Journal: International Journal of Molecular Sciences

Article Title: Chimeric Anti-Glypican 1 Antibodies Exert Antitumor Activities in Xenograft Models of Lung and Pancreatic Cancers

doi: 10.3390/ijms27104181

Figure Lengend Snippet: Production of recombinant G 1 Mab-28-mG 2a and G 1 Mab-28-hG 1 . ( A ) After determination of CDRs of G 1 Mab-28 (mouse IgG 1 ), G 1 Mab-28-mG 2a (mouse IgG 2a ) and G 1 Mab-28-hG 1 (human IgG 1 ) were produced. The amino acid sequence of V H and V L CDRs was indicated. ( B ) PMab-231 (control mIgG 2a ), G 1 Mab-28-mG 2a , humCvMab-62 (control hIgG 1 ), and G 1 Mab-28-hG 1 were subjected to SDS-PAGE, and the gel was stained with Bio-Safe CBB G-250 Stain. ( C ) Flow cytometry using G 1 Mab-28-mG 2a (1 μg/mL; Red line) and G 1 Mab-28-hG 1 (1 μg/mL; Blue line) against CHO/GPC1 and CHO/PA16-mouse GPC1 (CHO/mouse GPC1). An anti-PA16 tag mAb (NZ-1) detected PA16-tagged mouse GPC1 (1 μg/mL; Green line). After treatment with primary mAbs or buffer control (Black line), cells were treated with Alexa Fluor 488-conjugated anti-mouse or rat IgG, or FITC-conjugated anti-human IgG. ( D ) Determination of the binding affinity of G 1 Mab-28-mG 2a and G 1 Mab-28-hG 1 . CHO/GPC1 was suspended in G 1 Mab-28-mG 2a and G 1 Mab-28-hG 1 at indicated concentrations, followed by Alexa Fluor 488-conjugated anti-mouse IgG or FITC-conjugated anti-human IgG treatment. The SA3800 Cell Analyzer was used to analyze fluorescence data. The dissociation constant ( K D ) values were determined using GraphPad Prism 6.

Article Snippet: The mouse GPC1 ( NM_016696.4 ) cDNA was obtained from OriGene Technologies, Inc. (Rockville, MD, USA).

Techniques: Recombinant, Produced, Sequencing, Control, SDS Page, Staining, Flow Cytometry, Binding Assay, Fluorescence

Journal: International Journal of Molecular Sciences

Article Title: Chimeric Anti-Glypican 1 Antibodies Exert Antitumor Activities in Xenograft Models of Lung and Pancreatic Cancers

doi: 10.3390/ijms27104181

Figure Lengend Snippet: ADCC and CDC by G 1 Mab-28-mG 2a against GPC1-positive tumor cells. The target cells labeled with Calcein AM (CHO/GPC1, PC-10, and PK-45H) were incubated with effector splenocyte derived from BALB/c nude mice ( A ) or rabbit complement ( B ) in the presence of G 1 Mab-28-mG 2a or control mIgG 2a . Calcein release into the medium was measured, and cytotoxicity was determined. Values are shown as the mean ± SEM. Asterisks indicate statistical significance (* p < 0.05, ** p < 0.01; two-tailed unpaired t -test).

Article Snippet: The mouse GPC1 ( NM_016696.4 ) cDNA was obtained from OriGene Technologies, Inc. (Rockville, MD, USA).

Techniques: Labeling, Incubation, Derivative Assay, Control, Two Tailed Test

Journal: International Journal of Molecular Sciences

Article Title: Chimeric Anti-Glypican 1 Antibodies Exert Antitumor Activities in Xenograft Models of Lung and Pancreatic Cancers

