- 44-668G - Invitrogen Antibodies EIF2AK2 antibody

Submitted references Clinical relevance of proteomic profiling in de novo pediatric acute myeloid leukemia: a Children's Oncology Group study.

Hoff FW, Van Dijk AD, Qiu Y, Hu CW, Ries RE, Ligeralde A, Jenkins GN, Gerbing RB, Gamis AS, Aplenc R, Kolb EA, Alonzo TA, Meshinchi S, Qutub AA, De Bont ESJM, Horton TM, Kornblau SM
Haematologica 2022 Oct 1;107(10):2329-2343

Therapeutic effects of the PKR inhibitor C16 suppressing tumor proliferation and angiogenesis in hepatocellular carcinoma in vitro and in vivo.

Watanabe T, Ninomiya H, Saitou T, Takanezawa S, Yamamoto S, Imai Y, Yoshida O, Kawakami R, Hirooka M, Abe M, Imamura T, Hiasa Y
Scientific reports 2020 Mar 20;10(1):5133

The SINEB1 element in the long non-coding RNA Malat1 is necessary for TDP-43 proteostasis.

Nguyen TM, Kabotyanski EB, Reineke LC, Shao J, Xiong F, Lee JH, Dubrulle J, Johnson H, Stossi F, Tsoi PS, Choi KJ, Ellis AG, Zhao N, Cao J, Adewunmi O, Ferreon JC, Ferreon ACM, Neilson JR, Mancini MA, Chen X, Kim J, Ma L, Li W, Rosen JM
Nucleic acids research 2020 Mar 18;48(5):2621-2642

Stimulated hepatic stellate cell promotes progression of hepatocellular carcinoma due to protein kinase R activation.

Imai Y, Yoshida O, Watanabe T, Yukimoto A, Koizumi Y, Ikeda Y, Tokumoto Y, Hirooka M, Abe M, Hiasa Y
PloS one 2019;14(2):e0212589

Restoring synaptic plasticity and memory in mouse models of Alzheimer's disease by PKR inhibition.

Hwang KD, Bak MS, Kim SJ, Rhee S, Lee YS
Molecular brain 2017 Dec 13;10(1):57

The small molecule '1-(4-biphenylylcarbonyl)-4-(5-bromo-2-methoxybenzyl) piperazine oxalate' and its derivatives regulate global protein synthesis by inactivating eukaryotic translation initiation factor 2-alpha.

Hong MN, Nam KY, Kim KK, Kim SY, Kim I
Cell stress & chaperones 2016 May;21(3):485-97

The infectious bursal disease virus RNA-binding VP3 polypeptide inhibits PKR-mediated apoptosis.

Busnadiego I, Maestre AM, Rodríguez D, Rodríguez JF
PloS one 2012;7(10):e46768

Transcriptional gene silencing of HIV-1 through promoter targeted RNA is highly specific.

Suzuki K, Ishida T, Yamagishi M, Ahlenstiel C, Swaminathan S, Marks K, Murray D, McCartney EM, Beard MR, Alexander M, Purcell DF, Cooper DA, Watanabe T, Kelleher AD
RNA biology 2011 Nov-Dec;8(6):1035-46

Inhibition of double-stranded RNA-dependent protein kinase strongly decreases cytokine production and release in peripheral blood mononuclear cells from patients with Alzheimer's disease.

Couturier J, Page G, Morel M, Gontier C, Claude J, Pontcharraud R, Fauconneau B, Paccalin M
Journal of Alzheimer's disease : JAD 2010;21(4):1217-31

Inhibition of double-stranded RNA-dependent protein kinase strongly decreases cytokine production and release in peripheral blood mononuclear cells from patients with Alzheimer's disease.

Couturier J, Page G, Morel M, Gontier C, Claude J, Pontcharraud R, Fauconneau B, Paccalin M
Journal of Alzheimer's disease : JAD 2010;21(4):1217-31

The double-stranded RNA-activated protein kinase mediates radiation resistance in mouse embryo fibroblasts through nuclear factor kappaB and Akt activation.

von Holzen U, Pataer A, Raju U, Bocangel D, Vorburger SA, Liu Y, Lu X, Roth JA, Aggarwal BB, Barber GN, Keyomarsi K, Hunt KK, Swisher SG
Clinical cancer research : an official journal of the American Association for Cancer Research 2007 Oct 15;13(20):6032-9

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Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Western Blot analysis using rabbit anti-PKR (pT451) polyclonal antibody. (Product # 44-668G)

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Figure 1 PKR inhibitor treatment suppresses HCC cell proliferation in a dose-dependent manner in vitro . Huh7 cells were seeded in a 6-well flat-bottomed plate, cultured at 37 degC for 24 h and treated with the PKR inhibitor at different concentrations: 500, 1000, 2000, and 3000 nM. DMSO was used as a control. Twenty-four hours after treatment with the PKR inhibitor, proteins were extracted and analyzed with Western blotting. The anti-phosphorylated PKR antibody using in this figure was product number 44-668 G (Life Technologies). Expression of phosphorylated PKR is downregulated in a dose-dependent manner. The bands of phosphorylated PKR are indicated by an arrow, and original gel images of Western blotting are shown in Supplemental Fig. S1 ( A ). Bands indicating total PKR and phosphorylated PKR were quantified, and the phosphorylated PKR:total PKR ratio is shown. The values in the figure represent fold change to those without PKR inhibitor treatment (0 nmol/L), and means +- SEM of three independent experiments are shown. *p < 0.05 compared to the group without the PKR inhibitor by Student's t -test ( B ). To investigate the effects on HCC cell proliferation in vitro with the MTS assay, Huh7 cells were seeded in a 96-well flat-bottomed plate with the PKR inhibitor at different concentrations: 500, 1000, 2000, and 3000 nM. Proliferation of Huh7 cells was markedly suppressed by treatment with the PKR inhibitor in a dose-dependent manner. Mean +- SEM of six replicates. *p < 0.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Figure 2 PKR inhibitor suppresses the growth of HCC cells in vivo in the xenograft model. Huh7 tumor cells (3 x 10 6 ) were inoculated subcutaneously into the flank of female BALB/c-nu/nu mice. The mice were injected i.p. with the PKR inhibitor at 300 mug/kg. Each single xenograft tumor at 0, 2, 4, and 24 h after C16 injection was isolated and each protein sample was extracted. The expression of phosphorylated PKR is suppressed over time after PKR inhibitor injection, as seen with Western blotting. The bands of phosphorylated PKR are indicated by an arrow, and original gel images of Western blotting are shown in Supplemental Fig. S5 ( A ). Bands indicating total PKR and phosphorylated PKR were quantified, and the phosphorylated PKR:total PKR ratio is shown (n = 1) ( B ). Huh7 tumor cells (3 x 10 6 ) were inoculated subcutaneously into the flank of female BALB/c-nu/nu mice (n = 6). The groups with and without the PKR inhibitor were injected i.p. every day for 4 weeks with the PKR inhibitor (300 mug/kg) or phosphate-buffered saline as a control. The body weights of the groups with and without PKR inhibitor injection ( C ) and the growth curves of tumor volumes are shown ( D ). The group with PKR inhibitor treatment shows markedly slower tumor growth. Mean +- SEM of six replicates. *p < 0.05 compared to the group without the PKR inhibitor by Student's t -test.

44-668G

Antibody data