Journal: Poultry Science

Article Title: Gut microbiota-derived taurolithocholic acid modulates myofiber-type switching via p38 MAPK/PGC-1α signaling underlying breed differences between Arbor Acres and Taoyuan chickens

doi: 10.1016/j.psj.2026.106914

Figure Lengend Snippet: Comparative analysis of growth performance and pectoral muscle development of postnatal broiler chickens (n = 6). A The sampling time of AA chickens at day 1 after hatching (D1), D7, D14, D21, D28, D42, D56 and TY chickens at D1, D7, D14, D21, D28, D42, D56, D77, D105. B The changes in body weight of AA and TY chickens. C The changes in pectoral muscle weight of AA and TY chickens. D Immunofluorescence staining of myofibers with MYH1A and MYH7B of AA and TY chickens. Scale bars: 20 μm. E Statistical analysis of immunofluorescence staining density values for pectoral muscle fibers in AA and TY chickens. Data were shown as mean ± SD; * P < 0.05, ⁎⁎ P < 0.01, ⁎⁎⁎ P < 0.001.

Article Snippet: Following blocking with 1% BSA, the sections were incubated with the primary antibody MYH1A (1:100, F59, DSHB, USA) and the AF647-labeled goat anti-mouse secondary antibody (1:500, A0473, Beyotime), with the primary antibody MYH7B (1:100, S58, DSHB) and the FITC-labeled goat anti-mouse secondary antibody (1:500, A0568, Beyotime).

Techniques: Sampling, Immunofluorescence, Staining

Journal: Poultry Science

Article Title: Gut microbiota-derived taurolithocholic acid modulates myofiber-type switching via p38 MAPK/PGC-1α signaling underlying breed differences between Arbor Acres and Taoyuan chickens

doi: 10.1016/j.psj.2026.106914

Figure Lengend Snippet: Intestinal microbiota transplantation (IMT) affects the growth and pectoral muscle development of chickens. A IMT experimental design. B The variation of body weight of AA and TY chickens during D1 to D28 (n = 6). C Pectoral muscle weight of AA and TY chickens at D21 and D28 (n = 12). d -E Morphology of the myofibers stained by hematoxylin and eosin and the statistics of muscle fiber diameter (MDia) and muscle fiber density (MDen) at D21( D ) and D28 ( E ). F-G The mRNA expression of MYH1A and MYH7B in the pectoral muscle at D21 ( F ) and D28 ( G ) (n = 6). Data were shown as mean ± SD; * P < 0.05, ⁎⁎ P < 0.01, ⁎⁎⁎ P < 0.001.

Article Snippet: Following blocking with 1% BSA, the sections were incubated with the primary antibody MYH1A (1:100, F59, DSHB, USA) and the AF647-labeled goat anti-mouse secondary antibody (1:500, A0473, Beyotime), with the primary antibody MYH7B (1:100, S58, DSHB) and the FITC-labeled goat anti-mouse secondary antibody (1:500, A0568, Beyotime).

Techniques: Transplantation Assay, Staining, Expressing

Journal: Poultry Science

Article Title: Gut microbiota-derived taurolithocholic acid modulates myofiber-type switching via p38 MAPK/PGC-1α signaling underlying breed differences between Arbor Acres and Taoyuan chickens

doi: 10.1016/j.psj.2026.106914

Figure Lengend Snippet: TLCA regulates mitochondrial biogenesis and altered myofiber type composition through the p38 MAPK/PGC-1α signaling pathway. A Cell viability of cells treated with different concentrations of TLCA for 24 h (n = 10). B & F The mRNA expression of MYH1A and MYH7B (n = 6). C & G Intracellular enzymatic activities of succinate dehydrogenase (SDH) and lactate dehydrogenase (LDH), ATP content and mitochondrial DNA (mtDNA) content (n = 6). D & H The mRNA expression of HK1, GPI, PGAM1, PGK1, PYGL, PGC-1α, NRF1 and TFAM (n = 6). E The protein expression of PGC-1α, p38 MAPK and phosphorylation p38 MAPK (n = 3). I The protein expression of PGC-1α (n = 3). Data were shown as mean ± SD; *Represents significant difference when compared with 0 μM TLCA or CON group, and # represents significant difference when compared with TLCA group. *& # P < 0.05, ⁎⁎ & ## P < 0.01, ⁎⁎⁎ & ### P < 0.001.

