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rabbit anti rab18 (Bioss)

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Bioss rabbit anti rab18
Rabbit Anti Rab18, supplied by Bioss, used in various techniques. Bioz Stars score: 93/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/rabbit anti rab18/product/Bioss
Average 93 stars, based on 3 article reviews

rabbit anti rab18 - by Bioz Stars, 2026-03

93/100 stars

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(A) The mRNA levels of the indicated RABs in sh RABs MARC-145 cells were analyzed by qRT-PCR analysis. Values below the black line are statistically significance. (B) sh RABs MARC-145 cells were infected with PRRSV-2-GFP (MOI = 10) for 36 h. GFP-positive cells were analyzed by flow cytometry. Values above the green line (green bar) and below the red line (red bar) are statistically significance. (C) Immunoblot analysis of RAB18 and ACTB in scramble, sh RAB18 -1, and sh RAB18 -2 MARC-145 cells. (D) Scrambled, sh RAB18 -1, and sh RAB18 -2 MARC-145 cells were infected with LP-PRRSV-2 (MOI = 10) and HP-PRRSV-2 (MOI = 10) for 36 h. Viral titers were assessed by the TCID 50 assay. *** P < 0.001. (E) Immunoblot analysis of RAB18 and ACTB in sgcontrol and sg RAB18 MARC-145 cells. (F) Sgcontrol and sg RAB18 MARC-145 cells were infected with LP-PRRSV-2 (MOI = 10) and HP-PRRSV-2 (MOI = 10) for 36 h. Viral titers were assessed by the TCID 50 assay. *** P < 0.001. (G) MARC-145 cells were transfected with plasmids encoding RAB18-mCherry WT, RAB18-mCherry S22N, and RAB18-mCherry Q67L for 12 h and then infected with LP-PRRSV-2 (MOI = 10) for 36 h. PRRSV-2-N was detected by immunofluorescence analysis. Asterisks indicate non-transfected cells. Scale bar: 10 μm. (H) Quantification of the relative fluorescence intensity of PRRSV-2-N from (G) (n = 20). ** P < 0.01, *** P < 0.001. (I) Sgcontrol and sg RAB18 MARC-145 cells were transfected with plasmids encoding RAB18-FLAG WT, RAB18-FLAG S22N, and RAB18-FLAG Q67L for 12 h and then infected with LP-PRRSV-2 (MOI = 10) and HP-PRRSV-2 (MOI = 10) for 36 h. Viral titers were assessed by the TCID 50 assay. ** P < 0.01, *** P < 0.001. ns, not significance.

Journal: PLOS Pathogens

Article Title: Porcine reproductive and respiratory syndrome virus 2 hijacks CMA-mediated lipolysis through upregulation of small GTPase RAB18

doi: 10.1371/journal.ppat.1012123

Figure Lengend Snippet: (A) The mRNA levels of the indicated RABs in sh RABs MARC-145 cells were analyzed by qRT-PCR analysis. Values below the black line are statistically significance. (B) sh RABs MARC-145 cells were infected with PRRSV-2-GFP (MOI = 10) for 36 h. GFP-positive cells were analyzed by flow cytometry. Values above the green line (green bar) and below the red line (red bar) are statistically significance. (C) Immunoblot analysis of RAB18 and ACTB in scramble, sh RAB18 -1, and sh RAB18 -2 MARC-145 cells. (D) Scrambled, sh RAB18 -1, and sh RAB18 -2 MARC-145 cells were infected with LP-PRRSV-2 (MOI = 10) and HP-PRRSV-2 (MOI = 10) for 36 h. Viral titers were assessed by the TCID 50 assay. *** P < 0.001. (E) Immunoblot analysis of RAB18 and ACTB in sgcontrol and sg RAB18 MARC-145 cells. (F) Sgcontrol and sg RAB18 MARC-145 cells were infected with LP-PRRSV-2 (MOI = 10) and HP-PRRSV-2 (MOI = 10) for 36 h. Viral titers were assessed by the TCID 50 assay. *** P < 0.001. (G) MARC-145 cells were transfected with plasmids encoding RAB18-mCherry WT, RAB18-mCherry S22N, and RAB18-mCherry Q67L for 12 h and then infected with LP-PRRSV-2 (MOI = 10) for 36 h. PRRSV-2-N was detected by immunofluorescence analysis. Asterisks indicate non-transfected cells. Scale bar: 10 μm. (H) Quantification of the relative fluorescence intensity of PRRSV-2-N from (G) (n = 20). ** P < 0.01, *** P < 0.001. (I) Sgcontrol and sg RAB18 MARC-145 cells were transfected with plasmids encoding RAB18-FLAG WT, RAB18-FLAG S22N, and RAB18-FLAG Q67L for 12 h and then infected with LP-PRRSV-2 (MOI = 10) and HP-PRRSV-2 (MOI = 10) for 36 h. Viral titers were assessed by the TCID 50 assay. ** P < 0.01, *** P < 0.001. ns, not significance.

