PERK Antibody / EIF2AK3 (RQ4206)

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PERK Antibody / EIF2AK3 (RQ4206)

Catalog No.
Formulation
Size

RQ4206
0.5mg/ml if reconstituted with 0.2ml sterile DI water
100 ug

Bulk quote request

Availability Species Reactivity Format

1-3 business days Human, Mouse, Rat Antigen affinity purified

Clonality Isotype

Polyclonal (rabbit origin) Rabbit IgG

Purity

Antigen affinity purified

Buffer

Lyophilized from 1X PBS with 2% Trehalose and 0.025% sodium azide Q9NZJ5

UniProt Applications

Western Blot : 0.5-1ug/ml Flow cytometry : 1-3ug/10^6 cells Direct ELISA : 0.1-0.5ug/ml

Limitations

This PERK antibody is available for research use only.

Western blot testing of human 1) HeLa, 2) COLO320, 3) A549, 4) SK-OV-3, 5) A431, 6) rat brain and 7) mouse brain lysate with PERK antibody at 0.5ug/ml. Predicted molecular weight ~125 kDa, observed here at ~140 kDa. Flow cytometry testing of human HepG2 cells with PERK antibody at 1ug/10^6 cells (blocked with goat sera); Red=cells alone, Green=isotype control, Blue= PERK antibody.

Description

Eukaryotic translation initiation factor 2-alpha kinase 3, also known as protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK), is an enzyme that in humans is encoded by the EIF2AK3 gene. The protein encoded by this gene phosphorylates the alpha subunit of eukaryotic translation-initiation factor 2, leading to its inactivation, and thus to a rapid reduction of translational initiation and repression of global protein synthesis. This protein is thought to modulate mitochondrial function. It is a type I membrane protein located in the endoplasmic reticulum (ER), where it is induced by ER stress caused by malfolded proteins. Mutations in this gene are associated with Wolcott-Rallison syndrome.

Application Notes

Optimal dilution of the PERK antibody should be determined by the researcher.

Immunogen

A recombinant human protein corresponding to amino acids R222-Q334 was used as the immunogen for the PERK antibody.

Storage

After reconstitution, the PERK antibody can be stored for up to one month at 4oC. For long-term, aliquot and store at -20oC. Avoid repeated freezing and thawing.

Ordering: Phone:858.663.9055 | Fax:1.267.821.0800 | Email:[email protected]

Recommended publications

De Novo EIF2AK1 and EIF2AK2 Variants Are Associated with Developmental Delay, Leukoencephalopathy, and Neurologic Decompensation

bioRxiv preprint doi: https://doi.org/10.1101/757039; this version posted September 16, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. De novo EIF2AK1 and EIF2AK2 variants are associated with developmental delay, leukoencephalopathy, and neurologic decompensation Dongxue Mao1,2, Chloe M. Reuter3,4, Maura R.Z. Ruzhnikov5,6, Anita E. Beck7, Emily G. Farrow8,9,10, Lisa T. Emrick1,11,12,13, Jill A. Rosenfeld12, Katherine M. Mackenzie5, Laurie Robak2,12,13, Matthew T. Wheeler3,14, Lindsay C. Burrage12,13, Mahim Jain15, Pengfei Liu12, Daniel Calame11,13, Sebastien Küry17,18, Martin Sillesen19, Klaus Schmitz-Abe20, Davide Tonduti21, Luigina Spaccini22, Maria Iascone23, Casie A. Genetti20, Madeline Graf16, Alyssa Tran12, Mercedes Alejandro12, Undiagnosed Diseases Network, Brendan H. Lee12,13, Isabelle Thiffault8,9,24, Pankaj B. Agrawal#,20, Jonathan A. Bernstein#,3,25, Hugo J. Bellen#,2,12,26,27,28, Hsiao- Tuan Chao#,1,2,11,12,13,28,27,29 #Correspondence should be addressed: [email protected] (P.A.), [email protected] (J.A.B.), [email protected] (H.J.B.), [email protected] (H.T.C.) 1Department of Pediatrics, Baylor College of Medicine (BCM), Houston, TX 2Jan and Dan Duncan Neurological Research Institute, Texas Children’s Hospital, Houston, TX 3Stanford Center for Undiagnosed Diseases, Stanford University, Stanford, CA 4Stanford Center for Inherited Cardiovascular Disease, Division of Cardiovascular Medicine,
Table S1. Complete Gene List. Genbank Refseq and Description of Each Gene Were Provided By