doi: 10.3390/ijms27104181

Figure Lengend Snippet: Antitumor activity of G 1 Mab-28-mG 2a against human tumor xenografts. ( A – C ) CHO/GPC1 ( A ), PC-10 ( B ), and PK-45H ( C ) cells were subcutaneously injected into BALB/c nude mice (day 0). G 1 Mab-28-mG 2a (100 μg) or control mIgG 2a (100 μg) were intraperitoneally injected into each mouse on days 7 and 13 (arrows). The tumor volume is represented as the mean ± SEM. ** p < 0.01 (two-way ANOVA with Sidak’s post hoc test). ( D – F ) After cell inoculation, the mice were euthanized on day 20. The tumor weights (left) and appearance (right) of CHO/GPC1 ( D ), PC-10 ( E ), and PK-45H ( F ) xenografts were measured. Values are presented as the mean ± SEM. ** p < 0.01 (two-tailed unpaired t -test). Scale bar, 1 cm. ( G – I ) Body weight (mean ± SEM) of xenograft-bearing mice treated with mAbs is presented. There is no significant difference (two-way ANOVA with Sidak’s post hoc test).

Article Snippet: The mouse GPC1 ( NM_016696.4 ) cDNA was obtained from OriGene Technologies, Inc. (Rockville, MD, USA).

Techniques: Activity Assay, Injection, Control, Two Tailed Test

Journal: International Journal of Molecular Sciences

Article Title: Chimeric Anti-Glypican 1 Antibodies Exert Antitumor Activities in Xenograft Models of Lung and Pancreatic Cancers

doi: 10.3390/ijms27104181

Figure Lengend Snippet: ADCC and CDC by G 1 Mab-28-hG 1 against GPC1-positive tumor cells. The target cells labeled with Calcein AM (CHO/GPC1, PC-10, and PK-45H) were incubated with effector splenocyte derived from BALB/c nude mice ( A ) or rabbit complement ( B ) in the presence of G 1 Mab-28-hG 1 or control hIgG 1 . Calcein release into the medium was measured, and cytotoxicity was determined. Values are shown as the mean ± SEM. Asterisks indicate statistical significance (* p < 0.05; two-tailed unpaired t -test).

Article Snippet: The mouse GPC1 ( NM_016696.4 ) cDNA was obtained from OriGene Technologies, Inc. (Rockville, MD, USA).

Techniques: Labeling, Incubation, Derivative Assay, Control, Two Tailed Test

Journal: International Journal of Molecular Sciences

Article Title: Chimeric Anti-Glypican 1 Antibodies Exert Antitumor Activities in Xenograft Models of Lung and Pancreatic Cancers

doi: 10.3390/ijms27104181

Figure Lengend Snippet: Antitumor activity of G 1 Mab-28-hG 1 against human tumor xenografts. ( A – C ) CHO/GPC1 ( A ), PC-10 ( B ), and PK-45H ( C ) cells were subcutaneously injected into BALB/c nude mice (day 0). G 1 Mab-28-hG 1 (100 μg) or control hIgG 1 (100 μg) were intraperitoneally injected into each mouse on days 7 and 13 (arrows). The tumor volume is represented as the mean ± SEM. * p < 0.05, ** p < 0.01 (two-way ANOVA with Sidak’s post hoc test). ( D – F ) After cell inoculation, the mice were euthanized on day 20. The tumor weights (left) and appearance (right) of CHO/GPC1 ( D ), PC-10 ( E ), and PK-45H ( F ) xenografts were measured. Values are presented as the mean ± SEM. * p < 0.05, ** p < 0.01 (two-tailed unpaired t -test). Scale bar, 1 cm. ( G – I ) Body weight (mean ± SEM) of xenograft-bearing mice treated with the mAbs is presented. There is no significant difference (two-way ANOVA with Sidak’s post hoc test).

Article Snippet: The mouse GPC1 ( NM_016696.4 ) cDNA was obtained from OriGene Technologies, Inc. (Rockville, MD, USA).

