36A2 , SLC38A1 , and SLC38A2 ) between WT and Cx43‐KO iPSC‐CMs. n = 4 independently biological repeats. (B–D) Western blot analysis of the protein expression of SNAT2 (sodium‐coupled neutral amino acid transporter) and <t>PRODH</t> (proline dehydrogenase) in WT and Cx43‐KO iPSC‐CMs. GAPDH is used as the loading control. n = 3 independently biological repeats. (E) Co‐immunoprecipitation (co‐IP) assay showing that SNAT2 was detected in anti‐Cx43 immunoprecipitates in WT iPSC‐CMs. (F) Molecular docking simulation using AutoDockTools and GRAMM. Cx43 and SNAT2 are represented as slate and cyan cartoon models, respectively. (G) Measurement of proline contents through a proline assay kit in Cx43‐KO iPSC‐CMs transfected with green fluorescent protein (GFP) only (negative control, NC) (KO + NC) or SNAT2 protein labeled with GFP (SNAT2‐OE) (KO + SNAT2‐OE). OE, overexpressing. n = 5 independently biological repeats. (H) Bar graph to compare the mitochondrial ROS level among WT, KO + NC, and KO + SNAT2‐OE iPSC‐CMs. n = 4 independently biological repeats. (I) Bar graph to compare the GSH/GSSG among WT, KO + NC, and KO + SNAT2‐OE iPSC‐CMs. n = 3 independently biological repeats. (J) Bar graph to compare the proline content among WT iPSC‐CMs transfected with scrambled siRNA (WT + NC), WT iPSC‐CMs transfected with SNAT2 small interfering RNA (siRNA) (WT + SNAT2‐KD), and KO iPSC‐CMs. KD, knockdown. n = 5 independently biological repeats. (K–N) Bar graphs to compare the calcium amplitude, peak calcium, maximum rising rate, and maximum decay rate among WT + NC1, WT + SNAT2‐KD, KO + NC2, and KO + SNAT2‐OE iPSC‐CMs. n = 21–24 cells. (O) The diagram depicting the traces of OCR on WT and Cx43‐KO iPSC‐CMs treated with PBS (vehicle) or proline (100 n m , 24 h) after sequentially administration of 1.5 µ m oligomycin, 4 µ m FCCP, and 1 µ m antimycin A, respectively. (P–S) Bar graphs to compare a series of fundamental parameters of mitochondrial function among different groups in Panel O, including basal OCR, spare respiratory capacity, maximal respiration, and ATP production. n = 2–4 independently biological repeats. (T) Measurement of mitochondrial ROS levels in WT and Cx43‐KO iPSC‐CMs with or without ISO (100 n m , 2 h) stimulation and/or proline (100 n m , 24 h) supplementation. n = 4 independently biological repeats. (A–D,G–T) “KO” in the figure panels refers to combined data from KO‐1 and KO‐2 analyzed in parallel. (A,C,D,G) p values were calculated using unpaired two‐tailed Student's t ‐test, (H) Brown–Forsythe ANOVA test/Welch ANOVA test followed by Dunnett T3 multiple comparisons test, (I) one‐way ANOVA followed by Dunnett's multiple comparisons test, (J) one‐way ANOVA followed by Dunnett's multiple comparisons test, (K,M,N) Kruskal–Wallis test followed by Dunn's multiple comparisons test, (L,T) one‐way ANOVA followed by Tukey's multiple comparisons test, and (P–S) two‐way ANOVA followed by Tukey's multiple comparisons test. Data were shown as mean ± SEM.

Prodh, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 23 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+prodh/PRODH+Antibody/pmc13045320-336-25-26
Average 93 stars, based on 23 article reviews

prodh - by Bioz Stars, 2026-09

93/100 stars

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1) Product Images from "Connexin43 Deficiency Leads to Ventricular Arrhythmias by Reprogramming Proline Metabolism"

Article Title: Connexin43 Deficiency Leads to Ventricular Arrhythmias by Reprogramming Proline Metabolism