Document downloaded from http://www.elsevier.es, day 24/09/2021. This copy is for personal use. Any transmission of this document by any media or format is strictly prohibited. Table S1. Complete gene list. GenBank RefSeq and description of each gene were provided by the array supplier. Unigene GeneBank Symbol Description Gene Name/s Rn.11422 NM_033230 Akt1 V-akt murine thymoma viral oncogene homolog 1 Akt Rn.2104 NM_019288 App Amyloid beta (A4) precursor protein - Rn.23323 NM_001034933 Arsa Arylsulfatase A MGC125207 Rn.94004 NM_033443 Arsb Arylsulfatase B - Rn.6224 NM_001038495 Atg12 ATG12 autophagy related 12 Apg12l, MGC125080 Rn.101734NM_001108809 Atg16l1 ATG16 autophagy related 16-like 1 Apg16l, Wdr30 Rn.104199NM_001191560 Atg16l2 ATG16 autophagy related 16-like 2 RGD1311400 Rn.3084 NM_134394 Atg3 ATG3 autophagy related 3 Apg3l, PIG-1, Pig1 Rn.163086NM_001025711 Atg4b ATG4 autophagy related 4 homolog B Apg4b, MGC112887 Rn.23378 NM_001107948 Atg4c ATG4 autophagy related 4 homolog C - Rn.98385 NM_001014250 Atg5 ATG5 autophagy related 5 - Rn.162765NM_001012097 Atg7 ATG7 autophagy related 7 Apg7l Rn.35248 NM_001014218 Atg9a ATG9 autophagy related 9 homolog A MGC105908, RGD1310450 Rn.36696 NM_022698 Bad BCL2-associated agonist of cell death MGC72439 Rn.14598 NM_053812 Bak1 BCL2-antagonist/killer 1 MGC108627 Rn.10668 NM_017059 Bax Bcl2-associated X protein - Rn.9996 NM_016993 Bcl2 B-cell CLL/lymphoma 2 Bcl-2 Rn.10323 NM_031535 Bcl2l1 Bcl2-like 1 Bcl-xl, Bcl2l, Bclx, bcl-X Rn.2776 NM_053739 Becn1 Beclin 1, autophagy related - Rn.31142 NM_022684
LIM and Cysteine-Rich Domains 1 (LMCD1) Regulates Skeletal Muscle Hypertrophy, Calcium Handling, and Force Duarte M

Ferreira et al. Skeletal Muscle (2019) 9:26 https://doi.org/10.1186/s13395-019-0214-1 RESEARCH Open Access LIM and cysteine-rich domains 1 (LMCD1) regulates skeletal muscle hypertrophy, calcium handling, and force Duarte M. S. Ferreira1, Arthur J. Cheng2,3, Leandro Z. Agudelo1,4, Igor Cervenka1, Thomas Chaillou2,5, Jorge C. Correia1, Margareta Porsmyr-Palmertz1, Manizheh Izadi1,6, Alicia Hansson1, Vicente Martínez-Redondo1, Paula Valente-Silva1, Amanda T. Pettersson-Klein1, Jennifer L. Estall7, Matthew M. Robinson8, K. Sreekumaran Nair8, Johanna T. Lanner2 and Jorge L. Ruas1* Abstract Background: Skeletal muscle mass and strength are crucial determinants of health. Muscle mass loss is associated with weakness, fatigue, and insulin resistance. In fact, it is predicted that controlling muscle atrophy can reduce morbidity and mortality associated with diseases such as cancer cachexia and sarcopenia. Methods: We analyzed gene expression data from muscle of mice or human patients with diverse muscle pathologies and identified LMCD1 as a gene strongly associated with skeletal muscle function. We transiently expressed or silenced LMCD1 in mouse gastrocnemius muscle or in mouse primary muscle cells and determined muscle/cell size, targeted gene expression, kinase activity with kinase arrays, protein immunoblotting, and protein synthesis levels. To evaluate force, calcium handling, and fatigue, we transduced the flexor digitorum brevis muscle with a LMCD1-expressing adenovirus and measured specific force and sarcoplasmic reticulum Ca2+ release in individual fibers. Finally, to explore the relationship between LMCD1 and calcineurin, we ectopically expressed Lmcd1 in the gastrocnemius muscle and treated those mice with cyclosporine A (calcineurin inhibitor). In addition, we used a luciferase reporter construct containing the myoregulin gene promoter to confirm the role of a LMCD1- calcineurin-myoregulin axis in skeletal muscle mass control and calcium handling.
Biomarkers, Master Regulators and Genomic Fabric Remodeling in a Case of Papillary Thyroid Carcinoma