Techniques: Activity Assay, Injection, Control, Two Tailed Test

Journal: bioRxiv

Article Title: Neuronal overexpression of mouse potassium channel subunit Kcnn1 in A53T α-synuclein mice more than doubles median survival time, associated with suppression of phospho-S129 α-synuclein formation

doi: 10.64898/2026.03.09.709927

Figure Lengend Snippet: Kaplan-Meier survival plots for A53T α-synuclein transgenic mice, A53T/Kcnn1-3copy mice, and A53T/Kcnn1-6copy mice. Median survival time was extended by 47% for the A53T/ Kcnn1-3copy mice and >100% for the A53T/Kcnn1-6copy mice. The two Kcnn1 transgenes are independent. See text for the different motor phenotypes of the A53T and A53T/Kcnn1-6copy mice.

Article Snippet: The mouse Kcnn1 cDNA sequence (NM_032397), was PCR-amplified from OriGene Technologies plasmid MR208601, omitting the 3’-terminal Myc-DDK tag sequence.

Techniques: Transgenic Assay

Journal: bioRxiv

Article Title: Neuronal overexpression of mouse potassium channel subunit Kcnn1 in A53T α-synuclein mice more than doubles median survival time, associated with suppression of phospho-S129 α-synuclein formation

doi: 10.64898/2026.03.09.709927

Figure Lengend Snippet: Absence of serine129 phospho-α-synuclein (Psynuclein) immunostaining in 12 mo A53T/Kcnn1-6copy mouse as compared with A53T endstage (9 mo) mouse. A. Location of superior colliculus (purple). Sagittal and coronal cross-sections of brain are shown, to illustrate midbrain dorsal position in the sagittal section and paired left and right structures in the coronal views. B. Sagittal views of superior colliculus, from 20 µm sagittal sections ∼1.2 mm from midline, showing presence of Kcnn1 overexpression in A53T/Kcnn1-6copy 12 month old mouse is associated with absence of α-synuclein disease-associated Psynuclein. Upper panels, A53T endstage 9 month old mouse sagitally sectioned and immunostained to reveal copious Psynuclein (left) and endogenous levels of Kcnn1 (right). Lower panels, absence of Psynuclein associated with overexpression of Kcnn1. Red arrow likely denotes intermediate gray layer. Scale bar, 200 μm.

Article Snippet: The mouse Kcnn1 cDNA sequence (NM_032397), was PCR-amplified from OriGene Technologies plasmid MR208601, omitting the 3’-terminal Myc-DDK tag sequence.

Techniques: Immunostaining, Over Expression

Journal: bioRxiv

Article Title: Neuronal overexpression of mouse potassium channel subunit Kcnn1 in A53T α-synuclein mice more than doubles median survival time, associated with suppression of phospho-S129 α-synuclein formation

doi: 10.64898/2026.03.09.709927

Figure Lengend Snippet: Stereotactic injection of AAV9-CMV-Kcnn1 virus into the right superior colliculus of an asymptomatic 6 month old A53T mouse leads to overexpression of Kcnn1 in right superior colliculus (upper panel, outlined in light blue), associated with absence of Psynuclein (lower panel outlined in blue) observed after 54 days. Shown in upper and lower panels are separately immunostained neighboring 20 µm cryosections of flash-frozen brain. Upper panel, coronal section of brain showing right superior colliculus with clusters of fluorescent anti-Kcnn1-positive cells in what appear to be the bands of superficial, intermediate, and deep gray layers. Fluorescent cells are also observed beyond the boundaries of the superior colliculus, including crossing the midline and ventrally (see text). Lower panel, almost complete absence of Psynuclein staining in injected right superior colliculus region vs non-injected left (outlined and labeled in blue). (For detail on Psynuclein accumulation outside superior colliculus, see text). Scale bar 250 μm.

Article Snippet: The mouse Kcnn1 cDNA sequence (NM_032397), was PCR-amplified from OriGene Technologies plasmid MR208601, omitting the 3’-terminal Myc-DDK tag sequence.

