• 🛑Hello, this board in now turned off and no new posting.
    Please REGISTER at Anabolic Steroid Forums, and become a member of our NEW community! 💪
  • 🔥Check Out Muscle Gelz HEAL® - A Topical Peptide Repair Formula with BPC-157 & TB-500! 🏥

can anyone explain to me what this means?

titans13ae

Registered User
Registered
Joined
Apr 3, 2003
Messages
82
Reaction score
0
Points
0
Age
40
Location
arkansas
IML Gear Cream!
It is important to take your creatine with a protein powder that is not enriched with glutamine (this means you cannot take it with mrp's as most are enriched with glutamine) because the two amino's use the same substrate to transport them into your muscle cells and when taken within 1-1/2 hour apart will not absorb.
I dont understand what is happeining there, i just ordered creatine and protein with glut in it, what should i do?
 
I don't think that is true..................
 
Many people put it in protein shakes.
 
I've read many different studies stating that you can take and can't take creatine and glutamine together because they fight for absorbsion .......Hell,I never had a problem or maybe I'm just to dumb to reralize it,but I do put creatine in my protein
 
I'd love to see a study that says that.
 
I used to know the name of the glutamine receptor.

I've since forgotten.
 
Funny how relationships fade..;)
 
What, the relationship between me and my memory?
 
Originally posted by Twin Peak
I'd love to see a study that says that.

.

The guanine nucleotide-binding regulatory protein alpha-subunit, Galpha(16), is primarily expressed in hemopoietic cells, and interacts with a large number of seven-membrane span receptors including chemoattractant receptors. We investigated the biological functions resulting from Galpha(16) coupling of chemoattractant receptors in a transfected cell model system. HeLa cells expressing a kappaB-driven luciferase reporter, Galpha(16), and the formyl peptide receptor responded to fMLP with a approximately 7- to 10-fold increase in luciferase activity. This response was accompanied by phosphorylation of IkappaBalpha and elevation of nuclear kappaB-DNA binding activity, indicating activation of NF-kappaB. In contrast to Galpha(16), expression of Galpha(q), Galpha(13), and Galpha(i2) resulted in a marginal increase in kappaB luciferase activity. A GTPase-deficient, constitutively active Galpha(16) mutant (Q212L) could replace agonist stimulation for activation of NF-kappaB. Furthermore, expression of Galpha(16) (Q212L) markedly enhanced TNF-alpha-induced kappaB reporter activity. The Galpha(16)-mediated NF-kappaB activation was paralleled by an increase in phospholipase C-beta activity, and was blocked by pharmacological inhibitors of protein kinase C (PKC) and by buffering of intracellular Ca(2+). The involvement of a conventional PKC isoform was confirmed by the finding that expression of PKCalpha enhanced the effect of Galpha(16), and a dominant negative PKCalpha partially blocked Galpha(16)-mediated NF-kappaB activation. In addition to formyl peptide receptor, Galpha(16) also enhanced NF-kappaB activation by the C5a and C3a receptors, and by CXC chemokine receptor 2 and CCR8. These results suggest a potential role of Galpha(16) in transcriptional regulation downstream of chemoattractant receptors.

PMID: 11359849 [PubMed - indexed for MEDLINE]
 
Back
Top