Direct Link === https://urluss.com/2tkQLp
You can directly connect to IBM Cloud services to extend your on-premises network to IBM Cloud. For example, you can connect to VPCs or connect your direct links to other local or remote transit gateways.
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An antiserum raised against chemically acetylated histone H4 was found to recognize the epitope epsilon-N-acetyl lysine. Affinity-purified antibodies were used to fractionate oligo- and mononucleosomal chromatin fragments from the nuclei of 15-day chicken embryo erythrocytes. Antibody-bound chromatin was found to contain elevated levels of acetylated core histones. On probing with sequences of alpha D globin, an actively transcribed gene, the antibody-bound chromatin was 15- to 30-fold enriched relative to the input chromatin. Using ovalbumin sequences as a probe, no enrichment was observed. The results demonstrate directly that transcriptionally active genes carry acetylated core histones.
On Windows and macOS, Storage Explorer supports URIs with the storageexplorer:// protocol. These URIs are referred to as direct links. A direct link points to an Azure Storage resource in Storage Explorer. Following a direct link will open Storage Explorer and navigate to the resource it points to. This article describes how direct links work and how you can use them.
Storage Explorer uses the tree view to visualize resources in Azure. A direct link contains the hierarchical information for the linked resource node in the tree. When a direct link is followed, Storage Explorer opens and receives the parameters in the direct link. Storage Explorer then uses these parameters to navigate to the linked resource in the tree view.
Here is an example direct link to a blob container.storageexplorer://v=1&accountid=/subscriptions/the_subscription_id/resourceGroups/the_resource_group_name/providers/Microsoft.Storage/storageAccounts/the_storage_account_name&subscriptionid=the_subscription_id&resourcetype=Azure.BlobContainer&resourcename=the_blob_container_name
You can use Storage Explorer to get a direct link for a resource. Open the context menu of the node for the resource in the tree view. Then use the \"Copy Direct Link\" action to copy its direct link to the clipboard.
Among the genes differentially expressed in Mitfmi-vga9/+ McSCs, we were particularly interested in IFN regulatory factor 4, Irf4. In human melanocytes, MITF binds and activates Irf4 via an intronic enhancer , and in turn, IRF4 can transcriptionally regulate IFN signaling by repressing the master regulatory factor for IFN gene expression, Irf7 [43,44]. A genome-wide association study of Latin Americans also identified Irf4 as a locus associated with hair graying . Because Irf4 and Irf7 exhibit a reciprocal relationship in Mitfmi-vga9/+ McSCs (Irf4 is down and Irf7 is up; S2 Data), we asked whether Irf4 may be indirectly responsible for the up-regulation of ISGs in Mitfmi-vga9/+ melanocytes. However, within the 48-hour time frame that is sufficient for Mitf knockdown to result in ISG up-regulation, we did not observe consistent down-regulation of Irf4 between the two Mitf siRNAs (Fig 4A). As a control, we further confirmed that cells being treated with either siMitf or siMitf-OM results in the predictable down-regulation of the melanosomal gene Pmel17, which MITF is known to transcriptionally activate (Fig 4A; ). Based on these observations, we anticipated that the up-regulation of ISGs observed with Mitf knockdown cannot be IRF4 dependent. Indeed, using two unique Irf4 siRNAs (siIrf4_a and siIrf4_b), Irf4 gene expression can be significantly reduced in comparison to a negative control siRNA (siNC1). However, when considering the results of both Irf4 siRNAs, Irf4 knockdown does not lead to the consistent up-regulation or Irf7 or any of the other ISGs analyzed (Fig 4B). Altogether, these results support a novel role for MITF in suppressing the basal IFN signature in melanocytes in vitro and indicate that MITF does not mediate this response through Irf4.
Recent genome-wide association studies have led to the identification of function-reducing mutations in interferon induced with helicase C domain 1 (Ifih1) as protective against vitiligo in humans . Ifih1 is one of the direct transcriptional targets of MITF identified above (Fig 4) and encodes for the protein MDA5. MDA5 sits at the top of the type I innate immune signaling cascade and functions as a cytoplasmic PRR that responds to pathogen-associated molecular patterns (PAMPs) like viral RNA . Gain-of-function mutations of Ifih1 in humans or overexpression of Ifih1 in mice is associated with a sustained IFN gene signature and makes it a reasonable candidate for mediating a similar effect downstream of Mitfmi-vga9/+ [55,56]. Thus, we were interested to evaluate whether Ifih1 haploinsufficiency would be sufficient to reduce the hair graying caused by Mitfmi-vga9 in the context of Tg(Dct-Sox10).