Techniques: Injection, Virus, Over Expression, Staining, Labeling

Journal: bioRxiv

Article Title: Neuronal overexpression of mouse potassium channel subunit Kcnn1 in A53T α-synuclein mice more than doubles median survival time, associated with suppression of phospho-S129 α-synuclein formation

doi: 10.64898/2026.03.09.709927

Figure Lengend Snippet: Absence of Psynuclein from right superior colliculus along ∼1 mm of rostro-caudal length of the AAV9-CMV-Kcnn1-injected mouse shown in (Mouse 1). The right and left superior colliculus are outlined in blue in all sections. Note that the shape of the outline is slightly altered from frame to frame to account for its position relative to surrounding landmarks (not shown) and compared with The Mouse Brain in Stereotaxic Coordinates, Franklin and Paxinos, 2007 . Coronal sections shown are spaced every 200 µm rostrocaudally. Consecutive 20 µm coronal sections of brain were taken, beginning at an arbitrary point several 100 µm rostral to superior colliculus and proceeding into the superior colliculus. Every 10 th section (sxn) was stained for Psynuclein. There is absence of Psynuclein from the injected right superior colliculus along the entire cut region. Section #89 appears to contain an artefact in its left aspect. Scale bar 250 μm. Figure 4B. A53T mouse injected with injection solution lacking virus (Control). Sections were collected and immunostained as in A. Superior colliculi circled in blue. There is symmetric presence of Psynuclein in the superior colliculi and outside of it. Scale bar 250 μm.

Article Snippet: The mouse Kcnn1 cDNA sequence (NM_032397), was PCR-amplified from OriGene Technologies plasmid MR208601, omitting the 3’-terminal Myc-DDK tag sequence.

Techniques: Injection, Staining, Virus, Control

Journal: bioRxiv

Article Title: Neuronal overexpression of mouse potassium channel subunit Kcnn1 in A53T α-synuclein mice more than doubles median survival time, associated with suppression of phospho-S129 α-synuclein formation

doi: 10.64898/2026.03.09.709927

Figure Lengend Snippet: Magnified views of corresponding regions of left and right superior colliculus from an AAV9 CMV-Kcnn1 virus-injected mouse at level of intermediate gray layers, immunostained with anti-Kcnn1 and anti-P-synuclein, showing near complete absence of Psynuclein in the presence of overexpressed Kcnn1. Displayed are 400 µm X 400 µm squares, taken from coronal section #60 (Kcnn1) and section #59 (Psynuclein) of Mouse 1, with their centers ∼1100 microns from either side of the midline. Anti-Kcnn1 (upper panels) shows brighter Kcnn1-immunoreactive cells on the virus-injected right side vs much less bright cells (endogenously expressing Kcnn1) on the uninjected left side. The number of Kcnn1-immunostained cells was roughly equal on the two sides (data not shown). Anti-Psynuclein (lower panels) shows copious intracellular Psynuclein on the left, in the setting of endogenous Kcnn1, and also that Psynuclein extends into processes and that a portion may be in glia or neuropil. On the right, in the setting of overexpressed Kcnn1, only four or five flecks of Psynuclein are visible, the rightmost of which appears to be intracellular. Scale bar 20 µm.

Article Snippet: The mouse Kcnn1 cDNA sequence (NM_032397), was PCR-amplified from OriGene Technologies plasmid MR208601, omitting the 3’-terminal Myc-DDK tag sequence.

Techniques: Virus, Injection, Expressing

Journal: bioRxiv

Article Title: Scn4b Modulates Huntington’s Disease Phenotype Severity in vivo

doi: 10.64898/2026.03.08.708251

Figure Lengend Snippet: (A) Volcano plots of significantly differentially expressed genes (DEGs) in a CAG-length-dependent manner in the direct (dSPNs) and indirect (iSPNs) pathway spiny projection neurons of an HD mouse model allelic series (Q50, Q111, Q170, zQ175), as reported by translating ribosome affinity purification (TRAP) profiling. (B) Representative RNAScope in situ hybridization images showing striatal caudate nucleus SCN4B RNA (yellow) reduction across human HD grades 1-3 compared to pathologically normal (PN) caudate tissues. Scale bar, 5 µm. (C) Quantification of normalized (to PN) SCN4B puncta per cell. Data are shown as mean ± SD ( n =3 biological replicates per condition; 10 images (63x) per donor). One-sided t-test: ** p = 0.0031 (PN vs. HD1) and 0.0081 (PN vs. HD2); *** p = 0.0007 (PN vs. HD3).