Journal: Advanced Science

doi: 10.1002/advs.202516090

Downregulation of the Cx43‐interacting protein SNAT2 leads to disorders of proline metabolism and disturbances in redox balance of Cx43‐KO iPSC‐CMs. (A) Bar graph to compare the mRNA expression of the proline transporters ( SLC36A1 , SLC36A2 , SLC38A1 , and SLC38A2 ) between WT and Cx43‐KO iPSC‐CMs. n = 4 independently biological repeats. (B–D) Western blot analysis of the protein expression of SNAT2 (sodium‐coupled neutral amino acid transporter) and PRODH (proline dehydrogenase) in WT and Cx43‐KO iPSC‐CMs. GAPDH is used as the loading control. n = 3 independently biological repeats. (E) Co‐immunoprecipitation (co‐IP) assay showing that SNAT2 was detected in anti‐Cx43 immunoprecipitates in WT iPSC‐CMs. (F) Molecular docking simulation using AutoDockTools and GRAMM. Cx43 and SNAT2 are represented as slate and cyan cartoon models, respectively. (G) Measurement of proline contents through a proline assay kit in Cx43‐KO iPSC‐CMs transfected with green fluorescent protein (GFP) only (negative control, NC) (KO + NC) or SNAT2 protein labeled with GFP (SNAT2‐OE) (KO + SNAT2‐OE). OE, overexpressing. n = 5 independently biological repeats. (H) Bar graph to compare the mitochondrial ROS level among WT, KO + NC, and KO + SNAT2‐OE iPSC‐CMs. n = 4 independently biological repeats. (I) Bar graph to compare the GSH/GSSG among WT, KO + NC, and KO + SNAT2‐OE iPSC‐CMs. n = 3 independently biological repeats. (J) Bar graph to compare the proline content among WT iPSC‐CMs transfected with scrambled siRNA (WT + NC), WT iPSC‐CMs transfected with SNAT2 small interfering RNA (siRNA) (WT + SNAT2‐KD), and KO iPSC‐CMs. KD, knockdown. n = 5 independently biological repeats. (K–N) Bar graphs to compare the calcium amplitude, peak calcium, maximum rising rate, and maximum decay rate among WT + NC1, WT + SNAT2‐KD, KO + NC2, and KO + SNAT2‐OE iPSC‐CMs. n = 21–24 cells. (O) The diagram depicting the traces of OCR on WT and Cx43‐KO iPSC‐CMs treated with PBS (vehicle) or proline (100 n m , 24 h) after sequentially administration of 1.5 µ m oligomycin, 4 µ m FCCP, and 1 µ m antimycin A, respectively. (P–S) Bar graphs to compare a series of fundamental parameters of mitochondrial function among different groups in Panel O, including basal OCR, spare respiratory capacity, maximal respiration, and ATP production. n = 2–4 independently biological repeats. (T) Measurement of mitochondrial ROS levels in WT and Cx43‐KO iPSC‐CMs with or without ISO (100 n m , 2 h) stimulation and/or proline (100 n m , 24 h) supplementation. n = 4 independently biological repeats. (A–D,G–T) “KO” in the figure panels refers to combined data from KO‐1 and KO‐2 analyzed in parallel. (A,C,D,G) p values were calculated using unpaired two‐tailed Student's t ‐test, (H) Brown–Forsythe ANOVA test/Welch ANOVA test followed by Dunnett T3 multiple comparisons test, (I) one‐way ANOVA followed by Dunnett's multiple comparisons test, (J) one‐way ANOVA followed by Dunnett's multiple comparisons test, (K,M,N) Kruskal–Wallis test followed by Dunn's multiple comparisons test, (L,T) one‐way ANOVA followed by Tukey's multiple comparisons test, and (P–S) two‐way ANOVA followed by Tukey's multiple comparisons test. Data were shown as mean ± SEM.

