goat serum  (Bio-Rad)

Journal: Genes & Diseases

Article Title: Activation of the Jak2/Stat3 pathway by ROS-dependent signaling cascades initiates hepatitis B virus-induced hepatic inflammatory responses

doi: 10.1016/j.gendis.2025.101857

Figure Lengend Snippet: Hepatic ROS levels and Jak2/Stat3 activity were increased simultaneously at the early stage of liver inflammation in a persistent HBV-replication mouse model. (A) Schematic representation of experiment design and procedures. A persistent HBV replication mouse model was established by HDI of 6 μg pAAV-HBV 1.2 plasmid into 5 to 6-week-old male C57BL/6J mice. As normal controls, mice were injected hydrodynamically with the same volume of phosphate-buffered saline (PBS). Serum and liver samples from HBV-replication mice and normal controls were collected at 2, 3, 4, and 5 weeks after HDI for later experiments. (B) Dynamic changes in serum ALT levels of HBV-replication mice and normal controls collected at 2, 3, 4, and 5 weeks after HDI, or HBsAg, HBeAg, and HBV-DNA levels in HBV-replication mice. (C) Representative images of hematoxylin-eosin staining of liver tissue sections from normal controls (top row) and HBV-replication mice (bottom row). Ishak scoring system was used to evaluate the degrees of liver inflammation and fibrosis. (D) Detection of hepatic ROS on frozen section of liver tissue using DCFH-DA dye by fluorescence confocal microscope. The ROS levels were expressed as MFI of DCFH-DA dye and compared among these groups. (E) Measurement of GSH or GSSG in fresh liver tissues obtained from HBV-replication mice or controls. Reduced ratio of GSH to GSSG indicated increased oxidative stress. (F) Protein expression of p-Stat3, p-Jak2, Nrf2, Stat3, and Jak2 in liver tissues from the 2-week group (normal ALT levels and no obvious liver inflammation) and the 4-week group (increased ALT levels and early stage of significant liver inflammation) of HBV-replication mice and their controls. The relative protein expression was shown as fold-change in comparison with the 2-week group of controls. (G) Serum levels of IL-6 and IL-8 in the 2-week and 4-week groups of HBV-replication mice and their controls were assessed by ELISA. (H) Relative mRNA expression of downstream target genes of p-Stat3 (Saa1, S100a9, Icam1, and Socs3) in liver tissues from the 4-week group of HBV-replication mice and their controls was detected by real-time PCR. All data were shown as mean ± standard error of the mean. Each dot represented an individual mouse, and each group consisted of 5 or 6 mice. P -values < 0.05 were considered statistically significant (∗ P < 0.05, ∗∗ P < 0.01, or ∗∗∗ P < 0.001 between two indicated groups). HDI, hydrodynamic injection; MFI, mean fluorescence intensity; GSH, reduced glutathione; GSSG, oxidized glutathione; ROS, reactive oxygen species; HBV, hepatitis B virus.

Article Snippet: The chemiluminescence microparticle immunoassay (CMIA) method was employed to quantify the HBsAg and HBeAg levels with Alinity HBsAg and HBeAg detection kits (Abbott Laboratories, Illinois, USA).

Techniques: Activity Assay, Plasmid Preparation, Injection, Saline, Staining, Fluorescence, Microscopy, Expressing, Comparison, Enzyme-linked Immunosorbent Assay, Real-time Polymerase Chain Reaction, Virus

