Journal: Materials Today Bio

Article Title: Lactoferrin-cyanidin-3-glucoside nanoparticles alleviate inflammation and oxidative stress via Sesn2/Nrf2 activation in mastitis

doi: 10.1016/j.mtbio.2025.102491

Figure Lengend Snippet: Schematic illustration of lactoferrin-cyanidin-3-glucoside-encapsulated nanoparticles alleviating LTA-induced inflammation and oxidative stress via Sesn2/Nrf2 activation in mastitis.

Article Snippet: Following this, sections were blocked using goat serum to minimize non-specific binding and incubated overnight at 4 °C with a rabbit-derived primary antibody specific for SESN2 (Proteintech, 66297-1-Ig), Nrf2 (Proteintech, 16396-1-AP), and TNF-α (Abmart, PY19810) at a 1:300 dilution.

Techniques: Activation Assay

Journal: Materials Today Bio

Article Title: Lactoferrin-cyanidin-3-glucoside nanoparticles alleviate inflammation and oxidative stress via Sesn2/Nrf2 activation in mastitis

doi: 10.1016/j.mtbio.2025.102491

Figure Lengend Snippet: Effect of LF-C3GNPs on H 2 O 2 -induced oxidative stress and inflammation in HC11 cells via Sesn2/Nrf2 signaling activation. (A – D) Antioxidant enzyme activity of SOD, CAT, GPx and lipid peroxidation marker (MDA) levels in HC11 cells (n = 3). (E – L) RT-qPCR analysis (E – K) and Western blotting (L) of key redox regulators biomarkers (Nrf2, SLC7A11, Keap1, Sesn2, NQO1, HO-1, and GPX4) under different treatments (n = 3). (M – O) Immunofluorescence staining (M) and quantification (N, O) of Nrf2 and Sesn2 in HC11 (n = 3). Scale bar: 50 μm. Mean ± SD; # p<0.05 compared to the untreated control group; ∗ p<0.05 , ∗∗ p<0.01 , ∗∗∗ p<0.001 , and ∗∗∗∗ p<0.0001 relative to the H 2 O 2 -treated groups.

Article Snippet: Following this, sections were blocked using goat serum to minimize non-specific binding and incubated overnight at 4 °C with a rabbit-derived primary antibody specific for SESN2 (Proteintech, 66297-1-Ig), Nrf2 (Proteintech, 16396-1-AP), and TNF-α (Abmart, PY19810) at a 1:300 dilution.

Techniques: Activation Assay, Activity Assay, Marker, Quantitative RT-PCR, Western Blot, Immunofluorescence, Staining, Control

Journal: Materials Today Bio

Article Title: Lactoferrin-cyanidin-3-glucoside nanoparticles alleviate inflammation and oxidative stress via Sesn2/Nrf2 activation in mastitis

doi: 10.1016/j.mtbio.2025.102491

Figure Lengend Snippet: Effect of LF-C3GNPs on S. aureus -induced oxidative stress and inflammation in mice via Sesn2/Nrf2 signaling activation . (A – D) Antioxidant enzyme activity of SOD, CAT, GPx and lipid peroxidation marker (MDA) levels in S. aureus -infected mammary tissue (n = 3). (E – L) Western blotting (E) and RT-qPCR analysis (F – L) of key redox regulators biomarkers (Nrf2, Sesn2, Keap1, SLC7A11, NQO1, HO-1, and GPX4) under different treatments (n = 3). (M – O) Immunofluorescence staining (M) and quantification (N, O) of Nrf2 and Sesn2 in S. aureus -infected mammary tissue (n = 3). Scale bar: 50 μm. Mean ± SD; # p<0.05 compared to the untreated control group; ∗ p<0.05 , ∗∗ p<0.01 , ∗∗∗ p<0.001 , and ∗∗∗∗ p<0.0001 relative to the S. aureus -treated groups.

Article Snippet: Following this, sections were blocked using goat serum to minimize non-specific binding and incubated overnight at 4 °C with a rabbit-derived primary antibody specific for SESN2 (Proteintech, 66297-1-Ig), Nrf2 (Proteintech, 16396-1-AP), and TNF-α (Abmart, PY19810) at a 1:300 dilution.