Article Snippet: Sections were then washed and further blocked with mouse and rabbit IgG (Proteintech, B900620 and 30000-0-AP) for 30 minutes before incubation with an Alexa Fluor 488-labeled mouse anti-PRRSV-2-N antibody and an Alexa Fluor 568-labeled rabbit anti-RAB18 antibody.

Techniques: Quantitative RT-PCR, Infection, Flow Cytometry, Western Blot, Transfection, Immunofluorescence, Fluorescence

(A and B) PAM (A) and MARC-145 (B) cells were infected with LP-PRRSV-2 (MOI = 10) for 0–36 h. The mRNA levels of RAB18 were analyzed by qRT-PCR. * P < 0.05, ** P < 0.01, *** P < 0.001. (C and D) MARC-145 cells were infected with LP-PRRSV-2 (MOI = 10, C) and HP-PRRSV-2 (MOI = 10, D) for 0–36 h. RAB18 and ACTB were analyzed by immunoblot analysis. (E) Immunohistochemistry for RAB18 and PRRSV-2-N in mock-infected or LP-PRRSV-2-infected porcine lungs (left). Asterisks indicate non-infected cells. Scale bar: 200 μm. The quantification of relative fluorescence intensity of PRRSV-2-N is shown on the right (n = 20). *** P < 0.001. (F) MARC-145 cells were transfected with the indicated RAB18-LUC plasmids for 12 h and then mock-infected or infected with LP-PRRSV-2 (MOI = 10) for 24 h. RAB18 promoter activities were assessed by dual-luciferase reporter assay. *** P < 0.001. ns, not significance. (G) MARC-145 cells were transfected with sicontrol or si RELA -1 for 24 h, followed by infection with LP-PRRSV-2 (MOI = 10) for 24 h. ChIP assays were performed with IgG or an antibody against RELA. The RAB18 promoter was amplified by primer-1 (146 bp) and primer-2 (96 bp). (H) The treatment of MARC-145 cells was as described in (G). ChIP assays were performed with IgG or an antibody against RELA. *** P < 0.001. (I) MARC-145 cells were transfected with sicontrol, siR IG-I -1, si RIG-I -2, si MAVS -1, si MAVS -2, si RELA -1, si RELA -2, si RELB -1, and si RELB -2 for 36 h. The mRNA levels of RIG-I, MAVS, RELA, and RELB were analyzed by qRT-PCR analysis. *** P < 0.001. (J) MARC-145 cells were transfected with sicontrol, siR IG-I -1, si RIG-I -2, si MAVS -1, si MAVS -2, si RELA -1, si RELA -2, si RELB -1, and si RELB -2 for 24 h, then infected with LP-PRRSV-2 (MOI = 10) for 0–48 h. The mRNA levels of RAB18 were analyzed by qRT-PCR analysis. * P < 0.05, ** P < 0.01.

Journal: PLOS Pathogens

Article Title: Porcine reproductive and respiratory syndrome virus 2 hijacks CMA-mediated lipolysis through upregulation of small GTPase RAB18