Journal: iScience

Article Title: A key role for the exoribonuclease XRN1 in regulating the hepatitis B viral transcriptome

doi: 10.1016/j.isci.2026.116328

Figure Lengend Snippet: XRN1 limits HBV RNAs (A) HBV infection and pAp treatment. Arrested HepG2-NTCP cells were infected with HBV for 16 h, inoculum removed, and cells treated with vehicle or 4 mM 3′, 5′-bisphosphate (pAp) for 72 h. RNA was extracted and total HBV RNAs quantified by RT-qPCR, normalized to the housekeeping gene B2M and expressed relative to vehicle-treated cells (mean ± SD, n = 9 from 3 independent experiments, one-way ANOVA, with multiple comparisons, ∗∗∗ p < 0.001). Cytotoxicity was evaluated by LDH assay with data expressed relative to cells treated with 0.05% Triton X-100 (Pos). (B) HBV infection of WT and XRN1 KO cells. WT and KO HepG2-NTCP cells were assessed for XRN1 expression by western blotting and treated with 50 nM Alexa 647 conjugated preS1 2-48 peptide in the presence or absence of excess unlabeled peptide (200 nM). After washing, the cells were incubated with DAPI and visualized by microscopy with a 20 × objective, scale bars, 150 μm. WT and XRN1 KO HepG2-NTCP cells were inoculated with HBV for 16 h. Intracellular DNA was extracted after 16 h post-infection and RNA at 72 h post-infection. HBV DNA, cccDNA, and total HBV RNAs were quantified by qPCR and normalized to the housekeeping genes, PrP or B2M , respectively. Data are plotted relative to the WT cells (mean ± SD, n = 6 from 2 independent experiments). (C) HBV life cycle and kinetic analysis of infection. WT and XRN1 KO HepG2-NTCP cells were inoculated with HBV for 16 h in the presence or absence of preS1 2-48 peptide, unbound virus removed by washing, and the cells cultured for 3, 6, 9, or 10 days. The schematic depicts steps in the HBV life cycle that were evaluated. Intracellular HBV RNA and secreted HBeAg were quantified at 3, 6, and 9 dpi by RT-qPCR and ELISA, respectively. RT-qPCR data are expressed relative to the housekeeping gene, B2M (mean ± SD, n = 9 from 3 independent experiments). Intracellular rcDNA and core-associated HBV DNA were quantified by qPCR (mean ± SD, n = 6 from 3 independent experiments). XRN1, HBs, HBc, and β-Actin proteins were detected at 10 dpi. Statistical significance was determined using Mann-Whitney tests, with Bonferroni correction for multiple comparisons; ∗∗ p < 0.01, ∗∗∗ p < 0.005, and ∗∗∗∗ p < 0.0001. Please see also .

Article Snippet: HBsAg ELISA , Autobio , Cat# CL0310-2.

Techniques: Infection, Quantitative RT-PCR, Lactate Dehydrogenase Assay, Expressing, Western Blot, Incubation, Microscopy, Virus, Cell Culture, Enzyme-linked Immunosorbent Assay, MANN-WHITNEY

Journal: iScience

Article Title: A key role for the exoribonuclease XRN1 in regulating the hepatitis B viral transcriptome

doi: 10.1016/j.isci.2026.116328

Figure Lengend Snippet: HBV induces P-bodies (A and B) Effect of HBV infection on XRN1 and EDC4 expression. Mock or HBV-infected HepG2-NTCP cells were cultured for up to 9 days (A) P-body components XRN1 and EDC4, together with HBsAg and β-actin, were detected at 3, 6, and 9 dpi by western blotting. (B) EDC4 (green) and DAPI nuclei (blue) were detected by immunofluorescence at 6 dpi, with a representative image shown (scale bars, 25 μm). The average number of EDC4 puncta relative to nuclei was quantified in 9 images from 3 independent experiments, with significance assessed using a Mann-Whitney test (∗∗∗ p < 0.001, ∗ p < 0.05). (C) Abundance of viral and host RNAs. Total HBV RNAs (HBV-total, yellow) and host Peptidylprolyl isomerase B RNA (PPIB, red) and nuclear DAPI (blue) were imaged at 6 dpi (scale bars, 20 μm). (D) Replication of in vitro transcribed HBV pgRNA. A schematic of in vitro transcribed (IVT) WT or Δε pgRNA and their viral products. Mock or IVT HBV RNA-transfected (100 ng) Huh 7.5 cells were cultured for 2, 4, or 6 days. Cells were imaged for HBc (magenta) (scale bars, 75 μm), intracellular HBV DNA, and secreted HBsAg assessed by qPCR or ELISA, respectively. (E) pCpg RNA levels after 6 days were measured by RT-qPCR, and the data were normalized to a housekeeping gene, B2M , respectively. (F) EDC4 puncta in HBV RNA-transfected cells. Mock or IVT HBV RNA-transfected (100 ng) Huh 7.5 cells (6 days) were stained for EDC4 expression and puncta number and size quantified in 15 images from 3 independent experiments. Mean EDC4 values are expressed relative to the number of nuclei per image, with statistical significance assessed using a Mann-Whitney test with correction for multiple comparisons (∗∗∗ p < 0.001 and ∗ p < 0.05).