Techniques: Activation Assay, Activity Assay, Marker, Infection, Western Blot, Quantitative RT-PCR, Immunofluorescence, Staining, Control

Journal: Cancers

Article Title: Docosahexaenoic Acid Enhances Oxaliplatin-Induced Autophagic Cell Death via the ER Stress/Sesn2 Pathway in Colorectal Cancer

doi: 10.3390/cancers11070982

Figure Lengend Snippet: Combinatorial treatment upregulates expression of SESN2 in human CRC. ( A ) mRNA expression levels of SESN2 in normal and tumor tissues were evaluated using the mRNA expression data of the IlluminaHiSeq of TCGA CRC. **, p < 0.01. ( B ) SESN2 protein levels in normal and tumor tissues were evaluated using western blotting. ( C , D ) Comparison of endogenous expression levels of SESN2 mRNA and protein in normal human cells and human CRC cells using quantitative real-time polymerase chain reaction (qRT-PCR) analysis ( C ), immunoblotting ( D ). ***, p < 0.001. ( E , F ) SESN2 protein levels in the Oxaliplatin and DHA combination was analyzed by immunoblotting ( E ) and immunofluorescence ( F ) (Scale bar, 10 μm). ( G , H ) Following transfection with control small interfering RNA (siRNA) or SESN2 siRNA, cells were exposed to the Oxaliplatin and DHA combination. The mRNA ( G ) and protein ( H ) expression of LC3 and p62 were evaluated using qRT-PCR and western blotting. ***, p < 0.001.

Article Snippet: HCT116 cells were transfected with SESN2 siRNA and CHOP small interfering RNA (siRNA) that were purchased from Santa Cruz Biotechnology (Santa Cruz).

Techniques: Expressing, Western Blot, Comparison, Real-time Polymerase Chain Reaction, Quantitative RT-PCR, Immunofluorescence, Transfection, Control, Small Interfering RNA

Journal: Cancers

Article Title: Docosahexaenoic Acid Enhances Oxaliplatin-Induced Autophagic Cell Death via the ER Stress/Sesn2 Pathway in Colorectal Cancer

doi: 10.3390/cancers11070982

Figure Lengend Snippet: CHOP regulates SESN2 activity by binding directly to the SESN2 promoter region. ( A ) The correlation of SESN2 expression and ER stress-related genes in CRC patients. ( B ) HCT116 cells were pre-treated with thapsigargin for 1 h and then exposed to the Oxaliplatin and DHA combination for 24 h. SESN2 protein expression was confirmed with western blotting. ( C – F ) Following transfection with control siRNA, CHOP siRNA, or SESN2 siRNA, the SESN2 and CHOP protein levels were determined using qRT-PCR ( C , E ) and immunoblotting ( D , F ). ***, p < 0.001. ( G ) Illustration of the three predicted CHOP binding sites (BS) and ATF BS in the SESN2 promoter. ( H ) Cells were treated with Oxaliplatin and DHA, and then immunoprecipitated with either IgG or CHOP.

Article Snippet: HCT116 cells were transfected with SESN2 siRNA and CHOP small interfering RNA (siRNA) that were purchased from Santa Cruz Biotechnology (Santa Cruz).

Techniques: Activity Assay, Binding Assay, Expressing, Western Blot, Transfection, Control, Quantitative RT-PCR, Immunoprecipitation

Journal: Cancers

Article Title: Docosahexaenoic Acid Enhances Oxaliplatin-Induced Autophagic Cell Death via the ER Stress/Sesn2 Pathway in Colorectal Cancer

doi: 10.3390/cancers11070982

Figure Lengend Snippet: Combinatorial treatment with DHA and Oxaliplatin increases CHOP expression and in vivo autophagy. ( A – D ) Nude mice were subcutaneously inoculated with 1 × 107 HCT116-Luc+ Cells. When tumor volume reached approximately 200 mm 3 , the mice were treated with EtOH, DHA (10 mg/kg), Oxaliplatin (10 mg/kg), or the combinatorial treatment of DHA and Oxaliplatin (10 mg/kg), administered 3 times a week for 2 weeks. ( A ) Mice were imaged using the NightOWL LB983 bioluminescence imaging (BLI) system. ( B ) Line graph illustrating the tumor volume (mm 3 ). ***, p < 0.001. ( C ) Tumor tissues were harvested on day 14 and then imaged using a digital camera. ( D ) Graph illustrating body weight. **, p < 0.01. ( E , F ) Immunohistochemistry (IHC) showing LC3 (upper panel), CHOP (middle panel), and SESN2 (lower panel) in the tumors from xenograft at a 400× magnification. (Scale bar, 20 μm). **, p < 0.01 and ***, p < 0.001.