Figure Legend Snippet: Downregulation of the Cx43‐interacting protein SNAT2 leads to disorders of proline metabolism and disturbances in redox balance of Cx43‐KO iPSC‐CMs. (A) Bar graph to compare the mRNA expression of the proline transporters ( SLC36A1 , SLC36A2 , SLC38A1 , and SLC38A2 ) between WT and Cx43‐KO iPSC‐CMs. n = 4 independently biological repeats. (B–D) Western blot analysis of the protein expression of SNAT2 (sodium‐coupled neutral amino acid transporter) and PRODH (proline dehydrogenase) in WT and Cx43‐KO iPSC‐CMs. GAPDH is used as the loading control. n = 3 independently biological repeats. (E) Co‐immunoprecipitation (co‐IP) assay showing that SNAT2 was detected in anti‐Cx43 immunoprecipitates in WT iPSC‐CMs. (F) Molecular docking simulation using AutoDockTools and GRAMM. Cx43 and SNAT2 are represented as slate and cyan cartoon models, respectively. (G) Measurement of proline contents through a proline assay kit in Cx43‐KO iPSC‐CMs transfected with green fluorescent protein (GFP) only (negative control, NC) (KO + NC) or SNAT2 protein labeled with GFP (SNAT2‐OE) (KO + SNAT2‐OE). OE, overexpressing. n = 5 independently biological repeats. (H) Bar graph to compare the mitochondrial ROS level among WT, KO + NC, and KO + SNAT2‐OE iPSC‐CMs. n = 4 independently biological repeats. (I) Bar graph to compare the GSH/GSSG among WT, KO + NC, and KO + SNAT2‐OE iPSC‐CMs. n = 3 independently biological repeats. (J) Bar graph to compare the proline content among WT iPSC‐CMs transfected with scrambled siRNA (WT + NC), WT iPSC‐CMs transfected with SNAT2 small interfering RNA (siRNA) (WT + SNAT2‐KD), and KO iPSC‐CMs. KD, knockdown. n = 5 independently biological repeats. (K–N) Bar graphs to compare the calcium amplitude, peak calcium, maximum rising rate, and maximum decay rate among WT + NC1, WT + SNAT2‐KD, KO + NC2, and KO + SNAT2‐OE iPSC‐CMs. n = 21–24 cells. (O) The diagram depicting the traces of OCR on WT and Cx43‐KO iPSC‐CMs treated with PBS (vehicle) or proline (100 n m , 24 h) after sequentially administration of 1.5 µ m oligomycin, 4 µ m FCCP, and 1 µ m antimycin A, respectively. (P–S) Bar graphs to compare a series of fundamental parameters of mitochondrial function among different groups in Panel O, including basal OCR, spare respiratory capacity, maximal respiration, and ATP production. n = 2–4 independently biological repeats. (T) Measurement of mitochondrial ROS levels in WT and Cx43‐KO iPSC‐CMs with or without ISO (100 n m , 2 h) stimulation and/or proline (100 n m , 24 h) supplementation. n = 4 independently biological repeats. (A–D,G–T) “KO” in the figure panels refers to combined data from KO‐1 and KO‐2 analyzed in parallel. (A,C,D,G) p values were calculated using unpaired two‐tailed Student's t ‐test, (H) Brown–Forsythe ANOVA test/Welch ANOVA test followed by Dunnett T3 multiple comparisons test, (I) one‐way ANOVA followed by Dunnett's multiple comparisons test, (J) one‐way ANOVA followed by Dunnett's multiple comparisons test, (K,M,N) Kruskal–Wallis test followed by Dunn's multiple comparisons test, (L,T) one‐way ANOVA followed by Tukey's multiple comparisons test, and (P–S) two‐way ANOVA followed by Tukey's multiple comparisons test. Data were shown as mean ± SEM.

Techniques Used: Expressing, Western Blot, Control, Co-Immunoprecipitation Assay, Transfection, Negative Control, Labeling, Small Interfering RNA, Knockdown, Two Tailed Test

other:

Article Title: The treatment of primary CoQ deficiency requires the targeting of multiple pathogenic mechanisms.
Article Snippet: The following primary antibodies were used: anti-COQ4 (Proteintech, 16654-1-AP), anti-COQ5 (Proteintech, 17453-AP), anti-COQ7 (Proteintech, 15083-1-AP), anti-PRODH(Cell Signaling, #22980), antiSQRDL (Proteintech, 17256-1-AP), anti-CBS (Proteintech, 14787-1-AP), antiEIF2AK2 (Proteintech, 18244-1-AP), anti-PSAT1 (Proteintech, 10501-1AP), anti-VDAC1 (Abcam, ab14734) and anti-ACTIN (Invitrogen, #MA515739-HRP).

Article Title: High levels of Myc expression are required for the robust proliferation of hepatocytes, but not for the sustained weak proliferation.
Article Snippet: In contrast to the robust proliferation exhibited following acute liver injury, hepatocytes exhibit long-lasting proliferative activity in chronic liver injury.. The mechanistic differences between these distinct modes of proliferation are unclear.. Hepatocytes exhibited robust proliferation that peaked at 2 days following partial hepatectomy in mice, but this proliferation was completely inhibited by hepatocyte-specific expression of MadMyc, a Myc-suppressing chimeric protein.