Article Snippet: HBsAg ELISA , Autobio , Cat# CL0310-2.

Techniques: Infection, Expressing, Cell Culture, Western Blot, Immunofluorescence, MANN-WHITNEY, In Vitro, Transfection, Enzyme-linked Immunosorbent Assay, Quantitative RT-PCR, Staining

Journal: iScience

Article Title: A key role for the exoribonuclease XRN1 in regulating the hepatitis B viral transcriptome

doi: 10.1016/j.isci.2026.116328

Figure Lengend Snippet: HBV induces P-bodies (A and B) Effect of HBV infection on XRN1 and EDC4 expression. Mock or HBV-infected HepG2-NTCP cells were cultured for up to 9 days (A) P-body components XRN1 and EDC4, together with HBsAg and β-actin, were detected at 3, 6, and 9 dpi by western blotting. (B) EDC4 (green) and DAPI nuclei (blue) were detected by immunofluorescence at 6 dpi, with a representative image shown (scale bars, 25 μm). The average number of EDC4 puncta relative to nuclei was quantified in 9 images from 3 independent experiments, with significance assessed using a Mann-Whitney test (∗∗∗ p < 0.001, ∗ p < 0.05). (C) Abundance of viral and host RNAs. Total HBV RNAs (HBV-total, yellow) and host Peptidylprolyl isomerase B RNA (PPIB, red) and nuclear DAPI (blue) were imaged at 6 dpi (scale bars, 20 μm). (D) Replication of in vitro transcribed HBV pgRNA. A schematic of in vitro transcribed (IVT) WT or Δε pgRNA and their viral products. Mock or IVT HBV RNA-transfected (100 ng) Huh 7.5 cells were cultured for 2, 4, or 6 days. Cells were imaged for HBc (magenta) (scale bars, 75 μm), intracellular HBV DNA, and secreted HBsAg assessed by qPCR or ELISA, respectively. (E) pCpg RNA levels after 6 days were measured by RT-qPCR, and the data were normalized to a housekeeping gene, B2M , respectively. (F) EDC4 puncta in HBV RNA-transfected cells. Mock or IVT HBV RNA-transfected (100 ng) Huh 7.5 cells (6 days) were stained for EDC4 expression and puncta number and size quantified in 15 images from 3 independent experiments. Mean EDC4 values are expressed relative to the number of nuclei per image, with statistical significance assessed using a Mann-Whitney test with correction for multiple comparisons (∗∗∗ p < 0.001 and ∗ p < 0.05).

Article Snippet: Antibodies used in this study (and their supplier) are: EDC4 (FORTIS), DDX6 (FORTIS), HBsAg (Stratech), HBcAg (Dako), HBcAg (Beacle Inc.) XRN1 (Thermo Fisher Scientific), β-Actin (Sigma), HBsAg (Abcam), anti-mouse Immunoglobulin HRP (Dako), anti-rabbit IgG HRP (Cytiva), anti-mouse IgG HRP (Abcam), anti-rabbit IgG (Alexa Fluor 488, 594 and 633, Thermo Fisher Scientific) and anti-7-methylguanosine (m 7 G)-Cap (Caltag Medsystems Ltd).