doi: 10.1371/journal.ppat.1012123

Figure Lengend Snippet: (A and B) PAM (A) and MARC-145 (B) cells were infected with LP-PRRSV-2 (MOI = 10) for 0–36 h. The mRNA levels of RAB18 were analyzed by qRT-PCR. * P < 0.05, ** P < 0.01, *** P < 0.001. (C and D) MARC-145 cells were infected with LP-PRRSV-2 (MOI = 10, C) and HP-PRRSV-2 (MOI = 10, D) for 0–36 h. RAB18 and ACTB were analyzed by immunoblot analysis. (E) Immunohistochemistry for RAB18 and PRRSV-2-N in mock-infected or LP-PRRSV-2-infected porcine lungs (left). Asterisks indicate non-infected cells. Scale bar: 200 μm. The quantification of relative fluorescence intensity of PRRSV-2-N is shown on the right (n = 20). *** P < 0.001. (F) MARC-145 cells were transfected with the indicated RAB18-LUC plasmids for 12 h and then mock-infected or infected with LP-PRRSV-2 (MOI = 10) for 24 h. RAB18 promoter activities were assessed by dual-luciferase reporter assay. *** P < 0.001. ns, not significance. (G) MARC-145 cells were transfected with sicontrol or si RELA -1 for 24 h, followed by infection with LP-PRRSV-2 (MOI = 10) for 24 h. ChIP assays were performed with IgG or an antibody against RELA. The RAB18 promoter was amplified by primer-1 (146 bp) and primer-2 (96 bp). (H) The treatment of MARC-145 cells was as described in (G). ChIP assays were performed with IgG or an antibody against RELA. *** P < 0.001. (I) MARC-145 cells were transfected with sicontrol, siR IG-I -1, si RIG-I -2, si MAVS -1, si MAVS -2, si RELA -1, si RELA -2, si RELB -1, and si RELB -2 for 36 h. The mRNA levels of RIG-I, MAVS, RELA, and RELB were analyzed by qRT-PCR analysis. *** P < 0.001. (J) MARC-145 cells were transfected with sicontrol, siR IG-I -1, si RIG-I -2, si MAVS -1, si MAVS -2, si RELA -1, si RELA -2, si RELB -1, and si RELB -2 for 24 h, then infected with LP-PRRSV-2 (MOI = 10) for 0–48 h. The mRNA levels of RAB18 were analyzed by qRT-PCR analysis. * P < 0.05, ** P < 0.01.

Techniques: Infection, Quantitative RT-PCR, Western Blot, Immunohistochemistry, Fluorescence, Transfection, Luciferase, Reporter Assay, Amplification

(A) PAM, scramble and sh RAB18 -1 MARC-145 cells were infected with LP-PRRSV-2 (MOI = 10) for 0–24 h. LDs were analyzed by Oil Red O staining. Scale bar: 10 μm. (B) Quantification of LDs numbers per cell from (A) by ImageJ (n = 16). ** P < 0.01, *** P < 0.001. (C) Oil Red O staining of mock-infected or LP-PRRSV-2-infected porcine lungs. Scale bar: 200 μm. (D) Scramble and sh RAB18 -1 MARC-145 cells were infected with LP-PRRSV-2 (MOI = 10) for 24 h. PRRSV-2-N was detected by immunofluorescence analysis and LDs were examined by BODIPY staining. Uninfected cells, indicated by asterisks, were outlined with dashed lines. Scale bar: 10 μm. (E) Quantification of relative BODIPY fluorescence intensity in cells from (D) by ImageJ (n = 16). ** P < 0.01. (F and G) PAM were infected with LP-PRRSV-2 (MOI = 10) for 0–24 h. TG (F) and NEFA (G) were quantified using biochemical kits. * P < 0.05, ** P < 0.01. (H and I) Scramble and sh RAB18 -1 MARC-145 cells were infected with LP-PRRSV-2 (MOI = 10) for 0–24 h. TG (H) and NEFA (I) were quantified using biochemical kits. ** P < 0.01. ns, no significance. (J) Sgcontrol and sg RAB18 MARC-145 cells were infected with LP-PRRSV-2 (MOI = 10) for 0–36 h. HSL, ATGL, PRRSV-2-N, RAB18, and ACTB were analyzed by immunoblot analysis. (K) Scramble and sh RAB18 -1 MARC-145 cells were infected with LP-PRRSV-2 (MOI = 10) for 36 h. Viral assembly in the supernatants was determined by comparing the infectious titers (TCID 50 /mL) with the total PRRSV-2 genome equivalents (GE). ** P < 0.01.

Journal: PLOS Pathogens

Article Title: Porcine reproductive and respiratory syndrome virus 2 hijacks CMA-mediated lipolysis through upregulation of small GTPase RAB18

