both CD11c-Cre and Mafb-Cre will target macrophages in many organs, not We prove that retinal microglia have a unique CD45 lo CD11c lo F4/80 lo I-A/I-E Once the tamoxifen is not longer bioavailable, Cre is inactive and no new YFP + cells can express RFP
However, there remains a lack of consensus on the optimal route and dosage of TAM administration in vivo
This system allows for deletion of the genes of interest in specific cells, tissues and the whole organism to generate a diversity of conditional knockout mouse strains
However, this effect is not permanent, as discontinuation of tamoxifen LN, axillary lymph nodes
Newell, Berenice Cabrera-Martinez, Justin Cre is a bacterial recombinase that catalyzes recombination between paired DNA recognition sites termed LoxP sites ( 4, 5 )
However, DT treatment also reduced Mg and DCs in Itgax-cre (CD11c-Cre) Tg mice (B6
These Cd11c-Cre transgenic mice are a Cre-lox tool for deletion of floxed sequences in CD8 - , CD8 >+ dendritic cells, tissue-derived dendritic cells from lymph Tg (Itgax-cre/ERT)61Gkl
3) T and B cells Cre-lox系统虽然能有效帮助我们在特定的组织中进行基因敲除,但Cre重组酶表达的时间是由其启动子决定的。如果您希望在特定时间段人为操纵Cre重组酶的活性,比如说要研究某个基因在小鼠发育特定时期的功能,应该怎么办 呢?本篇将给大家介绍一种时空特异性敲除系统:Tamoxifen诱导型CreER重组酶。 in cancer cells from Tsc1fl/flPyMT and CD11cCreTsc1fl/flPyMT mice, an approximate 6-fold increase of CC3+ cancer cells were observed in CD11cCreTsc1fl/flPyMT mice (Figure 3A)
Although leakiness of tdTomato expression was observed in CAMs and microglia in Cre + mice without tamoxifen treatment, blood monocytes showed no tdTomato expression, For instance, Irf8 was described to be crucial at the MDP to CDP transition in the BM, leading to cDC1 defect in the periphery
CD11c-Cre and CD11c-Cre IL-33 fl/fl mice were injected (intraperitoneally) with 2 × 10 6 Flt3L-producing EL4 cells, A tamoxifen inducible Cre recombinase cDNA (CreERT2) was cloned downstream of a CD68 promoter, consisting of 2
A major tamoxifen administration is performed by intraperitoneal administration or oral administration
Figure 1 Generation and validation of a tamoxifen-inducible CD4 + T-cell-specific Cre Efficiency of Cre activity by tdTomato expression was dose Tamoxifen-induced gene deletion was only initiated at day 3 post-infection when hemorrhagic lung injury has resolved, further supporting the importance of IEC
Flow cytometric analysis showed peritoneal F4/80 hi macrophages were not affected by IRF4 deficiency in CD11c cre × IRF4 fl/fl (CD11c ΔIRF4) mice
Mice carrying loxP-site-flanked (floxed) Hydroxy-tamoxifen (OH-TAM) was applied three days prior to analysis
TAMs can function as antigen-presenting cells and regulate cytotoxic T lymphocyte responses in tumor
129 (Cg)-Gt(ROSA)26Sor tm4(ACTB-tdTomato,-EGFP)Luo /J) and endothelin converting enzyme-1 floxed transgenic mouse line (D) Immunohistochemical analysis of spleens from Gata2 f/f /ER-Cre mice treated with tamoxifen or corn oil
Upon blue light stimulation following tamoxifen treatment, the TamPA-Cre system exhibits sensitivity to low intensity, short durations of blue light exposure to induce robust Cre-loxP Mutation details: A transgenic construct containing sequence encoding cre recombinase under the control of the mouse integrin alpha X (Cd11c) promoter, and a bovine growth hormone poly A signal sequence, was introduced into B6CBAF1/J donor eggs
Male CD11c-Cre + Fcgr2b fl/fl recipients also a reduction in other genes such HMGCoA reductase (Hmcgr) in the cholesterol synthesis pathway and macrophage scavenger receptor-1 (Msr1) (Fig
By contrast, using Cd11c cre (Cd11c Is also known as Itgax) to delete TIM-3 In DCs (TIM-3 conditional knockout (Havcr2 cko)), we observed significantly reduced tumour growth mice were orally gavaged with 8 mg tamoxifen 3 days before tumour implantation and every 3 days thereafter for the duration of the experiments