Article Snippet: Following blocking with 1% BSA, the sections were incubated with the primary antibody MYH1A (1:100, F59, DSHB, USA) and the AF647-labeled goat anti-mouse secondary antibody (1:500, A0473, Beyotime), with the primary antibody MYH7B (1:100, S58, DSHB) and the FITC-labeled goat anti-mouse secondary antibody (1:500, A0568, Beyotime).

Techniques: Expressing, Phospho-proteomics

Journal: Poultry Science

Article Title: Gut microbiota-derived taurolithocholic acid modulates myofiber-type switching via p38 MAPK/PGC-1α signaling underlying breed differences between Arbor Acres and Taoyuan chickens

doi: 10.1016/j.psj.2026.106914

Figure Lengend Snippet: Comparative analysis of growth performance and pectoral muscle development of postnatal broiler chickens (n = 6). A The sampling time of AA chickens at day 1 after hatching (D1), D7, D14, D21, D28, D42, D56 and TY chickens at D1, D7, D14, D21, D28, D42, D56, D77, D105. B The changes in body weight of AA and TY chickens. C The changes in pectoral muscle weight of AA and TY chickens. D Immunofluorescence staining of myofibers with MYH1A and MYH7B of AA and TY chickens. Scale bars: 20 μm. E Statistical analysis of immunofluorescence staining density values for pectoral muscle fibers in AA and TY chickens. Data were shown as mean ± SD; * P < 0.05, ⁎⁎ P < 0.01, ⁎⁎⁎ P < 0.001.

Article Snippet: Following blocking with 1% BSA, the sections were incubated with the primary antibody MYH1A (1:100, F59, DSHB, USA) and the AF647-labeled goat anti-mouse secondary antibody (1:500, A0473, Beyotime), with the primary antibody MYH7B (1:100, S58, DSHB) and the FITC-labeled goat anti-mouse secondary antibody (1:500, A0568, Beyotime).

Techniques: Sampling, Immunofluorescence, Staining

Journal: Poultry Science

Article Title: Gut microbiota-derived taurolithocholic acid modulates myofiber-type switching via p38 MAPK/PGC-1α signaling underlying breed differences between Arbor Acres and Taoyuan chickens

doi: 10.1016/j.psj.2026.106914

Figure Lengend Snippet: Intestinal microbiota transplantation (IMT) affects the growth and pectoral muscle development of chickens. A IMT experimental design. B The variation of body weight of AA and TY chickens during D1 to D28 (n = 6). C Pectoral muscle weight of AA and TY chickens at D21 and D28 (n = 12). d -E Morphology of the myofibers stained by hematoxylin and eosin and the statistics of muscle fiber diameter (MDia) and muscle fiber density (MDen) at D21( D ) and D28 ( E ). F-G The mRNA expression of MYH1A and MYH7B in the pectoral muscle at D21 ( F ) and D28 ( G ) (n = 6). Data were shown as mean ± SD; * P < 0.05, ⁎⁎ P < 0.01, ⁎⁎⁎ P < 0.001.

Article Snippet: Following blocking with 1% BSA, the sections were incubated with the primary antibody MYH1A (1:100, F59, DSHB, USA) and the AF647-labeled goat anti-mouse secondary antibody (1:500, A0473, Beyotime), with the primary antibody MYH7B (1:100, S58, DSHB) and the FITC-labeled goat anti-mouse secondary antibody (1:500, A0568, Beyotime).

Techniques: Transplantation Assay, Staining, Expressing

Journal: Poultry Science

Article Title: Gut microbiota-derived taurolithocholic acid modulates myofiber-type switching via p38 MAPK/PGC-1α signaling underlying breed differences between Arbor Acres and Taoyuan chickens

doi: 10.1016/j.psj.2026.106914

Figure Lengend Snippet: TLCA regulates mitochondrial biogenesis and altered myofiber type composition through the p38 MAPK/PGC-1α signaling pathway. A Cell viability of cells treated with different concentrations of TLCA for 24 h (n = 10). B & F The mRNA expression of MYH1A and MYH7B (n = 6). C & G Intracellular enzymatic activities of succinate dehydrogenase (SDH) and lactate dehydrogenase (LDH), ATP content and mitochondrial DNA (mtDNA) content (n = 6). D & H The mRNA expression of HK1, GPI, PGAM1, PGK1, PYGL, PGC-1α, NRF1 and TFAM (n = 6). E The protein expression of PGC-1α, p38 MAPK and phosphorylation p38 MAPK (n = 3). I The protein expression of PGC-1α (n = 3). Data were shown as mean ± SD; *Represents significant difference when compared with 0 μM TLCA or CON group, and # represents significant difference when compared with TLCA group. *& # P < 0.05, ⁎⁎ & ## P < 0.01, ⁎⁎⁎ & ### P < 0.001.

