Secretory Pathway Puns

what are they and what's the difference ?

and how proteins destined to function as membrane receptors are only partially translocated into the ER before forming into secretory vesicles?

please explain in details if possible

The following is a big dump of info related to an earlier post about MTORC1 here (full thread on hppdonline here) and its relation to Mast Cells which I need to sort into a coherent train of though outside of just my brain...: basically how does mtor relate to mast cells and/or how does hppd effect mast cells (secondary disease state) and/or how does mast cells effect hppd (onset) and/or mtor and mast cells cascading effect and how it can relate to anxiety, memory, and visuals.

keywords:

Mast cell

degranulation

5ht2a

microglia

astrocyte

mTORC1

MMP3

Histamine

AMPA

NMDA

Interleukin1-b (and more...)

Endocannabinoid

CB1

Pre Frontal Cortex PFC

retinal ganglion cell (RGC)

cytokine

chemokine

a ton more

Little is known about the signals downstream of PI3K which regulate mast cell homeostasis and function following FcepsilonRI aggregation and Kit ligation. In this study, we investigated the role of the mammalian target of rapamycin complex 1 (mTORC1) pathway in these responses. In human and mouse mast cells, stimulation via FcepsilonRI or Kit resulted in a marked PI3K-dependent activation of the mTORC1 pathway, as revealed by the wortmannin-sensitive sequential phosphorylation of tuberin, mTOR, p70S6 kinase (p70S6K), and 4E-BP1. In contrast, in human tumor mast cells, the mTORC1 pathway was constitutively activated and this was associated with markedly elevated levels of mTORC1 pathway components. Rapamycin, a specific inhibitor of mTORC1, selectively and completely blocked the FcepsilonRI- and Kit-induced mTORC1-dependent p70S6K phosphorylation and partially blocked the 4E-BP1 phosphorylation. In parallel, although rapamycin had no effect on FcepsilonRI-mediated degranulation or Kit-mediated cell adhesion, it inhibited cytokine production, and kit-mediated chemotaxis and cell survival. Furthermore, Rapamycin also blocked the constitutive activation of the mTORC1 pathway and inhibited cell survival of tumor mast cells. These data provide evidence that mTORC1 is a point of divergency for the PI3K-regulated downstream events of FcepsilonRI and Kit for the selective regulation of mast cell functions. Specifically, the mTORC1 pathway may play a critical role in normal and dysregulated control of mast cell homeostasis.

[https://www.researchgate.net/publication/5498643_A

I don't want to step on anybody's toes here, but the amount of non-dad jokes here in this subreddit really annoys me. First of all, dad jokes CAN be NSFW, it clearly says so in the sub rules. Secondly, it doesn't automatically make it a dad joke if it's from a conversation between you and your child. Most importantly, the jokes that your CHILDREN tell YOU are not dad jokes. The point of a dad joke is that it's so cheesy only a dad who's trying to be funny would make such a joke. That's it. They are stupid plays on words, lame puns and so on. There has to be a clever pun or wordplay for it to be considered a dad joke.

Again, to all the fellow dads, I apologise if I'm sounding too harsh. But I just needed to get it off my chest.

Continuation of mTORC1 p2: Mast cells.... p1 --> Link

2. Overview and activation of MCs

Although the role of MCs is overlooked compared with microglia, MCs remain an important factor in the immune signaling pathway (29). MCs, the effector cells of the innate immune system, are derived from hematopoietic stem cells and multifunctional antigen-presenting cells and have a pivotal role in immunoglobulin type E (IgE)-associated allergic and inflammation-associated diseases (35). Despite their low numbers in most organs, MCs are present in both healthy and disease states. MCs are the first line of defense against invading pathogens and are distributed in almost all organs and vascularized tissues (36). Blood MCs express CD34 and contain cytoplasmic granules filled with heparin and histamine, the latter of which is released after binding to IgE. Unlike other myeloid-derived cells, tissue MCs have a hematopoietic developmental lineage (37,38). During MC development, immature lineage progenitors enter the circulation and are recruited to peripheral tissues by endothelial cells, regulating the appearance of granules with proteases (37,38). Human MCs may be classified into mucosal and connective tissue types according to the type of proteases present in their cytoplasmic granules; the mucosal type contains tryptase, whereas the connective tissue type contains both tryptase and chymase (39). MCs act as first responders and environmental ‘sensors’ to interact with other cellular elements involved in physiological and immune responses, promoting the neuroinflammation process (40). MCs are present in various areas of the brain and meninges. Although less distributed in the brain, they are generally found in the subthalamic nucleus, choroid plexus and the parenchyma of the hypothalamic region (41). The pathogenic roles of MCs were indicated to extend from allergic disease to autoimmune diseases and carcinogenesis (42-47).

The most common way through which MCs perform their function is degranulation. The activation of the inflammatory process results in a rapid release of MC granules into the interstitium. MC granules contain pre-formed and newly synthesized reactive chemicals known as MC mediators. These mediators include histamine, tryptase, chymase, interleukin families, tumor necrosis factor-α (TNF-α), serotonin, heparin, proteoglycans, vascular endothelial growth factor (VEGF), prosta

Do your worst!

I'm surprised it hasn't decade.