Article Snippet: The GFP sequence was replaced with Scn4b sequence, amplified from the mouse Scn4b cDNA ORF plasmid (Scn4b #MR226154; Origene, Rockville, MD) for the pAAV GPR88 :: Scn4b OX construct.

Techniques: Affinity Purification, RNAscope, In Situ Hybridization

Journal: bioRxiv

Article Title: Scn4b Modulates Huntington’s Disease Phenotype Severity in vivo

doi: 10.64898/2026.03.08.708251

Figure Lengend Snippet: (A) Schematic showing the Scn4b knockdown (KD) approach in adult wild-type mice and the experimental timeline for behavioral testing. (B) Representative RNAScope in situ hybridization images of striatal tissue from mice injected with 5E12 vg/mouse of AAV PHP.eB hSyn::CRISPR/CasRx containing guides targeting Scn4b showing the reduction of Scn4b signal (yellow). FLuc denotes data from tissue with the guides targeting Firefly Luciferase, which is not present in the mouse genome. Scale bar, 25 µm (top) and 5 µm (bottom). (C) Relative quantification of Scn4b puncta count. Data are shown as mean ± SD ( n =4 mice per condition; 25 images (63x) per mouse). One-sided t-test: p = 0.0038. (D) Horizontal distance and (E) vertical time traveled as measured by open field test over a 30 min testing period. (F) Latency to fall in the rotarod test. (G) Stride length measured from paw prints from gait analysis. (H) Percentage of food pellets burrowed (by total mass) in the burrowing test. (I) Righting reflex time. Data are shown as mean ± SEM for all longitudinal time course data and mean ± SD for single-time-point comparisons ( n =8-10 mice per group). One-sided t-test: * p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001, **** p ≤ 0.0001. (J) Schematic showing the Scn4b knockout (KO) approach in conditional Scn4b floxed mice and the experimental timeline for behavioral testing. (K) Representative RNAScope in situ hybridization FISH images of striatal tissue from mice injected with 5E12 vg/mouse of AAV PHP.eB hSyn::GFP/iCre virus showing the reduction of Scn4b signal (yellow). Scale bar, 1 mm (left), 75 µm (middle) and 15 µm (right). (L) Relative quantification of Scn4b signal intensity. Data are shown as mean ± SD ( n = 4 mice per condition; 10 images (40x) per mouse). (M) Horizontal distance and (N) vertical time traveled as measured by open field test over a 60 min testing period. (O) Number of falls during rotarod training and (P) latency to fall in the rotarod test. (Q) Measured stride length of the paw prints from gait analysis. (R) Righting reflex time. Data are shown as mean ± SEM for all line graphs and as mean ± SD for all bar graphs ( n =13 mice per group). One-sided t-test: * p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001, **** p ≤ 0.0001. Figures in panels A and J were created with BioRender.

Article Snippet: The GFP sequence was replaced with Scn4b sequence, amplified from the mouse Scn4b cDNA ORF plasmid (Scn4b #MR226154; Origene, Rockville, MD) for the pAAV GPR88 :: Scn4b OX construct.

Techniques: Knockdown, RNAscope, In Situ Hybridization, Injection, CRISPR, Luciferase, Quantitative Proteomics, Knock-Out, Virus