G C A T T A C G G C A T genes Article Biomarkers, Master Regulators and Genomic Fabric Remodeling in a Case of Papillary Thyroid Carcinoma Dumitru A. Iacobas Personalized Genomics Laboratory, CRI Center for Computational Systems Biology, Roy G Perry College of Engineering, Prairie View A&M University, Prairie View, TX 77446, USA; [email protected]; Tel.: +1-936-261-9926 Received: 1 August 2020; Accepted: 1 September 2020; Published: 2 September 2020 Abstract: Publicly available (own) transcriptomic data have been analyzed to quantify the alteration in functional pathways in thyroid cancer, establish the gene hierarchy, identify potential gene targets and predict the effects of their manipulation. The expression data have been generated by profiling one case of papillary thyroid carcinoma (PTC) and genetically manipulated BCPAP (papillary) and 8505C (anaplastic) human thyroid cancer cell lines. The study used the genomic fabric paradigm that considers the transcriptome as a multi-dimensional mathematical object based on the three independent characteristics that can be derived for each gene from the expression data. We found remarkable remodeling of the thyroid hormone synthesis, cell cycle, oxidative phosphorylation and apoptosis pathways. Serine peptidase inhibitor, Kunitz type, 2 (SPINT2) was identified as the Gene Master Regulator of the investigated PTC. The substantial increase in the expression synergism of SPINT2 with apoptosis genes in the cancer nodule with respect to the surrounding normal tissue (NOR) suggests that SPINT2 experimental overexpression may force the PTC cells into apoptosis with a negligible effect on the NOR cells. The predictive value of the expression coordination for the expression regulation was validated with data from 8505C and BCPAP cell lines before and after lentiviral transfection with DDX19B.
S41598-018-20541-8.Pdf

www.nature.com/scientificreports OPEN Ormeloxifene-induced unfolded protein response contributes to autophagy-associated apoptosis Received: 28 September 2016 Accepted: 19 January 2018 via disruption of Akt/mTOR and Published: xx xx xxxx activation of JNK Arindam Bhattacharjee1, Mohammad Hasanain2, Manoj Kathuria1, Akhilesh Singh2, Dipak Datta2,3, Jayanta Sarkar2,3 & Kalyan Mitra1,3 Autophagy, a regulated nutrient recycling program can afect both cell survival and cell death. Here, we show that Ormeloxifene (ORM), a selective estrogen receptor modulator approved for oral contraceptive use induces autophagic fux in ovarian cancer cells, which is activated by an ER stress response upstream of autophagy. The ER stress response is characterized by activation of IRE1α, PERK and ATF6 and is under regulation of JNK. Pharmacological inhibition of either autophagy or ER stress increased cell survival, as did silencing of autophagy proteins LC3 and Beclin 1, implying that ORM-induced autophagy is pro-death in nature. Ultrastructural observations of treated cells confrmed stages of autophagic maturation. Caspase-dependent apoptosis succeeded these events and was characterized by generation of reactive oxygen species and disruption of mitochondrial membrane potential. A concomitant inhibition of the Akt/mTOR axis was also observed with possible regulation of Akt by ORM. ORM inhibited tumor growth in ovarian xenograft model and displayed autophagic activity. In summary, in vitro and in vivo results reveal that ORM induces autophagy-associated cell death to attenuate proliferation of ovarian cancer cells. Our results demonstrate that using ORM in combination with ER stress and autophagy modulators could ofer better therapeutic outcome in ovarian cancer. Ovarian cancer is one of the leading gynecological malignancies among women in terms of mortality1.
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Table S1. Gene List Genes Chr Genes Chr Genes Chr Genes Chr SEPT9

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Tyrosine Phosphorylation: from Discovery to the Kinome and Beyond

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Page 1 Exploring the Understudied Human Kinome For

bioRxiv preprint doi: https://doi.org/10.1101/2020.04.02.022277; this version posted June 30, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. Exploring the understudied human kinome for research and therapeutic opportunities Nienke Moret1,2,*, Changchang Liu1,2,*, Benjamin M. Gyori2, John A. Bachman,2, Albert Steppi2, Rahil Taujale3, Liang-Chin Huang3, Clemens Hug2, Matt Berginski1,4,5, Shawn Gomez1,4,5, Natarajan Kannan,1,3 and Peter K. Sorger1,2,† *These authors contributed equally † Corresponding author 1The NIH Understudied Kinome Consortium 2Laboratory of Systems Pharmacology, Department of Systems Biology, Harvard Program in Therapeutic Science, Harvard Medical School, Boston, Massachusetts 02115, USA 3 Institute of Bioinformatics, University of Georgia, Athens, GA, 30602 USA 4 Department of Pharmacology, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA 5 Joint Department of Biomedical Engineering at the University of North Carolina at Chapel Hill and North Carolina State University, Chapel Hill, NC 27599, USA Key Words: kinase, human kinome, kinase inhibitors, drug discovery, cancer, cheminformatics, † Peter Sorger Warren Alpert 432 200 Longwood Avenue Harvard Medical School, Boston MA 02115 [email protected] cc: [email protected] 617-432-6901 ORCID Numbers Peter K. Sorger 0000-0002-3364-1838 Nienke Moret 0000-0001-6038-6863 Changchang Liu 0000-0003-4594-4577 Ben Gyori 0000-0001-9439-5346 John Bachman 0000-0001-6095-2466 Albert Steppi 0000-0001-5871-6245 Page 1 bioRxiv preprint doi: https://doi.org/10.1101/2020.04.02.022277; this version posted June 30, 2020.
Characterization of a Novel PERK Kinase Inhibitor with Antitumor and Anti-Angiogenic Activity