Article Snippet: HCT116 cells were transfected with SESN2 siRNA and CHOP small interfering RNA (siRNA) that were purchased from Santa Cruz Biotechnology (Santa Cruz).

Techniques: Expressing, In Vivo, Imaging, Immunohistochemistry

Journal: Cell death & disease

Article Title: HGK-sestrin 2 signaling-mediated autophagy contributes to antitumor efficacy of Tanshinone IIA in human osteosarcoma cells.

doi: 10.1038/s41419-018-1016-9

Figure Lengend Snippet: Fig. 4 SESN2 but not Beclin 1 contributed to TIIA-induced autophagic induction and anchorage-independent growth inhibition in human osteosarcoma cells. a 143B cells were treated with various concentrations of TIIA (1, 5, 10, and 20 μM) as indicated for 24 h, after which BECN1, class III PI3K, ATG5, ATG7, SESN2, AMPK-α, p-AMPK-α, JNK1, p-SAPK/JNK, c-Jun, and p-c-Jun were measured by western blot. b–d shRNA SESN2 or shRNA BECN1 was stably transfected into 143B cells and the stable transfectants were identified (b). Following treatment with TIIA (20 μM) in 143B SESN2KD

Article Snippet: For knockdown of SESN2, BECN1, and HGK, pGFP-VRS plasmid encoding shRNA against human SESN2 (TG301755), BECN1 (TG314484), and HGK (TG320615) were purchased from OriGene (Rockville, MD).

Techniques: Inhibition, Western Blot, shRNA, Stable Transfection, Transfection

Journal: Cell death & disease

Article Title: HGK-sestrin 2 signaling-mediated autophagy contributes to antitumor efficacy of Tanshinone IIA in human osteosarcoma cells.

doi: 10.1038/s41419-018-1016-9

Figure Lengend Snippet: Fig. 6 HGK acted an upstream regulator that mediated initiation of the JNK MAP kinase and SESN2-dependent autophagy following TIIA treatment. a Western-assisted analysis of HGK after TIIA treatment as indicated for 24 h in 143B and MG63 cells. b 143B cells were pretreated with GNE-495 (8 nM, 1 h) followed by TIIA treatment as indicated for 24 h. Total lysates were immunoblotted for LC3B, HGK, and p-SAPK/JNK expression. c, d shRNA HGK was stably transfected into 143B (c) and MG63 cells (d). Following treatment with TIIA (20 μM) for indicated time intervals, total lysates were immunoblotted for LC3B, HGK, SESN2, p-SAPK/JNK, JNK1, p-c-Jun, and total c-Jun expression. β-actin served as loading control. e, f Representative images of colonies of 143B-HGKKD (shHGK) and 143B-mock (nonsense) cells in a soft agar colony formation assay in the absence or presence of various concentrations of TIIA were captured using a microscope. Scale bar: 500 μm (e). Results were expressed as average number of colonies counted (in six microfields) (f). g, h 143B cells were transiently transfected with the AP-1 luciferase reporter construct (g) or SESN2 promoter luciferase reporter construct (h). After 24 h, the cells were treated with various concentrations of TIIA for another 12 h and the relative luciferase activity was measured and presented as relative AP-1 activity or relative SESN2 promoter activity. The results were expressed as the means ± SD from three independent experiments (n ≥3, *P < 0.05 compared with untreated control)

Article Snippet: For knockdown of SESN2, BECN1, and HGK, pGFP-VRS plasmid encoding shRNA against human SESN2 (TG301755), BECN1 (TG314484), and HGK (TG320615) were purchased from OriGene (Rockville, MD).

Techniques: Western Blot, Expressing, shRNA, Stable Transfection, Transfection, Control, Soft Agar Assay, Microscopy, Luciferase, Construct, Activity Assay

Journal: Cell death & disease

Article Title: HGK-sestrin 2 signaling-mediated autophagy contributes to antitumor efficacy of Tanshinone IIA in human osteosarcoma cells.

doi: 10.1038/s41419-018-1016-9

Figure Lengend Snippet: Fig. 7 SESN2 and p-AMPK-α downregulation is a common event in osteosarcoma tissues. a, b Representative immunohistochemical staining of the expression of SESN2 (a) and p-AMPK (b) in normal bone tissues and osteosarcoma tissues. c Schematic model of TIIA-mediated induction of autophagic cell death in osteosarcoma cells

Article Snippet: For knockdown of SESN2, BECN1, and HGK, pGFP-VRS plasmid encoding shRNA against human SESN2 (TG301755), BECN1 (TG314484), and HGK (TG320615) were purchased from OriGene (Rockville, MD).