Article Snippet: Following blocking with 1% BSA, the sections were incubated with the primary antibody MYH1A (1:100, F59, DSHB, USA) and the AF647-labeled goat anti-mouse secondary antibody (1:500, A0473, Beyotime), with the primary antibody MYH7B (1:100, S58, DSHB) and the FITC-labeled goat anti-mouse secondary antibody (1:500, A0568, Beyotime).

Techniques: Expressing, Phospho-proteomics

Journal: Molecular Therapy Oncology

Article Title: Stem cell-directed targeted chemotherapy primes drug-resistant metastatic ovarian tumors for elimination by natural killer cells

doi: 10.1016/j.omton.2026.201214

Figure Lengend Snippet: Evaluation of MICA/B expression on the surface of CSCs and its correlation with sensitivity to laNK92 cells (A–F) Flow cytometry analysis of OV-031-T, OV-172-M, and OV-054-R ovarian CSCs extracted from tumorspheres before (Ctrl) and after treatment with SN38 or 5-FU. n = 3 flasks, biological replicates. (G–I) Measurement of NK cell-mediated toxicity to PDCs using a cell viability assay. This figure shows that treatment of CSCs with SN38 or 5-FU upregulates expression of MICA/B on CSCs making them more vulnerable to NK cells. The data are presented as mean ± SD, n = 3 wells, biological replicates, ∗∗ p < 0.01.

Article Snippet: Three days post-transduction, the transduced OV-031-T, OV-172-M, or OV-054-R cell populations were treated with puromycin (InvivoGen, Cat# ant-pr-1) at final concentrations of 2, 0.5, and 1 μg/mL, respectively, for 1 week to select for fLuc-expressing cells.

Techniques: Expressing, Flow Cytometry, Viability Assay

Journal: Molecular Therapy Oncology

Article Title: Stem cell-directed targeted chemotherapy primes drug-resistant metastatic ovarian tumors for elimination by natural killer cells

doi: 10.1016/j.omton.2026.201214

Figure Lengend Snippet: Evaluation of the ability of laNK92 cells to eliminate SN38/5-FU-treated metastatic ovarian cancer cells in vivo (A, D, G) Bioluminescent imaging of CIEA NOG mice that were implanted with untreated and drug-treated OV-031-T n = 3, OV-172-M n = 4, and OV-054-R n = 4 cancer cells, followed by i.p. injection of laNK92 cells. (B, E, H) qBLI of the change in tumor burden (untreated and drug-treated) after injection of laNK92 cells over the 30-day period. (C, F, I) Statistical analysis of fold change in BLI between untreated and drug-treated cancer cells after NK therapy. This fold change in BLI corresponds to the change in tumor burden over the 30-day period. Data are presented as mean ± SD, t test, ∗ p < 0.05.

Article Snippet: Three days post-transduction, the transduced OV-031-T, OV-172-M, or OV-054-R cell populations were treated with puromycin (InvivoGen, Cat# ant-pr-1) at final concentrations of 2, 0.5, and 1 μg/mL, respectively, for 1 week to select for fLuc-expressing cells.

Techniques: In Vivo, Imaging, Injection

Journal: Molecular Therapy Oncology

Article Title: Stem cell-directed targeted chemotherapy primes drug-resistant metastatic ovarian tumors for elimination by natural killer cells

doi: 10.1016/j.omton.2026.201214

Figure Lengend Snippet: Bioluminescent imaging of OV-031-T, OV-172-M, and OV-054-R ovarian tumors, shown in green, and ASC-shCE2:yCD cells, shown in red, in mice over a three-day period Post euthanasia, OV-031-T (A), OV-172-M (B), and OV-054-R (C) tumors and organs were removed and imaged after addition of furimazine, which is a substrate for nLuc. This figure shows active localization of ASC-shCE2:yCD cells in ovarian tumors, validating their tumor tropic properties; n = 1 mouse per cell line.

Article Snippet: Three days post-transduction, the transduced OV-031-T, OV-172-M, or OV-054-R cell populations were treated with puromycin (InvivoGen, Cat# ant-pr-1) at final concentrations of 2, 0.5, and 1 μg/mL, respectively, for 1 week to select for fLuc-expressing cells.