Published OnlineFirst January 18, 2013; DOI: 10.1158/0008-5472.CAN-12-3109 Cancer Tumor and Stem Cell Biology Research Characterization of a Novel PERK Kinase Inhibitor with Antitumor and Anti-Angiogenic Activity Charity Atkins1, Qi Liu1, Elisabeth Minthorn1, Shu-Yun Zhang1, David J. Figueroa1, Katherine Moss1, Thomas B. Stanley3, Brent Sanders1, Aaron Goetz2, Nathan Gaul2, Anthony E. Choudhry2, Hasan Alsaid4, Beat M. Jucker4, Jeffrey M. Axten1, and Rakesh Kumar1 Abstract The unfolded protein response (UPR) is a signal transduction pathway that coordinates cellular adaptation to microenvironmental stresses that include hypoxia, nutrient deprivation, and change in redox status. These stress stimuli are common in many tumors and thus targeting components of the UPR signaling is an attractive therapeutic approach. We have identiﬁed a ﬁrst-in-class, small molecule inhibitor of the eukaryotic initiation factor 2-alpha kinase 3 (EIF2AK3) or PERK, one of the three mediators of UPR signaling. GSK2656157 is an ATP-competitive inhibitor of PERK enzyme activity with an IC50 of 0.9 nmol/L. It is highly selective for PERK with IC50 values >100 nmol/L against a panel of 300 kinases. GSK2656157 inhibits PERK activity in cells – with an IC50 in the range of 10 30 nmol/L as shown by inhibition of stress-induced PERK autophosphorylation, eIF2a substrate phosphorylation, together with corresponding decreases in ATF4 and CAAT/enhancer binding protein homologous protein (CHOP) in multiple cell lines. Oral administration of GSK2656157 to mice shows a dose- and time-dependent pharmacodynamic response in pancreas as measured by PERK autophosphoryla- tion. Twice daily dosing of GSK2656157 results in dose-dependent inhibition of multiple human tumor xenografts growth in mice.
Discovery and Characterization of Novel Inhibitors of Protein Kinase R

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Gene Expression Profiling of NB4 Cells Following Knockdown of Nucleostemin Using DNA Microarrays

MOLECULAR MEDICINE REPORTS 14: 175-183, 2016 Gene expression profiling of NB4 cells following knockdown of nucleostemin using DNA microarrays XIAOLI SUN1-5, YU JIA1,3-5, YUANYU WEI1,3-5, SHUAI LIU1,3-5 and BAOHONG YUE1,3-5 1Department of Laboratory, The First Affiliated Hospital of Zhengzhou University;2 Department of Laboratory, The First Affiliated Hospital of Henan University of TCM; 3Faculty of Laboratory Medicine, Zhengzhou University; 4The Key-Disciplines Laboratory Clinical Medicine in Henan Province; 5Key Lab of Clinical Laboratory Medicine of Henan Province, Zhengzhou, Henan 450052, P.R. China Received December 23, 2014; Accepted December 18, 2015 DOI: 10.3892/mmr.2016.5213 Abstract. Nucleostemin (NS) is mainly expressed in stem undifferentiated properties of self-renewal certain types of and tumor cells, and is necessary for the maintenance of stem cell (1,2) as well as germ cell tumors (3). Furthermore, their self-renewal and proliferation. Originally, NS was NS is abundantly expressed in numerous tumor types, thought to exert its effects through inhibiting p53, while including prostate cancer (4), esophageal cancer (5), breast recent studies have revealed that NS is also able to function carcinoma (6) and gastric adenocarcinoma (7). Elevated NS independently of p53. The present study performed a gene expression is associated with poor prognosis of patients with expression profiling analysis of p53-mutant NB4 leukeima various types of cancer (8,9). Furthermore, knockdown of NS cells following knockdown of NS in order to elucidate the was shown to inhibit cell proliferation as well as induce cell p53-independent NS pathway. NS expression was silenced cycle arrest and apoptosis (6,10-13).