Techniques: Immunohistochemical staining, Staining, Expressing

Journal: Frontiers in Cell and Developmental Biology

Article Title: Sestrin2 Regulates Osteoclastogenesis via the p62-TRAF6 Interaction

doi: 10.3389/fcell.2021.646803

Figure Lengend Snippet: The skeletal phenotype is altered in Sesn2 KO mice. For the in vivo experiments, distal femoral bones were isolated from WT and Sesn2 KO male mice and analyzed histologically and by micro-computed tomography (μCT). (A) Micro-radiographic analyses of femur obtained from 13 to 15-week old WT ( n = 6) and Sesn2 KO mice ( n = 9). The bone mass increased in Sesn2 KO mice. Bone volume over total volume (BV/TV), trabecular thickness (Tb.Th), trabecular number (Tb.N), and trabecular separation (Tb.Sp) were expressed as mean ± S.E.M. * p < 0.05 and ** p < 0.01 compared with WT mice. N.S. = not significant (Scale bar = 500 μm). (B) Trabecular surfaces of sectioned femurs from WT ( n = 5) and Sesn2 KO mice ( n = 7) were TRAP-stained. TRAP + osteoclasts along the trabecular surfaces on bone sections are indicated by arrows. There were fewer osteoclasts on the bone surface of Sesn2 KO mice than WT mice. The percentages of TRAP-labeled osteoclast surface over bone surface (Oc.S/BS) were calculated, and the results are presented as fold-change relative to WT mice (Scale bar = 100 μm). Oc.S/BS and number of osteoclast over bone surface (N.Oc/BS) were measured using Bio-Quant software and expressed as mean ± S.E.M. * p < 0.05 compared with WT.

Article Snippet: Sesn2 plasmid (pcDNA3.1 Flag-Sesn2; plasmid #61868) was obtained from Addgene (Cambridge, MA, United States).

Techniques: In Vivo, Isolation, Micro-CT, Staining, Labeling, Software

Journal: Frontiers in Cell and Developmental Biology

Article Title: Sestrin2 Regulates Osteoclastogenesis via the p62-TRAF6 Interaction

doi: 10.3389/fcell.2021.646803

Figure Lengend Snippet: Deletion of Sesn2 inhibits osteoclast differentiation. (A) Primary calvarial osteoblasts derived from WT and Sesn2 KO mice were stained for ALP and ARS after 14 day of cell culture ( n = 4). The Sesn2 deletion had no effects on osteoblast differentiation in Sesn2 KO mice. N.S. = not significant. (B) Primary BMMs derived from WT and Sesn2 KO mice were TRAP-stained after 6 days of cell culture ( n = 4). After staining, TRAP + MNCs with more than three nuclei were scored as osteoclasts. Osteoclast differentiation was reduced in Sesn2 KO mice (Scale bar = 50 μm). Data were expressed as mean ± S.E.M. * p < 0.05, ** p < 0.01, and *** p < 0.001 compared with RANKL-treated WT mice. (C) BMMs were plated on a pit assay plate and cultured for 6 days ( n = 4). The attached cells were removed and photographed under a light microscope. Pit areas were quantified using Bio-Quant software (Scale bar = 50 μm). RANKL-induced bone resorption was inhibited in Sesn2 KO BMMs. The data were normalized to the resorptive area in RANKL-treated BMMs from WT mice. Results were expressed as mean ± S.E.M. * p < 0.05 compared with RANKL-treated WT mice. (D) Expression of NFATc1 (90∼110 kDa), Sestrin2 (54 kDa), and tubulin (50 kDa) in WT and Sesn2 KO BMMs after RANKL stimulation were quantified by immunoblotting and ImageJ analysis ( n = 6). Expression of NFATc1 was lower in Sesn2 KO BMM cells than in WT BMM cells. Data were normalized to the expression in cells from WT mice and expressed as mean ± S.E.M. * p < 0.05, ** p < 0.01, and *** p < 0.001 compared with WT.

Article Snippet: Sesn2 plasmid (pcDNA3.1 Flag-Sesn2; plasmid #61868) was obtained from Addgene (Cambridge, MA, United States).