doi: 10.1371/journal.ppat.1012123

Figure Lengend Snippet: (A) PAM, scramble and sh RAB18 -1 MARC-145 cells were infected with LP-PRRSV-2 (MOI = 10) for 0–24 h. LDs were analyzed by Oil Red O staining. Scale bar: 10 μm. (B) Quantification of LDs numbers per cell from (A) by ImageJ (n = 16). ** P < 0.01, *** P < 0.001. (C) Oil Red O staining of mock-infected or LP-PRRSV-2-infected porcine lungs. Scale bar: 200 μm. (D) Scramble and sh RAB18 -1 MARC-145 cells were infected with LP-PRRSV-2 (MOI = 10) for 24 h. PRRSV-2-N was detected by immunofluorescence analysis and LDs were examined by BODIPY staining. Uninfected cells, indicated by asterisks, were outlined with dashed lines. Scale bar: 10 μm. (E) Quantification of relative BODIPY fluorescence intensity in cells from (D) by ImageJ (n = 16). ** P < 0.01. (F and G) PAM were infected with LP-PRRSV-2 (MOI = 10) for 0–24 h. TG (F) and NEFA (G) were quantified using biochemical kits. * P < 0.05, ** P < 0.01. (H and I) Scramble and sh RAB18 -1 MARC-145 cells were infected with LP-PRRSV-2 (MOI = 10) for 0–24 h. TG (H) and NEFA (I) were quantified using biochemical kits. ** P < 0.01. ns, no significance. (J) Sgcontrol and sg RAB18 MARC-145 cells were infected with LP-PRRSV-2 (MOI = 10) for 0–36 h. HSL, ATGL, PRRSV-2-N, RAB18, and ACTB were analyzed by immunoblot analysis. (K) Scramble and sh RAB18 -1 MARC-145 cells were infected with LP-PRRSV-2 (MOI = 10) for 36 h. Viral assembly in the supernatants was determined by comparing the infectious titers (TCID 50 /mL) with the total PRRSV-2 genome equivalents (GE). ** P < 0.01.

Techniques: Infection, Staining, Immunofluorescence, Fluorescence, Western Blot

(A) Sgcontrol and sg RAB18 MARC-145 cells were infected with LP-PRRSV-2 (MOI = 10) for 0–36 h. PLIN2, RAB18, PRRSV-2-N and ATCB were analyzed by immunoblot analysis. (B) MARC-145 cells were mock-infected or infected with LP-PRRSV-2 (MOI = 10) for 36 h. Immunoblot analysis of PLIN2 (LDs), GM130 (Golgi), LAMP1 (Lysosome) and PRRSV-2-N was performed with cell lysates subjected to iodixanol density gradient centrifugation. (C) LDs were purified from MARC-145 cells mock-infected or infected with LP-PRRSV-2 (MOI = 10) for 36 h. PLIN2, RAB18 and PRRSV-2-N were analyzed by immunoblot analysis. (D) Sgcontrol and sg RAB18 MARC-145 cells were transfected with a plasmid encoding GFP-RFP-PLIN2 for 12 h and then mock-infected or infected with LP-PRRSV-2 (MOI = 10) for 36 h. PRRSV-2-N was detected by immunofluorescence analysis and the fluorescence of GFP and RFP was monitored by fluorescence microscopy. Scale bar: 10 μm. (E) Quantification of the fluorescence intensity ratio of RFP/GFP from D by ImageJ (n = 10). ** P < 0.01. ns, no significance. (F) MARC-145 cells were mock-infected or infected with LP-PRRSV-2 (MOI = 10), and treated with vehicle or CQ (10 mM) for 0–36 h. PLIN2, RAB18, PRRSV-2-N and ATCB were analyzed by immunoblot analysis.

Journal: PLOS Pathogens

Article Title: Porcine reproductive and respiratory syndrome virus 2 hijacks CMA-mediated lipolysis through upregulation of small GTPase RAB18

doi: 10.1371/journal.ppat.1012123

Figure Lengend Snippet: (A) Sgcontrol and sg RAB18 MARC-145 cells were infected with LP-PRRSV-2 (MOI = 10) for 0–36 h. PLIN2, RAB18, PRRSV-2-N and ATCB were analyzed by immunoblot analysis. (B) MARC-145 cells were mock-infected or infected with LP-PRRSV-2 (MOI = 10) for 36 h. Immunoblot analysis of PLIN2 (LDs), GM130 (Golgi), LAMP1 (Lysosome) and PRRSV-2-N was performed with cell lysates subjected to iodixanol density gradient centrifugation. (C) LDs were purified from MARC-145 cells mock-infected or infected with LP-PRRSV-2 (MOI = 10) for 36 h. PLIN2, RAB18 and PRRSV-2-N were analyzed by immunoblot analysis. (D) Sgcontrol and sg RAB18 MARC-145 cells were transfected with a plasmid encoding GFP-RFP-PLIN2 for 12 h and then mock-infected or infected with LP-PRRSV-2 (MOI = 10) for 36 h. PRRSV-2-N was detected by immunofluorescence analysis and the fluorescence of GFP and RFP was monitored by fluorescence microscopy. Scale bar: 10 μm. (E) Quantification of the fluorescence intensity ratio of RFP/GFP from D by ImageJ (n = 10). ** P < 0.01. ns, no significance. (F) MARC-145 cells were mock-infected or infected with LP-PRRSV-2 (MOI = 10), and treated with vehicle or CQ (10 mM) for 0–36 h. PLIN2, RAB18, PRRSV-2-N and ATCB were analyzed by immunoblot analysis.