Techniques: Infection, Expressing, Cell Culture, Western Blot, Immunofluorescence, MANN-WHITNEY, In Vitro, Transfection, Enzyme-linked Immunosorbent Assay, Quantitative RT-PCR, Staining

Journal: Hepatology Communications

Article Title: Secretion of the HBV small surface antigen is driven by an ER autophagic pathway

doi: 10.1097/HC9.0000000000000939

Figure Lengend Snippet: The SHBs resides in the ER and late endosomal compartments. (A) Western blot (WB) analysis of culture medium (CM or EXT) and whole cell lysates (WCLs or INT) from either HepG2 parental cells or the HepG2-SHBs stable cell line. Distinct 27/24 kD bands are detectable using 2 distinct SHBs antibodies (Virostat and Biosynth) in both the EXT (CM) and INT (WCLs) in HepG2-SHBs stable cells, but not from the parental cell line. (B) Quantitation of extracellular SHBs by CLIA. (C–F) Immunofluorescence (IF) staining of HepG2-SHBs stable cells showing the intracellular distribution of the SHBs (red) with different compartment markers (green) including (C) the endoplasmic reticulum (ER, PDI), (D) the Golgi (GM130), (E) early endosomes (E. Endo, EEA1), and (F) multivesicular bodies (MVB)s/late endosomes (CD63). Intensity line scan quantitation of SHBs within the different compartments of the provided images. At least 10 cells were analyzed per condition, and the experiment was performed 3 times. p -value ****, <0.0001. Scale bar, 10 μm. Abbreviations: CD63, cluster of differentiation 63; CLIA, chemiluminescent immunoassay; CM, culture medium; EEA1, early endosome antigen 1; ER, endoplasmic reticulum; EXT, external/secreted; GM130, Golgi matrix protein 130; HepG2-SHBs, HepG2 cell line stably expressing SHBs; IF, immunofluorescence; INT, internal; MVB, multivesicular body; PDI, protein disulfide isomerase; SHBs, small hepatitis B surface antigen; WB, western blot; WCLs, whole cell lysates.

Article Snippet: Extracellular SHBs were quantified by a HBsAg chemiluminescence immunoassay (CLIA) (Autobio Diagnostics, Zhengzhou, China, CL0310-2).

Techniques: Western Blot, Stable Transfection, Quantitation Assay, Immunofluorescence, Staining, Expressing

Journal: Hepatology Communications

Article Title: Secretion of the HBV small surface antigen is driven by an ER autophagic pathway

doi: 10.1097/HC9.0000000000000939

Figure Lengend Snippet: VSV-G, but not SHBs protein, is visible in the Golgi under a low-temperature block. IF images of HepG2-SHBs cells profiling colocalization of vesicular stomatitis virus G protein (VSVG)-GFP (A–C) or SHBs (D, E) with Golgi. Cells were incubated at 20 °C for either (B, E) 2 hours or (C, F) 4 hours before fixation and staining. Corresponding intensity line scan quantitation of VSV-G or SHBs with the Golgi for each image. At least 10 cells were analyzed per condition, and the experiment was performed 3 times. Scale bar, 10 μm. Abbreviations: GFP, green fluorescent protein; HepG2-SHBs, HepG2 cell line stably expressing SHBs; IF, immunofluorescence; SHBs, small hepatitis B surface antigen; VSVG, vesicular stomatitis virus G protein.

Article Snippet: Extracellular SHBs were quantified by a HBsAg chemiluminescence immunoassay (CLIA) (Autobio Diagnostics, Zhengzhou, China, CL0310-2).

