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Bennett Lewis
Bennett Lewis

Parallels 12 Activation Key WORK

The activation key you will enter in the next step will be registered under the account you signed in to. If you would like to change the account you are signed in to, click on the Parallels Desktop menu and select Account & License. In the new window, click on the account email address and choose Sign Out.

Parallels 12 Activation Key

When Parallels Desktop prompts you to sign in, sign in to the account which contains your activation keys. After signing in, you will see the list of your license keys. Double-click on the license you would like to use for activation.

Hi, I am running a MacBook Air (2014) and bought a license for Windows 10 and installed it using Parallels 12. I tried it for a couple days and found it to be lagging a lot, especially for high demand processes. I want to instead run Windows 10 as a dual boot on my MacBook so I used Bootcamp to partition my hard drive and install a copy of windows 10 there. The problem is that I can't activate it as Microsoft is telling me that the activation key has already been activated (error 0xC004C008). Is there a way to deactivate the license on parallels and use that on the bootcamp/dualboot? I am using it on the same MacBook Air.

For anyone having the same issue, what I did was deactivated my Windows 10 key on Parallels Windows 10 VM (look up how to do this on google). Then I called Microsoft using the number that was given on the activation step, then followed through the automated representative until it transferred me to an actual representative, where he asked me to tell him the activation number (given when you click on "activate windows by phone") and he gave me a series of numbers to input and finished. Windows is Activated!

Triggering receptor expressed on myeloid cells-2 (TREM-2) is rapidly emerging as a key regulator of the innate immune response via its regulation of macrophage inflammatory responses. Here we demonstrate that proximal TREM-2 signaling parallels other DAP12-based receptor systems in its use of Syk and Src-family kinases. However, we find that the linker for activation of T cells (LAT) is severely reduced as monocytes differentiate into macrophages and that TREM-2 exclusively uses the linker for activation of B cells (LAB encoded by the gene Lat2(-/-)) to mediate downstream signaling. LAB is required for TREM-2-mediated activation of Erk1/2 and dampens proximal TREM-2 signals through a novel LAT-independent mechanism resulting in macrophages with proinflammatory properties. Thus, Lat2(-/-) macrophages have increased TREM-2-induced proximal phosphorylation, and lipopolysaccharide stimulation of these cells leads to increased interleukin-10 (IL-10) and decreased IL-12p40 production relative to wild type cells. Together these data identify LAB as a critical, LAT-independent regulator of TREM-2 signaling and macrophage development capable of controlling subsequent inflammatory responses.


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