X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

Phospho-AKT1 (Ser473) Monoclonal Antibody (SDRNR), APC, eBioscience(TM)

RRID:AB_2573309

Antibody ID

AB_2573309

Target Antigen

Phospho-AKT1 (Ser473) human

Proper Citation

(Thermo Fisher Scientific Cat# 17-9715-41, RRID:AB_2573309)

Clonality

monoclonal antibody

Comments

Applications: Flow (5 µL (0.5 µg)/test)

Clone ID

Clone SDRNR

Host Organism

mouse

Vendor

Thermo Fisher Scientific Go To Vendor

Cat Num

17-9715-41 also 17-9715

Publications that use this research resource

CRIg, a tissue-resident macrophage specific immune checkpoint molecule, promotes immunological tolerance in NOD mice, via a dual role in effector and regulatory T cells.

  • Yuan X
  • Elife
  • 2017 Nov 24

Literature context:


Abstract:

How tissue-resident macrophages (TRM) impact adaptive immune responses remains poorly understood. We report novel mechanisms by which TRMs regulate T cell activities at tissue sites. These mechanisms are mediated by the complement receptor of immunoglobulin family (CRIg). Using animal models for autoimmune type 1 diabetes (T1D), we found that CRIg+ TRMs formed a protective barrier surrounding pancreatic islets. Genetic ablation of CRIg exacerbated islet inflammation and local T cell activation. CRIg exhibited a dual function of attenuating early T cell activation and promoting the differentiation of Foxp3+ regulatory (Treg) cells. More importantly, CRIg stabilized the expression of Foxp3 in Treg cells, by enhancing their responsiveness to interleukin-2. The expression of CRIg in TRMs was postnatally regulated by gut microbial signals and metabolites. Thus, environmental cues instruct TRMs to express CRIg, which functions as an immune checkpoint molecule to regulate adaptive immunity and promote immune tolerance.

Funding information:
  • NIGMS NIH HHS - T32 GM07270(United States)

Regulatory T Cell Migration Is Dependent on Glucokinase-Mediated Glycolysis.

  • Kishore M
  • Immunity
  • 2017 Nov 21

Literature context:


Abstract:

Migration of activated regulatory T (Treg) cells to inflamed tissue is crucial for their immune-modulatory function. While metabolic reprogramming during Treg cell differentiation has been extensively studied, the bioenergetics of Treg cell trafficking remains undefined. We have investigated the metabolic demands of migrating Treg cells in vitro and in vivo. We show that glycolysis was instrumental for their migration and was initiated by pro-migratory stimuli via a PI3K-mTORC2-mediated pathway culminating in induction of the enzyme glucokinase (GCK). Subsequently, GCK promoted cytoskeletal rearrangements by associating with actin. Treg cells lacking this pathway were functionally suppressive but failed to migrate to skin allografts and inhibit rejection. Similarly, human carriers of a loss-of-function GCK regulatory protein gene-leading to increased GCK activity-had reduced numbers of circulating Treg cells. These cells displayed enhanced migratory activity but similar suppressive function, while conventional T cells were unaffected. Thus, GCK-dependent glycolysis regulates Treg cell migration.