Techniques: Imaging

Journal: Molecular Therapy Oncology

Article Title: Stem cell-directed targeted chemotherapy primes drug-resistant metastatic ovarian tumors for elimination by natural killer cells

doi: 10.1016/j.omton.2026.201214

Figure Lengend Snippet: Evaluation of therapy responses and cancer relapses by BLI in CIEA NOG mice bearing OV-054-R tumors (A) qBLI of mice in the untreated group, n = 5 mice. (B) qBLI of mice treated with irinotecan, 25 mg/kg, and 5-FC, 350 mg/kg, twice per week, n = 5 mice. (C) qBLI of mice treated with ASC-shCE2:yCD cells once per week plus irinotecan, 35 mg/kg, and 5-FC, 350 mg/kg, twice per week for 11 weeks, followed by 5 weeks of therapy with laNK92-nLuc cells, n = 4, 1 additional mouse for IHC. The blue arrows point to the days laNK92-nLuc cells were injected. The number of animals per group was estimated based on pilot studies, providing sufficient power to avoid type I and type II errors. The dashed line at 1 ×10 6 , radiance, shows the background bioluminescence of mice without any tumors. (D) IHC of excised OV-054-R tumor tissue from the ASC-treated group versus the untreated control group using an anti-GFP primary antibody. (E) BLI, nLuc imaging, of laNK92-nLuc cells, validating the viability of the NK cells during the immunotherapy phase. (F) Measurement of mouse body weight during the immunotherapy phase.

Article Snippet: Three days post-transduction, the transduced OV-031-T, OV-172-M, or OV-054-R cell populations were treated with puromycin (InvivoGen, Cat# ant-pr-1) at final concentrations of 2, 0.5, and 1 μg/mL, respectively, for 1 week to select for fLuc-expressing cells.

Techniques: Injection, Control, Imaging

Journal: bioRxiv

Article Title: Auxin is metabolized through kynurenine in Hypericum perforatum L

doi: 10.64898/2026.05.18.726114

Figure Lengend Snippet: (A) Schematic representation of major tryptophan (Trp)-derived metabolic pathways, including the kynurenine pathway (center), the indole-3-pyruvic acid (IPA)–indole-3-acetic acid (IAA) pathway, and the tryptamine– serotonin–melatonin branch (top). Solid, dashed, and double boxes indicate metabolites reported in animals, plants, or both, respectively. Enzymes are indicated at each step: IDO1/IDO2 (indoleamine 2,3-dioxygenase), TDO (tryptophan 2,3-dioxygenase), AFMID (arylformamidase), KAT (kynurenine aminotransferase), TDC (tryptophan decarboxylase), TAA1/TAR (tryptophan aminotransferase), KYNU (kynureninase), KMO (kynurenine 3-monooxygenase), HAAO (3-hydroxyanthranilate 3,4-dioxygenase), ACMSD (α-amino-β-carboxymuconate-ε-semialdehyde decarboxylase), and QPRT (quinolinate phosphoribosyltransferase). Inhibitor targets are indicated at the corresponding steps: JM6 and RO 61-8048 inhibit KMO, and PF-04859989 inhibits KAT. (B) Chemical structures of the kynurenine pathway metabolites quantified in this study: kynurenine, kynurenic acid (KYNA), and 3-hydroxyanthranilic acid (3-HAA). (C) Chemical structures of the inhibitors used in this study. Core structural differences between JM6 and RO 61-8048 are highlighted in red.

Article Snippet: The compound (R)-3-amino-1-hydroxy-3,4-dihydroquinolin-2(1H)-one (PF-04859989) was identified by a high-throughput screen of the Pfizer compound library as a high-affinity inhibitor of human kynurenine aminotransferase (KAT; ).

Techniques: Derivative Assay

Journal: bioRxiv

Article Title: Auxin is metabolized through kynurenine in Hypericum perforatum L

doi: 10.64898/2026.05.18.726114

Figure Lengend Snippet: ( A) Representative images of explants cultured on MSO (control), kynurenine (KYN), indole-3-acetic acid (IAA), and IAA combined with inhibitors (IAA + JM6, IAA + PF-04859989 [PF], and IAA + RO 61-8048 [RO]). Scale bar = 1 cm (B) Rooting frequency, (C) internodal length (cm per node), (D) root number, and (E) maximum root length (cm) of explants under each treatment. For rooting frequency (B), bars represent mean proportion rooted ± SE. For (C–E), boxplots represent median (center line), interquartile range (box), and range (whiskers). Differences relative to the MSO control were evaluated using Dunnett-adjusted contrasts (p < 0.05; n = 12–18 per treatment).