Techniques: Infection, Western Blot, Gradient Centrifugation, Purification, Transfection, Plasmid Preparation, Immunofluorescence, Fluorescence, Microscopy

(A) Sgcontrol and sg RAB18 MARC-145 cells stably expressing KFERQ-PS-CFP2 were photoconverted and maintained for 2 h, and then mock-infected or infected with LP-PRRSV-2 (MOI = 10) for 36 h. The fluorescence of KFERQ-PS-CFP2 was detected by fluorescence microscopy (left). Quantification of the KFERQ puncta per cell by ImageJ is shown on the right (n = 10). Scale bar: 10 μm. ** P < 0.01, *** P < 0.001. ns, no significance. (B) Sgcontrol and sg RAB18 MARC-145 cells were mock-infected or infected with LP-PRRSV-2 (MOI = 10) for 36 h. PLIN2, LAMP2A, HSPA8, and NPC1 in lysosome purified by iodixanol density gradient centrifugation were analyzed by immunoblot analysis. (C) Immunoblot analysis of HSPA8 and ACTB in scramble and sh HSPA8 MARC-145 cells. (D and E) Scramble and sh HSPA8 MARC-145 cells were infected with LP-PRRSV-2 (MOI = 10, D) and HP-PRRSV-2 (MOI = 10, E) for 36 h. Viral titers were assessed by the TCID 50 assay. ** P < 0.01. (F) Immunoblot analysis of LAMP2A and ACTB in scramble and sh LAMP2A MARC-145 cells. (G and H) Scramble and sh LAMP2A MARC-145 cells were infected with LP-PRRSV-2 (MOI = 10, G) and HP-PRRSV-2 (MOI = 10, H) for 36 h. Viral titers were assessed by the TCID 50 assay. ** P < 0.01.

Journal: PLOS Pathogens

Article Title: Porcine reproductive and respiratory syndrome virus 2 hijacks CMA-mediated lipolysis through upregulation of small GTPase RAB18

doi: 10.1371/journal.ppat.1012123

Figure Lengend Snippet: (A) Sgcontrol and sg RAB18 MARC-145 cells stably expressing KFERQ-PS-CFP2 were photoconverted and maintained for 2 h, and then mock-infected or infected with LP-PRRSV-2 (MOI = 10) for 36 h. The fluorescence of KFERQ-PS-CFP2 was detected by fluorescence microscopy (left). Quantification of the KFERQ puncta per cell by ImageJ is shown on the right (n = 10). Scale bar: 10 μm. ** P < 0.01, *** P < 0.001. ns, no significance. (B) Sgcontrol and sg RAB18 MARC-145 cells were mock-infected or infected with LP-PRRSV-2 (MOI = 10) for 36 h. PLIN2, LAMP2A, HSPA8, and NPC1 in lysosome purified by iodixanol density gradient centrifugation were analyzed by immunoblot analysis. (C) Immunoblot analysis of HSPA8 and ACTB in scramble and sh HSPA8 MARC-145 cells. (D and E) Scramble and sh HSPA8 MARC-145 cells were infected with LP-PRRSV-2 (MOI = 10, D) and HP-PRRSV-2 (MOI = 10, E) for 36 h. Viral titers were assessed by the TCID 50 assay. ** P < 0.01. (F) Immunoblot analysis of LAMP2A and ACTB in scramble and sh LAMP2A MARC-145 cells. (G and H) Scramble and sh LAMP2A MARC-145 cells were infected with LP-PRRSV-2 (MOI = 10, G) and HP-PRRSV-2 (MOI = 10, H) for 36 h. Viral titers were assessed by the TCID 50 assay. ** P < 0.01.