Techniques: Blocking Assay, Virus, Incubation, Staining, Quantitation Assay, Stable Transfection, Expressing, Immunofluorescence

Journal: Hepatology Communications

Article Title: Secretion of the HBV small surface antigen is driven by an ER autophagic pathway

doi: 10.1097/HC9.0000000000000939

Figure Lengend Snippet: Development of a novel SHBs-tagged probe to observe trafficking in live cells. (A, B) Schematic diagrams and domain maps of (A) GFP-tagged SHBs WT fusion protein (GFP-WT) and (B) truncated form missing the C-terminus (GFP-ΔHCR) of SHBs. Corresponding fluorescence images of these fusion proteins expressed in HepG2-SHBs stable cells co-stained with an MVB marker (red, white arrowheads). (C) WB analysis of the HepG2 parental and the HepG2-SHBs stable expressing cells (lanes 1, 2), co-expressing either the GFP-WT protein (lanes 3, 4) or the truncated GFP-ΔHCR protein (lanes 5, 6). Lane 3: Parental cells transiently expressing only full-length wild-type GFP-SHBs, which shows minimal secretion. Lane 4: HepG2-SHBs stable cells expressing full-length untagged SHBs, along with transiently expressed wild-type GFP-SHBs, supports ~50% secretion, though the protein localizes to an undefined compartment (see Supplemental Figure S3, http://links.lww.com/HC9/C332 ). Lane 5: Parental cells transiently expressing GFP-ΔHCR alone without co-expression of untagged SHBs for dimerization, secretion from these cells remains minimal. Lane 6: HepG2-SHBs stable cells expressing full-length untagged SHBs and GFP-ΔHCR show optimal secretion. (D) Densitometric quantitation of the ratios from 3 independent experiments of GFP-tagged WT and truncated ΔHCR proteins secreted into the culture medium (EXT) versus intracellular (INT) from WB. (E) Quantitation of secreted GFP constructs from HepG2 parental and HepG2-SHBs stable cells. p -value *, <0.05. p -value **, <0.01. p -value ***, <0.001. Scale bar, 10 μm. Abbreviations: AU, arbitrary units; EXT, external/secreted; GFP, green fluorescent protein; GFP-ΔHCR, GFP-tagged SHBs lacking the C-terminal hydrophobic region; GFP-WT, GFP-tagged wild-type SHBs; HepG2-SHBs, HepG2 cell line stably expressing SHBs; INT, internal; MVB, multivesicular body; SHBs, small hepatitis B surface antigen; WB, western blot.

Article Snippet: Extracellular SHBs were quantified by a HBsAg chemiluminescence immunoassay (CLIA) (Autobio Diagnostics, Zhengzhou, China, CL0310-2).

Techniques: Fluorescence, Staining, Marker, Expressing, Quantitation Assay, Construct, Stable Transfection, Western Blot

Journal: Hepatology Communications

Article Title: Secretion of the HBV small surface antigen is driven by an ER autophagic pathway

doi: 10.1097/HC9.0000000000000939

Figure Lengend Snippet: Intracellular trafficking of the SHBs probe bypasses the Golgi and matches the localization of wild-type, untagged SHBs. (A–C) Stills from time-lapse videos of the HepG2-SHBs stable cells expressing the mCh-ΔHCR SHBs probe and GFP-tagged marker proteins for (A) MVBs (CD63), (B) lysosomes (LAMP1), and (C) Golgi (GM130) for 24 hours before the initiation of image acquisition. Images were acquired every 10 minutes for over 60 hours. Images shown are at T=0 hour that indicates the start of image acquisition, and every 10 hours afterward. White arrows point to red mCh-ΔHCR protein that can be seen accumulating into large spherical organelles reminiscent of MVBs (A), or lysosomes (B), while never appearing to transit through the Golgi. (C) Large pools of mCh-ΔHCR in red represent nascent ER-residing probe that eventually transits out into autophagosomes/lysosomes. The original videos are available in the supplemental materials (Supplemental Movies 4A–C, http://links.lww.com/HC9/C332 ). Scale bar, 10 μm. Abbreviations: CD63, cluster of differentiation 63; ER, endoplasmic reticulum; GFP, green fluorescent protein; GM130, Golgi matrix protein 130; HepG2-SHBs, HepG2 cell line stably expressing SHBs; LAMP1, lysosomal-associated membrane protein 1; mCh-ΔHCR, monomeric cherry–tagged SHBs lacking the C-terminal hydrophobic region; MVB, multivesicular body; SHBs, small hepatitis B surface antigen.