Therefore, we crossed mice expressing green fluorescent protein (GFP) and Cre recombinase under the control of the CD11c promoter (encoded by Itgax) 25, 26 with mice possessing two loxP sites Graphical timeline of IMQ treatment for the different Cre‐Lines
The disease-propagating effects of these cells in experimental autoimmune A tamoxifen inducible Cre recombinase cDNA (CreERT2) was cloned downstream of a CD68 promoter, consisting of 2
(A) Schematic diagram of generating a VSMC-specific tamoxifen-inducible knockout (iKO) mice by crossing DGCR8 loxp/loxp with SMA-Cre Future studies which invoke long-term depletion of CD11c + cells through the use of CD11c-cre animals are required to definitively demonstrate that CD11c + cells are required for αSyn transport Stk11 fl/fl VECad-Cre ERT2 mice were generated by crossing breeding Stk11 fl/fl mice with VECad-Cre ERT2 mice
Until now there are very few lines for DC targeting available When fusing the Cre recombinase gene with the gene encoding estrogen receptor (ER), such Cre driver mice can be used for a temporal control of loxP-flanked transgene expression upon administration of tamoxifen, the estrogen antagonist
CD11c-Cre has been reported to target ResAM, although careful studies of its specificity and efficiency have not been published
5 mg tamoxifen on three alternating days and harvested at the indicated time after the last tamoxifen injection
A tamoxifen-inducible CD4 + T-cell-specific ThPOK CreERT2
A 2A receptor agonism depleted CD11c + T-bet + B cells in lupus-prone mice
These Cd11c-Cre transgenic mice are a Cre-lox tool for deletion of floxed sequences in CD8 - , CD8 + dendritic cells, tissue-derived dendritic cells from lymph nodes, lung and
To test whether CSF-1R signaling also controlled liMac homeostasis, we generated Cd11c Cre Csf1r fl/fl mice, in which Csf1r was specifically deleted in CD11c +
CD11c-Cre +;Flt3 −/ Mice were tamoxifen (TAM) induced 6–8 weeks earlier at 8–12 weeks of age
To further validate this finding, we generated CD11c + Mac–depleting (CD11c + Mac iDTR) mice by breeding CD11c Cre-GFP and Csf1r LoxP-stop-LoxP-DTR-mCherry mice
F4/80 hi and F4/80 lo macrophages were not affected in Cd11c Cre Csf1r fl/fl mice Tamoxifen was reconstituted with 100% ethanol in corn oil with a final concentration of 25 mg ml –1
The panel with CD11C staining shows a similar area to the panel with The putative mechanism of selective Cre-mediated recombination is Cre sequestration in the cytoplasm in the basal state with translocation to the nucleus only in the presence of tamoxifen
7,8 In addi-tion, CD11cCre targets DCs that capture tumor (D) Immunohistochemical analysis of spleens from Gata2 f/f /ER-Cre mice treated with tamoxifen or corn oil
9 kb of CD68 5’ flanking sequence with the 83-bp first intron (IVS-1) of the CD68 gene (PMID 11454064), together with a rabbit beta-globin polyadenylation sequence
Tamoxifen was given in the diet for 3 wk, and then animals were analyzed for reporter expression in peritoneal and pleural macrophages
In order to determine the role of Flip in cDC, Flip flox/flox mice were crossed with mice expressing GFP-Cre recombinase under the control of the CD11c promoter Future studies which invoke long-term depletion of CD11c + cells through the use of CD11c-cre animals are required to definitively demonstrate that CD11c + cells are required for αSyn transport In fact, c‐Jun expression was also not affected in CD11c expressing macrophages from c‐Jun Δ/Δ CD11c‐Cre mice as shown by qRT–PCR, demonstrating that c‐Jun deletion by CD11c‐Cre had not occurred in these cells (Fig 4D and E)
5, 3, or 7 days after the first CD11c-cre mice that express Cre recombinant under the control of CD11c promoter were bilateral stereotactic injected with either rAAV2/6M-DIO-taCasp3 (rAAV-taCasp3) or rAAV2/6M-DIO-EGFP (rAAV Animal studies