Journal: Journal of cellular and molecular medicine
Article Title: Hepatocyte-Specific HuR Protects Against Acetaminophen-Induced Liver Injury in Mice.
doi: 10.1111/jcmm.70246
Figure Lengend Snippet: FIGURE 4 | Conditional hepatocyte-specific HuR knockout leads to the reduction of proliferation, autophagy and antioxidant-related factors in APAP-treated mice. (A) CTR and cKO mice were treated with 300 mg/kg of APAP for 6 and 12 h, and total protein lysates from liver tissues were subjected to Western blot analysis for HuR, NRF2, cyclin A1, cyclin B1, cyclin D1, CDK2, ATG3, ATG5, ATG7, PCNA, P62, LC3-I, LC3-II and β- Tubulin (TUBB). Blots were processed from parallel gels. (B) The density of the protein signals for NRF2, cyclin A1, cyclin B1, cyclin D1, CDK2, ATG3, ATG5, ATG7, PCNA, P62, LC3-I and LC3-II expressions in mice livers at 6 h post-APAP dosing (CTR and cKO, n = 5), and relative mRNA levels of Nrf2, cyclin A1, cyclin B1, cyclin D1, Cdk2, Atg3, Atg5 and Atg7 in the livers of mice at 6 h post-APAP dosing (CTR and cKO, n = 5). Data are expressed as mean ± SD (blank columns, CTR; black columns, cKO). Significance was determined by a two-tailed Mann–Whitney U test (**p < 0.01). (C) The density of the signals for NRF2, cyclin A1, cyclin B1, cyclin D1, CDK2, ATG3, ATG5, ATG7, PCNA, P62, LC3-I and LC3-II expressions in mice livers at 12 h post-APAP (CTR and cKO, n = 5), and relative mRNA levels of Nrf2, cyclin A1, cyclin B1, cyclin D1, Cdk2, Atg3, Atg5 and Atg7 in the livers from CTR and cKO mice at 12 h post-APAP (CTR and cKO, n = 5). Data are expressed as mean ± SD (blank columns, CTR; black columns, cKO). Significance was determined by a two-tailed Mann–Whitney U test (*p < 0.05; **p < 0.01).
Article Snippet: Polyclonal anti- HuR (11910- 1), polyclonal antiCYP2E1 (19937- 1), polyclonal anti- NRF2 (16396- 1), polyclonal anti- PCNA (10205- 2), polyclonal anti- CYCLIN B1 (55004- 1), polyclonal anti- CYCLIN D1 (26939- 1), polyclonal anti- CDK2 (10122- 1), polyclonal anti- CDK4 (11026- 1), polyclonal anti- ATG3 (11262- 2), polyclonal anti- ATG5 (10181- 2), polyclonal anti- ATG7 (10088- 2), polyclonal anti- ATG12 (11264- 1), polyclonal anti- P62 (18420- 1), polyclonal anti- LC3 (14600- 1) and monoclonal anti- GAPDH (60004- 1) were from Proteintech.
Techniques: Knock-Out, Western Blot, Two Tailed Test, MANN-WHITNEY
Proteintech is a verified supplier 
![The graphical abstract on the dual roles of CXCR4 in promoting EBOV entry and mediating excessively expressed mature GP degradation via reticulophagy to facilitate viral fitness. CXCR4 interacts with EBOV GP, and such interaction could mediate internalization of protein complex into early endosomes, where GP further interacts with NPC1 to release its genome to cytosol. Mature GP is transported to the cell membrane for release of the mature viral particles, whereas mature GP anchored on the cell membrane could hijack CXCR4 sorting and transporting pathway by their interactions with HGS, and then GP could be carried back to endoplasmic reticulum by CXCR4, where the E3 ubiquitin ligase RNF185 was recruited to polyubiquitinate GP in a K27- and K63-linked manner. Finally, polyubiquitinated GP was degraded in lysosomes via reticulophagy by interacting with the reticulophagic receptor RETREG1, in an ATG3- and ATG5-dependent manner. Thus, our study uncovered dual roles of CXCR4 in EBOV life cycle and provided new evidence that EBOV hijacked the host machinery through efficient virus-host interactions to promote viral fitness. (this figure was created by BioRender.com.) [the nucleus is double membrane.].](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_9367/pmc12459367/pmc12459367__KAUP_A_2492877_F0008_C.jpg)