Journal: bioRxiv

Article Title: Scn4b Modulates Huntington’s Disease Phenotype Severity in vivo

doi: 10.64898/2026.03.08.708251

Figure Lengend Snippet: (A) Schematic showing the snRNA-seq experimental workflow. (B) UMAP representing all cell types captured from striatal tissue of the Scn4b KD and control ( FLuc ) mice. (C) Back-to-back bar chart showing the number of genes that are dysregulated in the striatum of Scn4b KD versus FLuc mice, per cell type (log 2 fold change abs( z ) >= 1 and p adj. FDR < 0.05). (D) Volcano plot showing significant DEGs (versus FLuc , log 2 fold change abs( z ) >= 1 and p adj. FDR < 0.05) in striatal matrix dSPNs and (E) iSPNs. (F) GO BP pathway enrichment analysis of Scn4b KD downregulated DEGs (versus FLuc ) in matrix dSPNs and iSPNs. (G) Venn diagram showing the overlap between downregulated DEGs of Scn4b KD mice and human HD in matrix dSPNs and (H) iSPNs. Fisher’s exact test p = 1.32 × 10 -7 and p = 1.61 × 10 -14 , respectively. (I) GO BP pathway enrichment analysis of the shared downregulated DEGs in matrix dSPNs and iSPNs from Scn4b KD mice and human HD. (J) Overlap of the Scn4b KD DEGs and top hub genes from Langfelder et al., 2016. Fisher’s exact test: p = 0.0097 (M2 dSPN.Matrix), 0.0771 (M2 iSPN.Matrix), 0.0337 (M25 dSPN.Matrix). Figure in panel A created with BioRender.

Article Snippet: The GFP sequence was replaced with Scn4b sequence, amplified from the mouse Scn4b cDNA ORF plasmid (Scn4b #MR226154; Origene, Rockville, MD) for the pAAV GPR88 :: Scn4b OX construct.

Techniques: Control

Journal: bioRxiv

Article Title: Scn4b Modulates Huntington’s Disease Phenotype Severity in vivo

doi: 10.64898/2026.03.08.708251

Figure Lengend Snippet: (A) Schematic showing the Scn4b OX approach in the zQ175 HD model mice and the timeline used for behavioral testing. (B) Representative RNAScope in situ hybridization images of striatal tissue from mice injected with 1E12 vg/mouse of AAV PHP.eB GPR88 ::GFP or GPR88 :: Scn4b OX showing the reduction of Scn4b (yellow) in zQ175 vs. WT-GFP OX and the overexpression of Scn4b in only zQ175- Scn4b vs GFP OX. Scale bar, 10 µm. (C) Relative quantification of Scn4b expression across the experimental groups. Data are shown as mean ± SD ( n =3 mice per condition; 25 images (63x) per mouse). (D) Vertical time and (E) jump time parameters as measured by open field test over a 60 min testing period. (F) Latency to fall in the rotarod test. (G) Latency to cross in the beam walk test. (H) Grip strength measurement. For all tests, data are shown as mean ± SD ( n =7 mice per group). One-sided t-test for all parameters: * p ≤ 0.05, ** p ≤ 0.01. (I) Representative IF images (targeting EM48) of striatal sections from zQ175 mice injected with 1E12 vg/mouse of AAV PHP.eB GPR88 ::GFP or GPR88 :: Scn4b , showing the reduction of EM48+ mHTT aggregate signal (red) in Scn4b OX zQ175 mice. Scale bar, 20 µm. (J) Quantification of EM48+ mHTT aggregate count. Data are shown as mean ± SD ( n =4 mice per condition; 15 images (40x) per mouse). (K) Representative IF images (using the P90 antibody) of striatal sections from zQ175 mice injected with 1E12 vg/mouse of AAV PHP.eB GPR88 ::GFP or GPR88 :: Scn4b , showing the reduction of P90+ mHTT aggregate signal (red) in Scn4b OX zQ175 mice. Scale bar, 20 µm. (L) Quantification of P90+ mHTT aggregate count. Data are shown as mean ± SD ( n =3 mice per condition; 25 images (63x) per mouse). (M) Schematic representation of whole-cell clamp recording from the dorsal striatum. (N) The mean ± SEM of action potential thresholds for dorsal striatum SPNs from mice of the indicated genotypes. Figure in panel A created with BioRender.

Article Snippet: The GFP sequence was replaced with Scn4b sequence, amplified from the mouse Scn4b cDNA ORF plasmid (Scn4b #MR226154; Origene, Rockville, MD) for the pAAV GPR88 :: Scn4b OX construct.