Article Title: The treatment of primary CoQ deficiency requires the targeting of multiple pathogenic mechanisms.
Article Snippet: The following primary antibodies were used: anti-COQ4 (Proteintech, 16654-1-AP), anti-COQ5 (Proteintech, 17453-AP), anti-COQ7 (Proteintech, 15083-1-AP), anti-PRODH(Cell Signaling, #22980), anti- SQRDL (Proteintech, 17256-1-AP), anti-CBS (Proteintech, 14787-1-AP), antiEIF2AK2 (Proteintech, 18244-1-AP), anti-PSAT1 (Proteintech, 10501-1- AP), anti-VDAC1 (Abcam, ab14734) and anti-ACTIN (Invitrogen, #MA515739-HRP).

Image Search Results

Journal: Advanced Science

Article Title: Connexin43 Deficiency Leads to Ventricular Arrhythmias by Reprogramming Proline Metabolism

doi: 10.1002/advs.202516090

Figure Lengend Snippet: Downregulation of the Cx43‐interacting protein SNAT2 leads to disorders of proline metabolism and disturbances in redox balance of Cx43‐KO iPSC‐CMs. (A) Bar graph to compare the mRNA expression of the proline transporters ( SLC36A1 , SLC36A2 , SLC38A1 , and SLC38A2 ) between WT and Cx43‐KO iPSC‐CMs. n = 4 independently biological repeats. (B–D) Western blot analysis of the protein expression of SNAT2 (sodium‐coupled neutral amino acid transporter) and PRODH (proline dehydrogenase) in WT and Cx43‐KO iPSC‐CMs. GAPDH is used as the loading control. n = 3 independently biological repeats. (E) Co‐immunoprecipitation (co‐IP) assay showing that SNAT2 was detected in anti‐Cx43 immunoprecipitates in WT iPSC‐CMs. (F) Molecular docking simulation using AutoDockTools and GRAMM. Cx43 and SNAT2 are represented as slate and cyan cartoon models, respectively. (G) Measurement of proline contents through a proline assay kit in Cx43‐KO iPSC‐CMs transfected with green fluorescent protein (GFP) only (negative control, NC) (KO + NC) or SNAT2 protein labeled with GFP (SNAT2‐OE) (KO + SNAT2‐OE). OE, overexpressing. n = 5 independently biological repeats. (H) Bar graph to compare the mitochondrial ROS level among WT, KO + NC, and KO + SNAT2‐OE iPSC‐CMs. n = 4 independently biological repeats. (I) Bar graph to compare the GSH/GSSG among WT, KO + NC, and KO + SNAT2‐OE iPSC‐CMs. n = 3 independently biological repeats. (J) Bar graph to compare the proline content among WT iPSC‐CMs transfected with scrambled siRNA (WT + NC), WT iPSC‐CMs transfected with SNAT2 small interfering RNA (siRNA) (WT + SNAT2‐KD), and KO iPSC‐CMs. KD, knockdown. n = 5 independently biological repeats. (K–N) Bar graphs to compare the calcium amplitude, peak calcium, maximum rising rate, and maximum decay rate among WT + NC1, WT + SNAT2‐KD, KO + NC2, and KO + SNAT2‐OE iPSC‐CMs. n = 21–24 cells. (O) The diagram depicting the traces of OCR on WT and Cx43‐KO iPSC‐CMs treated with PBS (vehicle) or proline (100 n m , 24 h) after sequentially administration of 1.5 µ m oligomycin, 4 µ m FCCP, and 1 µ m antimycin A, respectively. (P–S) Bar graphs to compare a series of fundamental parameters of mitochondrial function among different groups in Panel O, including basal OCR, spare respiratory capacity, maximal respiration, and ATP production. n = 2–4 independently biological repeats. (T) Measurement of mitochondrial ROS levels in WT and Cx43‐KO iPSC‐CMs with or without ISO (100 n m , 2 h) stimulation and/or proline (100 n m , 24 h) supplementation. n = 4 independently biological repeats. (A–D,G–T) “KO” in the figure panels refers to combined data from KO‐1 and KO‐2 analyzed in parallel. (A,C,D,G) p values were calculated using unpaired two‐tailed Student's t ‐test, (H) Brown–Forsythe ANOVA test/Welch ANOVA test followed by Dunnett T3 multiple comparisons test, (I) one‐way ANOVA followed by Dunnett's multiple comparisons test, (J) one‐way ANOVA followed by Dunnett's multiple comparisons test, (K,M,N) Kruskal–Wallis test followed by Dunn's multiple comparisons test, (L,T) one‐way ANOVA followed by Tukey's multiple comparisons test, and (P–S) two‐way ANOVA followed by Tukey's multiple comparisons test. Data were shown as mean ± SEM.

