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Rabbit Anti-beta-Actin Monoclonal Antibody, Biotin Conjugated, Clone 13E5

RRID:AB_10694076

Antibody ID

AB_10694076

Target Antigen

beta-Actin bovine, chicken/avian, horse, human, mouse, porcine, rat, simian, human, mouse, rat, monkey, pig, bovine, chicken, horse

Proper Citation

(Cell Signaling Technology Cat# 5057, RRID:AB_10694076)

Clonality

monoclonal antibody

Comments

Applications: W. Consolidation on 10/2018: AB_10694076, AB_1903888.

Clone ID

Clone 13E5

Host Organism

rabbit

Vendor

Cell Signaling Technology

Cat Num

5057

Publications that use this research resource

Helicobacter pylori Infection Modulates Host Cell Metabolism through VacA-Dependent Inhibition of mTORC1.

  • Kim IJ
  • Cell Host Microbe
  • 2018 May 9

Literature context:


Abstract:

Helicobacter pylori (Hp) vacuolating cytotoxin (VacA) is a bacterial exotoxin that enters host cells and induces mitochondrial dysfunction. However, the extent to which VacA-dependent mitochondrial perturbations affect overall cellular metabolism is poorly understood. We report that VacA perturbations in mitochondria are linked to alterations in cellular amino acid homeostasis, which results in the inhibition of mammalian target of rapamycin complex 1 (mTORC1) and subsequent autophagy. mTORC1, which regulates cellular metabolism during nutrient stress, is inhibited during Hp infection by a VacA-dependent mechanism. This VacA-dependent inhibition of mTORC1 signaling is linked to the dissociation of mTORC1 from the lysosomal surface and results in activation of cellular autophagy through the Unc 51-like kinase 1 (Ulk1) complex. VacA intoxication results in reduced cellular amino acids, and bolstering amino acid pools prevents VacA-mediated mTORC1 inhibition. Overall, these studies support a model that Hp modulate host cell metabolism through the action of VacA at mitochondria.

Funding information:
  • NIAID NIH HHS - R01 AI045928()
  • NIAID NIH HHS - R21 AI117497()
  • NIAID NIH HHS - U19 AI106772(United States)
  • NIGMS NIH HHS - R01 GM089771()

Glucocorticoid Receptor Signaling Is Not Required for In Vivo Adipogenesis.

  • Bauerle KT
  • Endocrinology
  • 2018 May 1

Literature context:


Abstract:

Regulation of adipogenesis is of major interest given that adipose tissue expansion and dysfunction are central to metabolic syndrome. Glucocorticoids (GCs) are important for adipogenesis in vitro. However, establishing a role for GCs in adipogenesis in vivo has been difficult. GC receptor (GR)‒null mice die at birth, a time at which wild-type (WT) mice do not have fully developed white adipose depots. We conducted several studies aimed at defining the role of GC signaling in adipogenesis in vitro and in vivo. First, we showed that GR-null mouse embryonic fibroblasts (MEFs) have compromised ability to form adipocytes in vitro, a phenotype that can be partially rescued with a peroxisome proliferator-activated receptor γ agonist. Next, we demonstrated that MEFs are capable of forming de novo fat pads in mice despite the absence of GR or circulating GCs [by bilateral adrenalectomy (ADX)]. However, ADX and GR-null fat pads and their associated adipocyte areas were smaller than those in controls. Second, using adipocyte-specific luciferase reporter mice, we identified adipocytes in both WT and GR-null embryonic day (E)18 mouse embryos. Lastly, positive perilipin staining in WT and GR-null E18 embryos confirmed the presence of early white inguinal and brown adipocytes. Taken together, these results provide compelling evidence that GCs and GR augment but are not required for the development of functional adipose tissue in vivo.

Funding information:
  • Intramural NIH HHS - ZIA BC010309-12(United States)
  • NCI NIH HHS - P30 CA091842()
  • NCI NIH HHS - P50 CA094056()
  • NIDCR NIH HHS - K99 DE024178()
  • NIDCR NIH HHS - R00 DE024178()
  • NIDDK NIH HHS - R01 DK106083()
  • NIDDK NIH HHS - T32 DK007120()

Diverse stimuli engage different neutrophil extracellular trap pathways.

  • Kenny EF
  • Elife
  • 2017 Jun 2

Literature context:


Abstract:

Neutrophils release neutrophil extracellular traps (NETs) which ensnare pathogens and have pathogenic functions in diverse diseases. We examined the NETosis pathways induced by five stimuli; PMA, the calcium ionophore A23187, nigericin, Candida albicans and Group B Streptococcus. We studied NET production in neutrophils from healthy donors with inhibitors of molecules crucial to PMA-induced NETs including protein kinase C, calcium, reactive oxygen species, the enzymes myeloperoxidase (MPO) and neutrophil elastase. Additionally, neutrophils from chronic granulomatous disease patients, carrying mutations in the NADPH oxidase complex or a MPO-deficient patient were examined. We show that PMA, C. albicans and GBS use a related pathway for NET induction, whereas ionophores require an alternative pathway but that NETs produced by all stimuli are proteolytically active, kill bacteria and composed mainly of chromosomal DNA. Thus, we demonstrate that NETosis occurs through several signalling mechanisms, suggesting that extrusion of NETs is important in host defence.

Funding information:
  • NIGMS NIH HHS - R35 GM118112()