Techniques: Stable Transfection, Expressing, Infection, Fluorescence, Microscopy, Purification, Gradient Centrifugation, Western Blot

(A) MARC-145 cells were mock-infected or infected with LP-PRRSV-2 (MOI = 10) for 36 h. The interaction of RAB18, PLIN2, and HSPA8 was analyzed by Co-IP analysis with IgG (control) or anti-RAB18 antibody. (B) HEK293T cells were co-transfected with Rab18-HA and PLIN2-FLAG or PLIN2 (aa 1–251)-FLAG for 24 h. The interaction of RAB18 with PLIN2 variants was analyzed by Co-IP analysis. (C) HEK293T cells were co-transfected with HSPA8-HA and RAB18-FLAG for 24 h. The interaction of HSPA8 with RAB18 was analyzed by Co-IP analysis. (D) HEK293T cells were co-transfected with RAB18-FLAG and indicated HSPA8-HA variants for 24 h. The interaction of RAB18 with HSPA8 variants was analyzed by Co-IP analysis. (E) HEK293T cells were co-transfected with HSPA8-HA and indicated RAB18-FLAG variants for 24 h. The interaction of HSPA8 with RAB18 variants was analyzed by Co-IP analysis. (F) The interaction of His-SUMO-HSPA8 with indicated GST-RAB18 variants was assessed by in vitro affinity isolation assays. (G) The interaction of His-SUMO-RAB18 with indicated GST-HSPA8 variants was assessed by in vitro affinity isolation assays. (H) The interaction of His-SUMO-HSPA8 with GST-PLIN2 CTD was assessed by in vitro affinity isolation assays. (I) The interaction of His-SUMO-RAB18 with GST-PLIN2 CTD was assessed by in vitro affinity isolation assays.

Journal: PLOS Pathogens

Article Title: Porcine reproductive and respiratory syndrome virus 2 hijacks CMA-mediated lipolysis through upregulation of small GTPase RAB18

doi: 10.1371/journal.ppat.1012123

Figure Lengend Snippet: (A) MARC-145 cells were mock-infected or infected with LP-PRRSV-2 (MOI = 10) for 36 h. The interaction of RAB18, PLIN2, and HSPA8 was analyzed by Co-IP analysis with IgG (control) or anti-RAB18 antibody. (B) HEK293T cells were co-transfected with Rab18-HA and PLIN2-FLAG or PLIN2 (aa 1–251)-FLAG for 24 h. The interaction of RAB18 with PLIN2 variants was analyzed by Co-IP analysis. (C) HEK293T cells were co-transfected with HSPA8-HA and RAB18-FLAG for 24 h. The interaction of HSPA8 with RAB18 was analyzed by Co-IP analysis. (D) HEK293T cells were co-transfected with RAB18-FLAG and indicated HSPA8-HA variants for 24 h. The interaction of RAB18 with HSPA8 variants was analyzed by Co-IP analysis. (E) HEK293T cells were co-transfected with HSPA8-HA and indicated RAB18-FLAG variants for 24 h. The interaction of HSPA8 with RAB18 variants was analyzed by Co-IP analysis. (F) The interaction of His-SUMO-HSPA8 with indicated GST-RAB18 variants was assessed by in vitro affinity isolation assays. (G) The interaction of His-SUMO-RAB18 with indicated GST-HSPA8 variants was assessed by in vitro affinity isolation assays. (H) The interaction of His-SUMO-HSPA8 with GST-PLIN2 CTD was assessed by in vitro affinity isolation assays. (I) The interaction of His-SUMO-RAB18 with GST-PLIN2 CTD was assessed by in vitro affinity isolation assays.

Techniques: Infection, Co-Immunoprecipitation Assay, Transfection, In Vitro, Isolation

PRRSV-2 infection activates the RIG-I/MAVS and canonical NF-κB pathways, which in turn upregulate RAB18 expression. RAB18 recruits PLIN2 through direct interaction with HSPA8 and thereby translocates PLIN2 to the lysosome for CMA-mediated degradation. Neutral lipases, such as ATGL, stimulate lipolysis, facilitating PRRSV-2 replication and assembly.

Journal: PLOS Pathogens

Article Title: Porcine reproductive and respiratory syndrome virus 2 hijacks CMA-mediated lipolysis through upregulation of small GTPase RAB18

doi: 10.1371/journal.ppat.1012123

Figure Lengend Snippet: PRRSV-2 infection activates the RIG-I/MAVS and canonical NF-κB pathways, which in turn upregulate RAB18 expression. RAB18 recruits PLIN2 through direct interaction with HSPA8 and thereby translocates PLIN2 to the lysosome for CMA-mediated degradation. Neutral lipases, such as ATGL, stimulate lipolysis, facilitating PRRSV-2 replication and assembly.

Techniques: Infection, Expressing

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