Article Snippet: Western blot was performed using standard protocol with the following antibodies: Cx43 (Abcam, ab11370, 1:1000), DRP1 (Proteintech, 12957‐1‐AP, 1:500), phospho‐DRP1 (Ser616) (Cell signaling, 3455S, 1:1000), PRODH (Proteintech, 22980‐1‐AP, 1:500), SNAT2 (Santa Cruz Biotechnology, sc‐514037, 1:500), Na + /K + ‐ATPase (Abcam, ab7671, 1:1000), Na v 1.5 (Alomone labs, ASC005, 1:500), Ca v 1.2 (Abcam, ab84814, 1:1000), NCX1 (Proteintech, 55075‐1‐AP, 1:1000), SERCA2a (Santa Cruz Biotechnology, sc‐53010, 1:200), and GAPDH (Abmart, M200006, 1:5000).

Techniques: Expressing, Western Blot, Control, Co-Immunoprecipitation Assay, Transfection, Negative Control, Labeling, Small Interfering RNA, Knockdown, Two Tailed Test

A. Schematic of study in which 5-week-old mice (R6/2 HD = 8, B6 WT = 8) receive daily gavage treatments ( N -PPG at 50 mg/kg or Veh) for 9 days before sacrifice and snap freezing of whole brain and kidney tissue samples for later immunoblotting, RNA sequencing, and metabolomic analyses. B. Immunoblots of WT and HD whole brain samples probed for Prodh, Yme1l1, and β-actin with densitometry to determine treatment ( N -PPG, Veh) induced Prodh/actin and Yme1l1/actin ratios. C. Quantification of the mean values (+/− SD) plotted in bar graphs; p values for treatment differences determined by ANOVA F testing.

Journal: Brain research

Article Title: Brain transcriptomic, metabolic and mitohormesis properties associated with N -propargylglycine treatment: A prevention strategy against neurodegeneration

doi: 10.1016/j.brainres.2023.148733

Figure Lengend Snippet: A. Schematic of study in which 5-week-old mice (R6/2 HD = 8, B6 WT = 8) receive daily gavage treatments ( N -PPG at 50 mg/kg or Veh) for 9 days before sacrifice and snap freezing of whole brain and kidney tissue samples for later immunoblotting, RNA sequencing, and metabolomic analyses. B. Immunoblots of WT and HD whole brain samples probed for Prodh, Yme1l1, and β-actin with densitometry to determine treatment ( N -PPG, Veh) induced Prodh/actin and Yme1l1/actin ratios. C. Quantification of the mean values (+/− SD) plotted in bar graphs; p values for treatment differences determined by ANOVA F testing.

Article Snippet: Antibodies used in this study included mouse monoclonals against β-actin (C4 sc-47778), Prodh (A-11 sc-376401), Dmgdh (E6 sc-393178, Gnmt (A-4 sc-166834), and Rieske FeS IgG (A-5 sc-271609) from Santa Cruz Biotechnology (Santa Cruz, CA); Yme1l1 (#11510–1-AP), Grp78 (#11587–1-AP), and Sardh (#22762–1-AP) rabbit polyclonals from ProteinTech TM (Rosemont, IL); Prodh2/Hypdh rabbit polyclonal (PA5–62366) from Thermo-Fisher (Ashville, NC); HRP-conjugated goat anti-mouse secondary (#1706516) from BioRad Laboratories, Inc. (Hercules, CA); and HRP-conjugated mouse anti-rabbit monoclonal (#211–032–171) from Jackson ImmunoResearch Laboratories (West Grove, PA).