Hair graying associated with Tg(Dct-Sox10) is most readily visible in mice that are homozygous for the transgene, with Tg(Dct-Sox10)/Tg(Dct-Sox10); Mitfmi-vga9/+ animals exhibiting robust graying at 110 days (Fig 1). Comparing Tg(Dct-Sox10)/Tg(Dct-Sox10); Mitfmi-vga9/+ mice to their littermates, we find that additional heterozygosity for Ifih1 (Ifih tm1.1Cln/+) does not reverse hair graying to the levels observed in Tg(Dct-Sox10)/Tg(Dct-Sox10) mice (Fig 6, S3 Fig). At most, and in a qualitative sense, Ifih tm1.1Cln/+ appears to produce a small reduction in the existing congenital white belly spot. These observations suggest that while MITF may repress Ifih1 in melanocytes in vitro, reduction of Ifih1 in vivo is insufficient to reverse hair graying associated with Mitfmi-vga9/+. This may indicate that the influence of MITF in innate immune regulation extends beyond the regulation of an individual gene, which is consistent with the fact that Ifih1 is not the only innate immune target gene directly downstream of MITF (as shown in Fig 4).
By assessing McSCs and melanoblasts in vivo and melanocytes in vitro, we identify a novel role for MITF in the transcriptional repression of target genes involved in type I innate immune signaling. Accordingly, we demonstrate that haploinsufficiency for Mitf incites a heightened and sustained IFN gene signature in McSCs, melanoblasts, and whole skin, and that Mitfmi-vga9/+ melanoblasts have an enhanced ability to respond to viral mimic. We show through siRNA knockdown and ChIP analysis in vitro that MITF transcriptionally represses several ISGs and that for some of these ISGs, this response may be through the direct binding of MITF to their gene promoter. Furthermore, we establish that postnatal melanocytes and McSCs are negatively affected by systemic activation of innate immune signaling in vivo and that this contributes to the pathogenesis of hair graying when considered in the context of a genetic background that is already at risk for this phenotype.
The participation of MITF in the regulation of innate immune target genes within the melanocyte lineage is unanticipated but is reported within other genomic datasets. For instance, RNA-seq analysis of human melanoma COLO829 cells transfected with MITF short hairpin RNA (shRNA) demonstrates an up-regulation of over 17 of the same 55 innate immune DEGs identified in Mitfmi-vga9/+ McSCs, including Ifih1, Ifit3, Irf7, Parp9, and Stat1 (GSE50686 ). Differential regulation of 15 of the 55 Mitfmi-vga9/+ innate immune DEGs is also observed after transient knockdown of MITF in the immortalized, human melanocytes Hermes 3A, although the direction of expression varies in comparison to our observations . Interestingly, animals that are homozygous for a loss-of-function mutation in the melanocortin 1 receptor gene (Mc1re/e) also exhibit differential expression of ISGs in skin and spleen . MC1R and MITF exist in a positive feedback regulatory loop, in which MC1R activation leads to cAMP/CREB-dependent up-regulation of Mitf , and MITF acts as a transcriptional activator of Mc1R gene expression [47,62]. These observations further highlight a link between key melanocyte proteins and the expression of genes involved in the innate immune response.
If the browser security settings on the Windows Server instance provide the permissions (for example, to http://*.s3.amazonaws.com), you can use a direct link for your region to download the CodeDeploy agent and then run the installer manually.
I don't want to use the chat widget on my website but I do want to provide my customers with a live chat option. Is it possible to create a direct link to a separate chat window to send to my customers
In such a situation, are there any known ways of adding custom tags, e.g. If an organization wanted to include the direct-to-chat link in an email, but also wanted to ensure that within the chat initiated that way, there was some information (e.g. as tags attached to the chat), that said chat came from an email (e.g. adding a query parameter to the chat link itself)
We want to update our Chat Widget to Messaging, but the limitation that does not allow a direct link to the live chat window is a huge setback. Is there any possibility of including this feature in the future.
How do I do this but show the web widget from a link with not only Live Chat. E.g. show the same UI as clicking on the web widget button (chat bot > contact us button > option to leave a message or live chat (if available). Some of my text links using the above method have ended up in this result, but I can't replicate this 100% of the time. 59ce067264