Techniques: Derivative Assay, Staining, Cell Culture, Light Microscopy, Software, Expressing, Western Blot

Journal: Frontiers in Cell and Developmental Biology

Article Title: Sestrin2 Regulates Osteoclastogenesis via the p62-TRAF6 Interaction

doi: 10.3389/fcell.2021.646803

Figure Lengend Snippet: Reduced expression of osteoclast differentiation marker genes in Sesn2 KO mice. (A) Expression of mRNAs for the master regulators of osteoclastogenesis were measured on 2 days after RANKL treatment. Osteoclastogenesis-related gene expression diminished in Sesn2 KO BMMs during osteoclast differentiation ( n = 4). Data were expressed as mean ± S.E.M. * p < 0.05 compared with WT. N.S. = not significant. (B) BMM cells were treated with 100 ng/ml RANKL for the period indicated. Protein expression of p-JNK (90∼110 kDa), p-ERK (44, 42 kDa), p-p38 (41 kDa), and IκBα (35 kDa) was quantified by immunoblotting and ImageJ analysis ( n = 3). The RANKL-induced activation of the TRAF6 downstream pathways was reduced in Sesn2 KO osteoclasts. Data were normalized to expression in WT cells and expressed as mean ± S.E.M.

Article Snippet: Sesn2 plasmid (pcDNA3.1 Flag-Sesn2; plasmid #61868) was obtained from Addgene (Cambridge, MA, United States).

Techniques: Expressing, Marker, Gene Expression, Western Blot, Activation Assay

Journal: Frontiers in Cell and Developmental Biology

Article Title: Sestrin2 Regulates Osteoclastogenesis via the p62-TRAF6 Interaction

doi: 10.3389/fcell.2021.646803

Figure Lengend Snippet: The p62 and TRAF6 interaction is inhibited in Sesn2 KO mice. (A) RANKL-induced ROS generation was measured in WT and Sesn2 KO BMMs ( n = 7). Deletion of Sesn2 had no effect on ROS generation in Sesn2 KO BMMs. The data were normalized to the amount of ROS generated in WT cells and expressed as mean ± S.E.M. *** p < 0.001 compared with control. N.S. = not significant (Scale bar = 10 μm). (B) The number of RANKL-induced [Ca 2+ ] i oscillations were measured in WT and Sesn2 KO BMMs ( n = 5). Deletion of Sesn2 had no effects on [Ca 2+ ] i oscillations. The data were expressed as means ± S.E.M. *** p < 0.001 compared with control. N.S. = not significant. (C) BMMs from WT and Sesn2 KO mice were treated with RANKL for the period indicated, immunoprecipitated with anti-TRAF6 antibody, and the precipitates were immunoblotted for p62 (55 kDa) and TRAF6 (60 kDa; n = 3). The Sesn2 deletion inhibited the interaction between p62 and TRAF6. Data were expressed as mean ± SEM. *** p < 0.001 compared with WT. (D) BMMs from Sesn2 KO mice were transfected with Flag- Sesn2 ( n = 3). At 24 h post-transfection, cells were harvested and lysed, and cell lysates were subjected to immunoprecipitation with anti-TRAF6 antibody. The inhibition of interaction between p62 and TRAF6 in the Sesn2 deletion was recovered by transfection of Sesn2 KO BMMs with Flag- Sesn2 . Data were expressed as mean ± SEM. * p < 0.05 compared with transfected WT. N.S. = not significant. (E) BMMs from WT and Sesn2 KO mice were transfected with pLVX-EIP and pLVX-EIP-Flag- Sesn2 ( n = 3). At 24 h post-infection, cells were treated 50 ng/ml RANKL for 6 days, and then TRAP-stained. TRAP + MNCs with more than ten nuclei were scored as osteoclasts. The reduction in TRAP + osteoclasts in the Sesn2 deletion was recovered to WT levels by transfection of pLVX-EIP-Flag- Sesn2 into Sesn2 KO BMMs when compared to transfection of pLVX-EIP into WT BMMs. Data were expressed as mean ± SEM (Scale bar = 50 μm). ** p < 0.01 and *** p < 0.001 compared with RANKL-treated WT BMMs.

Article Snippet: Sesn2 plasmid (pcDNA3.1 Flag-Sesn2; plasmid #61868) was obtained from Addgene (Cambridge, MA, United States).