Article Snippet: Extracellular SHBs were quantified by a HBsAg chemiluminescence immunoassay (CLIA) (Autobio Diagnostics, Zhengzhou, China, CL0310-2).

Techniques: Expressing, Marker, Stable Transfection, Membrane

Journal: Hepatology Communications

Article Title: Secretion of the HBV small surface antigen is driven by an ER autophagic pathway

doi: 10.1097/HC9.0000000000000939

Figure Lengend Snippet: Transit of the SHBs from the ER to late endosome/lysosome compartments is mediated by a conventional autophagic pathway as well as directly to the lysosome. (A) IF images of HepG2-SHBs cells transiently expressing the autophagic adaptor protein LC3-GFP (green), fixed and stained for SHBs (red). Arrows within enlargements point to structures showing colocalization. (B) Stills from live cell imaging of mCh-ΔHCR and LC3-GFP in HepG2-SHBs cells (Supplemental Movie 5B, http://links.lww.com/HC9/C332 ). Enlargements show LC3-GFP associating with mCh-ΔHCR structures (arrows). (C) WB analysis of culture medium (EXT) and cell lysates (INT) from HepG2-SHBs cells treated with either control (siNT) or targeted siRNA to the key autophagic protein ATG5 (siATG5) in the presence (Baf-A1) or absence (DMSO) of the lysosome inhibitor. (D–F) Densitometric quantitation of WB following siRNA treatment: (D) intracellular ATG5 levels, (E) intracellular (INT) SHBs, and (F) extracellular (EXT) SHBs. (G) CLIA quantification of extracellular SHBs. (H, I) IF staining of HepG2-SHBs cells expressing LC3-GFP and treated with (H) siRNA (siNT) or (I) siATG5; enlargements show SHBs associated (arrows) or not associated (arrowheads) with LC3-GFP. (J) Quantitation of the colocalization expressed as percentage of cells with LC3-GFP co-localizing with SHBs vesicles in cells treated with siNT or siATG5 (K, L). IF staining of HepG2-SHBs cells treated with (K) siNT or (L) siATG5; enlargements show SHBs associated with lysosomes (arrows) or not associated with lysosomes (arrowheads). (M) Quantitation of cells with colocalization between SHBs and lysosomes in cells treated with siNT control or siATG5. p -value **, <0.01. p -value ***, <0.001. p -value ****, <0.0001. Scale bar, 10 μm. Abbreviations: ATG5, autophagy-related 5; AU, arbitrary units; Baf-A1, bafilomycin-A1; CLIA, chemiluminescent immunoassay; DMSO, dimethyl sulfoxide; ER, endoplasmic reticulum; EXT, external/secreted; GFP, green fluorescent protein; HepG2-SHBs, HepG2 cell line stably expressing SHBs; IF, immunofluorescence; INT, internal; LC3, microtubule-associated proteins 1A/1B light chain 3B; mCh-ΔHCR, monomeric cherry–tagged SHBs lacking the C-terminal hydrophobic region; N.S., not significant; SHBs, small hepatitis B surface antigen; siATG5, small interfering RNA targeting ATG5; siNT, non-targeting small interfering RNA; WB, western blot.

Article Snippet: Extracellular SHBs were quantified by a HBsAg chemiluminescence immunoassay (CLIA) (Autobio Diagnostics, Zhengzhou, China, CL0310-2).