Article Snippet: The compound (R)-3-amino-1-hydroxy-3,4-dihydroquinolin-2(1H)-one (PF-04859989) was identified by a high-throughput screen of the Pfizer compound library as a high-affinity inhibitor of human kynurenine aminotransferase (KAT; ).

Techniques: Cell Culture, Control

Journal: bioRxiv

Article Title: Auxin is metabolized through kynurenine in Hypericum perforatum L

doi: 10.64898/2026.05.18.726114

Figure Lengend Snippet: (A–C) Representative extracted ion chromatograms (EICs) of PF-04859989 (A), RO 61-8048 (B), and JM6 (KMO inhibitor II) (C) detected in plant tissue by LC–HRMS. Each panel shows the precursor ion trace at the expected m/z and retention time. (D–F) Relative abundance of PF (D), RO (E), and JM6 (F) in roots and shoots following treatment with MSO (control), inhibitor alone, or IAA + inhibitor. Peak areas are shown as log□□-transformed values. Boxplots represent median (center line), interquartile range (box), and range (whiskers). Signals corresponding to each inhibitor were observed in treated tissues and were not detected in MSO controls. Detection was also observed in IAA co-application treatments.

Article Snippet: The compound (R)-3-amino-1-hydroxy-3,4-dihydroquinolin-2(1H)-one (PF-04859989) was identified by a high-throughput screen of the Pfizer compound library as a high-affinity inhibitor of human kynurenine aminotransferase (KAT; ).

Techniques: Control, Transformation Assay

Journal: bioRxiv

Article Title: Auxin is metabolized through kynurenine in Hypericum perforatum L

doi: 10.64898/2026.05.18.726114

Figure Lengend Snippet: Concentrations of (A, D) kynurenic acid (KYNA), (B, E) kynurenine (KYN), and (C, F) 3-hydroxyanthranilic acid (3-HAA) in shoots (A–C) and roots (D–F) of explants cultured on MSO (control), IAA, or IAA combined with kynurenine pathway inhibitors (IAA + JM6, IAA + PF-04859989, and IAA + RO 61-8048). Concentrations are shown as log□□ (ng g −1 FW). Boxplots represent median (center line), interquartile range (box), and range (whiskers). For shoots (A–C), different letters indicate significant differences among treatments (one-way ANOVA followed by Tukey’s HSD, p < 0.05; n = 3). For roots (D–F), differences relative to the MSO control were evaluated using Dunnett-adjusted contrasts (p < 0.05; n = 3).

Article Snippet: The compound (R)-3-amino-1-hydroxy-3,4-dihydroquinolin-2(1H)-one (PF-04859989) was identified by a high-throughput screen of the Pfizer compound library as a high-affinity inhibitor of human kynurenine aminotransferase (KAT; ).

Techniques: Cell Culture, Control

Journal: bioRxiv

Article Title: Auxin is metabolized through kynurenine in Hypericum perforatum L

doi: 10.64898/2026.05.18.726114

Figure Lengend Snippet: Indole-3-acetic acid (IAA) is primarily synthesized from tryptophan through the indole-3-pyruvate (IPyA) pathway via tryptophan aminotransferase (TAA) and YUCCA flavin monooxygenase (YUC). Free IAA may be regulated through conjugation, catabolism, oxidative transformation and through feedback effects on tryptophan-derived metabolism. Kynurenine pathway metabolism proceeds through N-formyl-kynurenine and kynurenine, which occupies a central branch point between kynurenic acid formation via kynurenine aminotransferase (KAT) and downstream oxidative metabolism toward 3-hydroxyanthranilic acid (3-HAA) via kynurenine monooxygenase (KMO). Reactive oxygen species (ROS), temperature, drought, iron, and Fe 2+ are shown as potential stress and redox inputs that may influence auxin and kynurenine-associated metabolism. The pharmacological inhibitors used in this study are shown at their proposed targets: PF-04859989 at KAT, and RO-61-8048 and JM6 at kynurenine monooxygenase (KMO). Dashed arrows indicate proposed interactions linking auxin catabolism or oxidative transformation with kynurenine-associated metabolite accumulation and potential feedback on tryptophan-dependent auxin biosynthesis.

Article Snippet: The compound (R)-3-amino-1-hydroxy-3,4-dihydroquinolin-2(1H)-one (PF-04859989) was identified by a high-throughput screen of the Pfizer compound library as a high-affinity inhibitor of human kynurenine aminotransferase (KAT; ).

Techniques: Synthesized, Conjugation Assay, Transformation Assay, Derivative Assay