Techniques: Generated, Control, Immunoprecipitation, Transfection, Inhibition, Infection, Staining

Journal: Nutrition & metabolism

Article Title: Sestrin2 knockout exacerbates high-fat diet induced metabolic disorders and complications in female mice.

doi: 10.1186/s12986-024-00834-8

Figure Lengend Snippet: Fig. 1 Sesn2 knockout aggravates obesity in female mice. (A-B) mice in four groups; (C) body weight; (D-E) fat mass; (F) FFA; (G) TG; (H) FBG; (I-J) OGTT and ITT; n = 4–6/group. *P < 0.05; #P < 0.05 vs. KO-NC. +P < 0.05 vs. WT-HFD

Article Snippet: Six-week-old female C57BL/6J mice (Pengyue Animal Breeding Co., Ltd.) and Sesn2 whole-body KO mice (Cyagen Biosciences Inc.) accommodated in ventilated cages.

Techniques: Knock-Out

Journal: Nutrition & metabolism

Article Title: Sestrin2 knockout exacerbates high-fat diet induced metabolic disorders and complications in female mice.

doi: 10.1186/s12986-024-00834-8

Figure Lengend Snippet: Fig. 2 Sesn2 knockout aggravates liver injury in female mice (A) ALT; (B) AST; (C) Ccl2 mRNA levels (D) Il6 mRNA levels; (E-G) H&E, Masson’s staining and Oil O Red; (H-J) Western blot for AMPK and mTOR; n = 4–5/group, *P < 0.05

Article Snippet: Six-week-old female C57BL/6J mice (Pengyue Animal Breeding Co., Ltd.) and Sesn2 whole-body KO mice (Cyagen Biosciences Inc.) accommodated in ventilated cages.

Techniques: Knock-Out, Staining, Western Blot

Journal: Nutrition & metabolism

Article Title: Sestrin2 knockout exacerbates high-fat diet induced metabolic disorders and complications in female mice.

doi: 10.1186/s12986-024-00834-8

Figure Lengend Snippet: Fig. 3 Sesn2 knockout aggravates cardiac dysfunction in female Mice. (A-B) cardiac dysfunction (E/F ratio and E/A ratio); (C-E) H&E and Masson’s staining; n = 4–5/group, *P < 0.05

Article Snippet: Six-week-old female C57BL/6J mice (Pengyue Animal Breeding Co., Ltd.) and Sesn2 whole-body KO mice (Cyagen Biosciences Inc.) accommodated in ventilated cages.

Techniques: Knock-Out, Staining

Journal: Nutrition & metabolism

Article Title: Sestrin2 knockout exacerbates high-fat diet induced metabolic disorders and complications in female mice.

doi: 10.1186/s12986-024-00834-8

Figure Lengend Snippet: Fig. 4 Sesn2 knockout aggravates renal injury in female mice (A) 24-hour UAE; (B) 24-hour urinary volume; (C, D) H&E and Masson’s staining; n = 5/group *P < 0.05

Article Snippet: Six-week-old female C57BL/6J mice (Pengyue Animal Breeding Co., Ltd.) and Sesn2 whole-body KO mice (Cyagen Biosciences Inc.) accommodated in ventilated cages.

Techniques: Knock-Out, Staining

Journal: Nutrition & metabolism

Article Title: Sestrin2 knockout exacerbates high-fat diet induced metabolic disorders and complications in female mice.

doi: 10.1186/s12986-024-00834-8

Figure Lengend Snippet: Fig. 5 Sesn2 knockout aggravates adipose dysfunction in female mice (A-B) Atgl and Lpl in inguinal WAT; (C-D) Cidea and Ucp1 in BAT; (E-F) Adrb3 and Ucp1 in inguinal WAT; (G-K) Pgc1α, Sirt1, Adipoq, Il6 and Tnf in inguinal WAT; (L) UCP-1 protein in BAT. n = 4–6, *P < 0.05

Article Snippet: Six-week-old female C57BL/6J mice (Pengyue Animal Breeding Co., Ltd.) and Sesn2 whole-body KO mice (Cyagen Biosciences Inc.) accommodated in ventilated cages.

Techniques: Knock-Out

Journal: Nutrition & metabolism

Article Title: Sestrin2 knockout exacerbates high-fat diet induced metabolic disorders and complications in female mice.

doi: 10.1186/s12986-024-00834-8

Figure Lengend Snippet: Fig. 6 Sesn2 knockout exacerbates high-fat diet induced metabolic disorders and complications in female mice

Article Snippet: Six-week-old female C57BL/6J mice (Pengyue Animal Breeding Co., Ltd.) and Sesn2 whole-body KO mice (Cyagen Biosciences Inc.) accommodated in ventilated cages.

Techniques: Knock-Out