Techniques: RNAscope, In Situ Hybridization, Injection, Over Expression, Quantitative Proteomics, Expressing

Journal: bioRxiv

Article Title: Scn4b Modulates Huntington’s Disease Phenotype Severity in vivo

doi: 10.64898/2026.03.08.708251

Figure Lengend Snippet: (A) Schematic showing the snRNA-seq experimental workflow. (B) UMAP representing all cell types captured from striatal tissue of all mice included in this OX study. (C) Back-to-back bar chart showing the number genes that are differentially expressed (DEGs) in the striatum of Scn4b OX mice (zQ175- Scn4b OX vs zQ175-GFP OX; log 2 fold change abs( z ) >= 1 and p adj. FDR < 0.05), per cell type. (D) Volcano plot showing these genes in matrix dSPNs and (E) iSPNs of Scn4b OX mice. X-axis limit is set to ±0.4 for visualization purposes; genes exceeding this range include Ttr (log 2 fold change = −0.778) and Cmss1 (log 2 fold change = −0.777) in dSPNs and Cmss1 (log 2 fold change = −0.818) in iSPNs. GO BP pathway enrichment analysis showing the upregulated and downregulated pathways of matrix (F) dSPNs and (G) iSPNs in the zQ175 and Scn4b OX comparisons. (H) Volcano plots showing genes that are changed in opposite directions in the zQ175 and Scn4b OX comparisons in matrix dSPNs and (I) iSPNs. GO BP pathway enrichment analysis of (J) genes that are downregulated in the Scn4b OX comparison and upregulated in the zQ175 comparison and (K) genes that are upregulated in the Scn4b OX comparison and downregulated in the zQ175 comparison. (L) Heatmap showing log 2 fold change of selected MMR genes in the zQ175 and Scn4b OX comparisons. *indicates significance using the log 2 fold change abs( z ) >= 1 and p adj. FDR < 0.05 cutoff. Figure in panel A created with BioRender.

Article Snippet: The GFP sequence was replaced with Scn4b sequence, amplified from the mouse Scn4b cDNA ORF plasmid (Scn4b #MR226154; Origene, Rockville, MD) for the pAAV GPR88 :: Scn4b OX construct.

Techniques: Comparison

Journal: Cell Communication and Signaling : CCS

Article Title: Activation of aryl hydrocarbon receptor alleviates cholestatic liver injury by inhibiting inflammation

doi: 10.1186/s12964-026-02755-w

Figure Lengend Snippet: Proposed working model of AHR signaling in cholestatic liver injury (CLI). Cholestasis is associated with gut microbiota dysbiosis, including a reduced abundance of tryptophan-metabolizing bacteria and an increased abundance of LPS-producing bacteria (e.g., Escherichia-Shigella ). These alterations are accompanied by disrupted tryptophan metabolism and enhanced translocation of microbial products such as LPS to the liver, which are associated with impaired AHR activation and amplified hepatic inflammatory responses, including increased chemokine expression (e.g., CCL2) and recruitment of inflammatory cells. Pharmacological activation of AHR by tryptophan-derived metabolites (such as ITE) or AAV-mediated AHR overexpression attenuates inflammatory responses and liver injury, at least in part through suppression of chemokine expression. Hepatocyte-intrinsic AHR signaling is depicted as one contributing node within a broader multicellular inflammatory network rather than a dominant determinant of disease severity. This schematic represents a proposed working model based on the present findings

Article Snippet: After 12 h of cell starvation, LPS (500 nM, MedChemExpress, Shanghai, China, # HY-D1056) was added, along with ITE (10 nM or 100 nM, MedChemExpress Shanghai, China, # HY-19317), or liposome transfection of AHR overexpression plasmid (1ug/mL, Sino Biological, Beijing, China, # MG50786-CM), and the AHR inhibitor CH223191 (CH) (10 μM, MedChemExpress, Shanghai, China, # HY-12684) was added when necessary.

Techniques: Bacteria, Translocation Assay, Activation Assay, Amplification, Expressing, Derivative Assay, Over Expression