Techniques: Expressing, Staining, Live Cell Imaging, Control, Quantitation Assay, Stable Transfection, Immunofluorescence, Small Interfering RNA, Western Blot

Journal: Hepatology Communications

Article Title: Secretion of the HBV small surface antigen is driven by an ER autophagic pathway

doi: 10.1097/HC9.0000000000000939

Figure Lengend Snippet: Expression of ER-phagy receptors is required for efficient secretion of the SHBs via the endosomal/autophagic pathway. (A) Representative WB of extracellular (EXT) or intracellular (INT) protein levels in HepG2-SHBs cells following treatment with control siRNA (siNT) or siRNAs targeted to reticuon-3 (RTN3), atlastin GTPase3 (ATL3), Sec62, cell-cycle progression protein 1 (CCPG1), or testis-expressed 264 (Tex264). (B) Densitometric quantitation from 3 independent WB for each of the proteins normalized to NT siRNA control. Densitometric quantitation of INT SHBs (C) and (D) EXT SHBs by WB. (E) Quantitation of SHBs by CLIA in culture medium. (F) IF staining of SHBs (green) and MVB (red) in HepG2-SHBs cells treated with control (NT) siRNA or siRNAs targeting either ATL3, Sec62, or Tex264. (G) A representative WB of culture medium (EXT) and intracellular protein (INT) from HepG2-SHBs stable cells treated with siATL3 or siNT in the presence or absence of Baf-A1. (H) Quantitation of western blots (n=3 independent replicates) for knockdown efficiency of siATL3 normalized to siNT control. Quantitation of western blots (n=3 independent replicates) for intracellular (INT) SHBs (I) and extracellular (EXT) SHBs (J). Quantitative measurement by CLIA of SHBs in culture medium (K). p -value *, <0.05; p -value **, <0.01; p -value ***, <0.001; p -value ****, <0.0001. Scale bar, 10 μm. Abbreviations: ATL3, atlastin 3; AU, arbitrary units; Baf-A1, bafilomycin-A1; CCPG1, cell-cycle progression gene 1; CLIA, chemiluminescent immunoassay; ER, endoplasmic reticulum; EXT, external/secreted; HepG2-SHBs, HepG2 cell line stably expressing SHBs; IF, immunofluorescence; INT, internal; MVB, multivesicular body; RTN3, reticulon 3; Sec62, ER protein Sec62; SHBs, small hepatitis B surface antigen; siATL3, small interfering RNA targeting ATL3; siNT, non-targeting small interfering RNA; Tex264, testis-expressed 264; WB, western blot.

Article Snippet: Extracellular SHBs were quantified by a HBsAg chemiluminescence immunoassay (CLIA) (Autobio Diagnostics, Zhengzhou, China, CL0310-2).

Techniques: Expressing, Control, Quantitation Assay, Staining, Western Blot, Knockdown, Stable Transfection, Immunofluorescence, Small Interfering RNA

Journal: Hepatology Communications

Article Title: Secretion of the HBV small surface antigen is driven by an ER autophagic pathway

doi: 10.1097/HC9.0000000000000939

Figure Lengend Snippet: Hepatocellular secretory pathways utilized by SHBs. Illustration of the 2 SHBs pathways observed in this current study. Created with BioRender.com. Abbreviations: AP, autophagic pathway; ATG5 KD, autophagy-related 5 knockdown; ATL3, atlastin 3; Baf-A1, bafilomycin-A1; ER, endoplasmic reticulum; ERGIC, ER-Golgi intermediate compartment; Lys, lysosome; MVB, multivesicular body; SHBs, small hepatitis B surface antigen.

Article Snippet: Extracellular SHBs were quantified by a HBsAg chemiluminescence immunoassay (CLIA) (Autobio Diagnostics, Zhengzhou, China, CL0310-2).

Techniques: Knockdown