Techniques: Western Blot, RNA Sequencing

A. Schematic of study in which 7-week-old WT mice received extended daily gavage treatments of Veh (n = 5) or N -PPG at doses of 100 mg/kg (n = 5) or 200 mg/kg (n = 6) for 8 weeks, followed by 8 weeks off all treatments before sacrifice and tissue collection (brain, blood, kidneys). B. Body weights during and after treatment demonstrate no significant treatment effect. C. Whole brain immunoblot measured densitometric ratios showed significant (p < 0.01) N -PPG induced mitochondrial rebound of Prodh/Rieske expression above normal (Veh). D. Metabolomic profiling of the post-treatment (100 mg/kg N -PPG) WT brain (cerebellum), kidney and blood samples showed no significant changes in brain or kidney proline or hydroxyproline levels, a nominal (but not significant) increase in kidney sarcosine levels, but persistent significant increases in blood proline and sarcosine levels. E. RNAseq of post-treatment Veh (n = 4) and N -PPG (100 mg/kg, n = 4) WT brain/striatum samples were analyzed by GSEA for significant NES showed that 10 of the 15 highest expressed (NES≥ +2, p < 0.01) GO enrichment terms in the post N -PPG treated samples specifically involved mitochondrial pathways, including mitochondrial respiratory chain complex 1 assembly (NES = +3, p < 0.01).

Journal: Brain research

Article Title: Brain transcriptomic, metabolic and mitohormesis properties associated with N -propargylglycine treatment: A prevention strategy against neurodegeneration

doi: 10.1016/j.brainres.2023.148733

Figure Lengend Snippet: A. Schematic of study in which 7-week-old WT mice received extended daily gavage treatments of Veh (n = 5) or N -PPG at doses of 100 mg/kg (n = 5) or 200 mg/kg (n = 6) for 8 weeks, followed by 8 weeks off all treatments before sacrifice and tissue collection (brain, blood, kidneys). B. Body weights during and after treatment demonstrate no significant treatment effect. C. Whole brain immunoblot measured densitometric ratios showed significant (p < 0.01) N -PPG induced mitochondrial rebound of Prodh/Rieske expression above normal (Veh). D. Metabolomic profiling of the post-treatment (100 mg/kg N -PPG) WT brain (cerebellum), kidney and blood samples showed no significant changes in brain or kidney proline or hydroxyproline levels, a nominal (but not significant) increase in kidney sarcosine levels, but persistent significant increases in blood proline and sarcosine levels. E. RNAseq of post-treatment Veh (n = 4) and N -PPG (100 mg/kg, n = 4) WT brain/striatum samples were analyzed by GSEA for significant NES showed that 10 of the 15 highest expressed (NES≥ +2, p < 0.01) GO enrichment terms in the post N -PPG treated samples specifically involved mitochondrial pathways, including mitochondrial respiratory chain complex 1 assembly (NES = +3, p < 0.01).

Techniques: Western Blot, Expressing

Scheme 1. Scheme of the metabolism of biogenic polyamines and adjacent pathways and their pharmacological inhibitors used in this study. Compounds that target metabolic enzymes are pre- sented in red. ARG—arginase, OTC—ornithine transcarbamoylase, ASS—argininosuccinate synthase, ASL—argininosuccinate lyase, ODC—ornithine decarboxylase, AMD—S-adenosylmethionine decar- boxylase, SRM—spermidine synthase, SMS—spermine synthase, SSAT—spermidine/spermine-N1- acetyltransferase, PAOX—acetylpolyamine oxidase, SMOX—spermine oxidase, PRODH—proline dehy- drogenase, P5C—∆1-pyrrolidine-5-carboxylate, PYCR—P5C reductase, ALDH—aldehyde dehydrogenase.

Journal: Cells

Article Title: Hepatitis C Virus Dysregulates Polyamine and Proline Metabolism and Perturbs the Urea Cycle.

doi: 10.3390/cells13121036

Figure Lengend Snippet: Scheme 1. Scheme of the metabolism of biogenic polyamines and adjacent pathways and their pharmacological inhibitors used in this study. Compounds that target metabolic enzymes are pre- sented in red. ARG—arginase, OTC—ornithine transcarbamoylase, ASS—argininosuccinate synthase, ASL—argininosuccinate lyase, ODC—ornithine decarboxylase, AMD—S-adenosylmethionine decar- boxylase, SRM—spermidine synthase, SMS—spermine synthase, SSAT—spermidine/spermine-N1- acetyltransferase, PAOX—acetylpolyamine oxidase, SMOX—spermine oxidase, PRODH—proline dehy- drogenase, P5C—∆1-pyrrolidine-5-carboxylate, PYCR—P5C reductase, ALDH—aldehyde dehydrogenase.

Article Snippet: Murine antibodies to OAT (sc-374243, 1:500), PRODH (sc-376401, 1:200), and PYCR (sc-243722, 1:200) were from Santa Cruz Biotechnology, Inc. (Dallas, TX, USA).

Techniques: