PKA RI-alpha (D54D9) Rabbit mAb 5675T from Cell Signaling Technology

Published Figures

Register or Sign In to View Figures.

eLife
January 24 2023

Fig 1: Recurrent PKA activating somatic alterations in human cancer.(A) Pathway illustrations of different PKA activating genomic alterations in order from top: PRKACA amplification, DNAJB1-PRKACA fusion, PRKACA activating mutation, and PRKAR1A inactivation or deletion. (B) TCGA PanCancer Project analysis showing the frequency of PRKACA gain-of-function (red and yellow) and PRKAR1A loss-of-function (green and blue) alterations in various cancer types. The reported frequency of DNAJB1-PRKACA fusion in fibrolamellar carcinoma (FLC) clinical samples is also included. (C) Cell lines used in this study, their PKA-related mutation, PRKACA dependency, and inclusion in proteomic analyses. (D) Immunoblots showing the change of PKA activity, as indicated by phospho-PKA substrate, in different cell lines with dox-inducible 3xFLAG-PRKACA or PRKAR1AG325D with 1 µg/ml doxycycline (dox) for 48 hr. Left: engineered cell lines with inducible 3xFLAG-PRKACA. Right: engineered cell lines with inducible 3xFLAG- PRKAR1AG325D. Figure 1—source data 1.Images for Figure 1A. Figure 1—source data 2.Table for Figure 1B. Figure 1—source data 3.Images for Figure 1D part 1/3. Figure 1—source data 4.Images for Figure 1D part 2/3. Figure 1—source data 5.Images for Figure 1D part 3/3.
Register or Sign In to View Figures.

eLife
January 24 2023

Fig 2: PKA activity correlates with c-MYC and n-MYC protein levels.(A) Immunoblots showing the change of PKA activity, as indicated by phospho-PKA substrate, and c-MYC and n-MYC expression in Colo741 and FLX1 cells after treatment with 50 μM forskolin (FSK) and 3-isobutyl-1-methylxanthine (IBMX) for 30 min, 2 hr, or 4 hr. n-MYC was not detected in Colo741 so is not shown. (B) Impact of 0–4 hr treatment with FSK/IBMX on MYC mRNA levels in Colo741 and FLX1; ± SD. Technical replicates from a representative experiment shown. (C) Immunoblots showing the change of PKA activity and c-MYC and n-MYC levels in engineered FLX1 cells with doxycycline (dox)-inducible 3xFLAG- PRKAR1AG325D with or without dox for 72 hr. (D) Immunoblots showing the basal level of PKA activity with phosphorylated PKA substrate and c-MYC expression in AML12 wild type (WT; left) and AML12DNAJ-PKAc cells (right). (E) Effect of 4 hr treatment with PKA-inhibiting tool compound H89 over a dose range from 1.25 to 20 μM on PKA substrate phosphorylation and c-MYC level. (F) Immunoblot showing the presence of DNAJ-PKAc and different level of c-MYC and n-MYC in fibrolamellar carcinoma (FLC) tumor samples (FLC) vs adjacent liver (N) from four FLC patients. (G) Summary gene set enrichment analysis (GSEA) of PRKACA amplified/mutant and PRKAR1A inactivated adrenocortical carcinoma or ovarian serous carcinoma vs. WT from TCGA. All significant ‘Hallmark’ gene sets are shown. Figure 3—source data 1.Images for Figure 3A. Figure 3—source data 2.Tables for Figure 3B. Figure 3—source data 3.Images for Figure 3C. Figure 3—source data 4.Images for Figure 3D. Figure 3—source data 5.Images for Figure 3E. Figure 3—source data 6.Images for Figure 3F. Figure 3—source data 7.Tables for Figure 3G.
Register or Sign In to View Figures.

Elife
January 24 2023

Fig 3: Recurrent PKA activating somatic alterations in human cancer.(A) Pathway illustrations of different PKA activating genomic alterations in order from top: PRKACA amplification, DNAJB1-PRKACA fusion, PRKACA activating mutation, and PRKAR1A inactivation or deletion. (B) TCGA PanCancer Project analysis showing the frequency of PRKACA gain-of-function (red and yellow) and PRKAR1A loss-of-function (green and blue) alterations in various cancer types. The reported frequency of DNAJB1-PRKACA fusion in fibrolamellar carcinoma (FLC) clinical samples is also included. (C) Cell lines used in this study, their PKA-related mutation, PRKACA dependency, and inclusion in proteomic analyses. (D) Immunoblots showing the change of PKA activity, as indicated by phospho-PKA substrate, in different cell lines with dox-inducible 3xFLAG-PRKACA or PRKAR1AG325D with 1 µg/ml doxycycline (dox) for 48 hr. Left: engineered cell lines with inducible 3xFLAG-PRKACA. Right: engineered cell lines with inducible 3xFLAG- PRKAR1AG325D. Figure 1—source data 1.Images for Figure 1A. Figure 1—source data 2.Table for Figure 1B. Figure 1—source data 3.Images for Figure 1D part 1/3. Figure 1—source data 4.Images for Figure 1D part 2/3. Figure 1—source data 5.Images for Figure 1D part 3/3.
Register or Sign In to View Figures.

Elife
January 24 2023

Fig 4: PKA activity correlates with c-MYC and n-MYC protein levels.(A) Immunoblots showing the change of PKA activity, as indicated by phospho-PKA substrate, and c-MYC and n-MYC expression in Colo741 and FLX1 cells after treatment with 50 μM forskolin (FSK) and 3-isobutyl-1-methylxanthine (IBMX) for 30 min, 2 hr, or 4 hr. n-MYC was not detected in Colo741 so is not shown. (B) Impact of 0–4 hr treatment with FSK/IBMX on MYC mRNA levels in Colo741 and FLX1; ± SD. Technical replicates from a representative experiment shown. (C) Immunoblots showing the change of PKA activity and c-MYC and n-MYC levels in engineered FLX1 cells with doxycycline (dox)-inducible 3xFLAG- PRKAR1AG325D with or without dox for 72 hr. (D) Immunoblots showing the basal level of PKA activity with phosphorylated PKA substrate and c-MYC expression in AML12 wild type (WT; left) and AML12DNAJ-PKAc cells (right). (E) Effect of 4 hr treatment with PKA-inhibiting tool compound H89 over a dose range from 1.25 to 20 μM on PKA substrate phosphorylation and c-MYC level. (F) Immunoblot showing the presence of DNAJ-PKAc and different level of c-MYC and n-MYC in fibrolamellar carcinoma (FLC) tumor samples (FLC) vs adjacent liver (N) from four FLC patients. (G) Summary gene set enrichment analysis (GSEA) of PRKACA amplified/mutant and PRKAR1A inactivated adrenocortical carcinoma or ovarian serous carcinoma vs. WT from TCGA. All significant ‘Hallmark’ gene sets are shown. Figure 3—source data 1.Images for Figure 3A. Figure 3—source data 2.Tables for Figure 3B. Figure 3—source data 3.Images for Figure 3C. Figure 3—source data 4.Images for Figure 3D. Figure 3—source data 5.Images for Figure 3E. Figure 3—source data 6.Images for Figure 3F. Figure 3—source data 7.Tables for Figure 3G.

Be the first to write a review!

Citations:

(16)

Figures:

$153.00 Inquire

from
Cell Signaling Technology for
PKA RI-alpha (D54D9) Rabbit mAb

Cell Signaling Technology's PKA RI-alpha (D54D9) Rabbit mAb is a Rabbit monoclonal antibody. The PKA RI-alpha (D54D9) Rabbit mAb Antibody was generated using PRKAR1A as the antigen. It reacts with Homo Sapiens, Human, Mouse, Rat, Hamster, and Non-Human Primate. This antibody has been shown to work in applications such as: Precipitation, Immunoprecipitation, and Western Blot.

Product Specs
ItemPKA RI-alpha (D54D9) Rabbit mAb
CompanyCell Signaling Technology
Price $153.00 Inquire
Catalog Number5675T
ApplicationsWB, IP
ReactivityHu, Ms, Rt, Hm, Mk
NCBI Gene AliasesACRDYS1, ADOHR, CAR, CNC, CNC1, PKR1, PPNAD1, PRKAR1, TSE1
NCBI Full Gene Nameprotein kinase cAMP-dependent type I regulatory subunit alpha
TargetPRKAR1A
Quantity20 µl
HostRabbit
ClonalityMonoclonal

Add to Compare List

Cell Signaling Technology

3 Trask Lane

Danvers, Massachusetts 01923

United States

Phone: 877-616-CELL
Phone: 978-867-2388
Fax: 866-432-6112
Fax: 978-867-2488

Company Profile

Website: http://www.cellsignal.com/

Website: Technical Support

(1) Bipolar and schizophrenia risk gene AKAP11 encodes an autophagy receptor coupling the regulation of PKA kinase network homeostasis to synaptic transmissionNature CommunicationsNovember 28, 2025You-Kyung Lee, Cong Xiao, Xiaoting Zhou, Le Wang, Meghan McReynolds, Zhiping Wu, Xian Han, Eric Purisic, Henry Kim, Xianting Li, et al.temperature. Primary antibodies, Rabbit anti-AKAP11 (LS-Bio, LS-C374339), Rabbit anti-RIα (Cell signaling, 5675S), Sheep anti-RIβ (R&D, AF4177), Mouse anti-SPHKAP60, Guinea pig anti-Synaptophysin (Synaptic Systems,

(2) Discovery of a Cushing's syndrome protein kinase A mutant that biases signaling through type I AKAPsScience advancesFebruary 23, 2024Omar MH, Byrne DP, Shrestha S, Lakey TM, Lee KS, Lauer SM, Collins KB, Daly LA, Eyers CE, Baird GS, et al.(IF and WB); PKAc, Cell Signaling Technology, 5842 (IP and WB); PKA RIα, Cell Signaling Technology, 5675 (WB); PKA RIIα, BD Biosciences, 612243 (WB); PKA RIIβ, BD Biosciences, 610626; V5-HRP, Invitrogen, 46-0708

(3) Simple visualization of submicroscopic protein clusters with a phase-separation-based fluorescent reporterCell SystemsFebruary 21, 2024Thomas R. Mumford, Diarmid Rae, Emily Brackhahn, Abbas Idris, David Gonzalez-Martinez, Ayush Aditya Pal, Michael C. Chung, Juan Guan, Elizabeth Rhoades, Lukasz J. Bugajfor 1 hour and incubated overnight with gentle shaking at 4°C with primary antibody against R1α (CST #5675). Primary antibody was used at a dilution of 1:1000 in TBS-T with 5% BSA. After washing with TBS-T,

(4) Inhibition of phosphodiesterase 4D suppresses mTORC1 signaling and pancreatic cancer growthJCI insightJuly 10, 2023Jeong MH, Urquhart G, Lewis C, Chi Z, Jewell JL.(catalog 9197), mTOR (catalog 2972), mLST8 (catalog 3274), PKA Catα (catalog 4782), PKA RIα (catalog 5675), pPKA substrate (RRXS/T; catalog 9621) (all Cell Signaling Technology); Raptor (Cell Signaling Technology,

(5) Oncogenic PKA signaling increases c-MYC protein expression through multiple targetable mechanismsElifeJanuary 24, 2023Gary KL Chan, Samantha Maisel, Yeonjoo C Hwang, Bryan C Pascual, Rebecca RB Wolber, Phuong Vu, Krushna C Patra, Mehdi Bouhaddou, Heidi L Kenerson, Huat C Lim, et al.(CST#12456), MAPK1/3 pThr202/Thr204 (CST#4370), MAPK1/3 (CST#4695), PKAC-α (CST#4782), PKAR1a (CST#5675), FLAG (Sigma#F1804), Actin (CST#3700), Vinculin (CST#13901), or COXIV (CST#5247). Afterward, blotted

(6) Oncogenic PKA signaling increases c-MYC protein expression through multiple targetable mechanismseLifeJanuary 24, 2023Gary K L Chan, Samantha Maisel, Yeonjoo C Hwang, Bryan C Pascual, Rebecca R B Wolber, Phuong Vu, Krushna C Patra, Mehdi Bouhaddou, Heidi L Kenerson, Huat C Lim, et al.(CST#12456), MAPK1/3 pThr202/Thr204 (CST#4370), MAPK1/3 (CST#4695), PKAC-α (CST#4782), PKAR1a (CST#5675), FLAG (Sigma#F1804), Actin (CST#3700), Vinculin (CST#13901), or COXIV (CST#5247). Afterward, blotted

(7) t-Darpp stimulates protein kinase A activity by forming a complex with its RI regulatory subunitCellular signallingDecember 1, 2017Theile D, Geng S, Denny EC, Momand J, Kane SE.t-Darpp, Cell Signaling #2306), phospho-Darpp Thr75 (Cell Signaling #2301), PKA-RIα (Cell Signaling #5675), PKA-RIβ (ThermoFisher Scientific #PA5-13798), PKA-RIIα (BD Biosciences #612242), PKA-RIIβ (BD Biosciences

(8) Factors Influencing Business Intelligence Data Collection StrategiesThe Indonesian Journal of Accounting ResearchMay 23, 2017Hanif Faidz Rahadian, Dekar Urumsah2 Item INS 3 Item INS 4 Loading 0,7640 0,9132 0,9039 0,8863 0,6435 0,7581 0,7616 0,7818 0,8445 0,9431 0,5675 0,8888 Item CST 1 Item CST 2 Item CST 3 Item CST 4 Item OTR 1 Item OTR 2 Item OTR 3 Item OTR 4 0,6301 0,9249 0,8817 0,9825 0,8083 0,9024 0,9089 0,8711 Item

(9) The GCN5-CITED2-PKA signalling module controls hepatic glucose metabolism through a cAMP-induced substrate switchNature communicationsNovember 22, 2016Sakai M, Tujimura-Hayakawa T, Yagi T, Yano H, Mitsushima M, Unoki-Kubota H, Kaburagi Y, Inoue H, Kido Y, Kasuga M, et al.1:1,000), to Ser157-phosphorylated VASP (#3111, 1:1,000), to PKACα (#5842, 1:1,000) and to PKARIα (#5675, 1:1,000) were obtained from Cell Signaling. Antibodies to GCN5 (sc-20698, 1:500; sc-365321, 1:500),

(10) Enhanced cAMP-stimulated protein kinase A activity in human fibrolamellar hepatocellular carcinomaPediatric researchJuly 1, 2016Riggle KM, Riehle KJ, Kenerson HL, Turnham R, Homma MK, Kazami M, Samelson B, Bauer R, McKnight GS, Scott JD, et al.Jose, CA), p-p44/42 MAPK (Erk1/2) (Thr202/Tyr204), total p44/42 MAPK (Erk1/2), and PKA RIα (9101, 9102, 5675, Cell Signaling, Danvers, MA), and β-Actin (A5441, Sigma, St. Louis, MO). Densitometry analysis was

(11) Hepatocyte Insulin Signaling is Required for Feeding-Induced Lipogenesis but Dispensable for the Suppression of Glucose ProductionCell MetabolismJune 14, 2016Paul M. Titchenell et al.p4EBP1 (#2855), 4EBP1 (#9452), Tsc1 (#6935), pPKA substrates (#9624), pS133 Creb (#9198), RI alpha (#5675) were from Cell Signaling Technology. Igfbp1 (sc-6000) and Tsc2 (sc-893) were from Santa Cruz. pPRAS40

(12) Chronic hyperglycemia downregulates GLP-1 receptor signaling in pancreatic β-cells via protein kinase AMolecular metabolismApril 1, 2015Rajan S, Dickson LM, Mathew E, Orr CM, Ellenbroek JH, Philipson LH, Wicksteed B.(Cell Signaling Technologies, cat # 4820, diluted 1:1000); anti-PKA-RIα (Cell Signaling Technologies, cat # 5675, diluted 1:1000); anti-PKA RIIα (BD Transduction Laboratories, cat # 612242, diluted 1:1000); anti-PKA-RIIβ

(13) Selective Expression of a Dominant-Negative Type Ια PKA Regulatory Subunit in Striatal Medium Spiny Neurons Impairs Gene Expression and Leads to Reduced Feeding and Locomotor ActivityThe Journal of NeuroscienceApril 2, 2014Linghai Yang, Merle L. Gilbert, Ruimao Zheng, G. Stanley McKnightantibodies: anti-RII␤ (BD Transduction Laboratory; #610626), anti-RI␣ (Cell Signaling Technology; #5675), anti-c-fos (Santa Cruz Biotechnology; sc-7202), and antiphospho-CREB (S133; Cell Signaling Technology;

(14) Pain modulators regulate the dynamics of PKA-RII phosphorylation in subgroups of sensory neuronsJournal of cell scienceJanuary 1, 2014Isensee J, Diskar M, Waldherr S, Buschow R, Hasenauer J, Prinz A, Allgöwer F, Herberg FW, Hucho T.Cell Science (2014) 127, 216–229 doi:10.1242/jcs.136580 RESEARCH ARTICLE (Cell Signaling, no. 5675; WB 1:5000, IC 1:1000), rabbit polyclonal antiRIb (Abm, no. Y051648; WB 1:2500, IC 1:500), mouse monoclonal

(15) Acamprosate suppresses ethanol-induced place preference in mice with ethanol physical dependenceJournal of pharmacological sciencesJanuary 1, 2013Kurokawa K, Mizuno K, Shibasaki M, Higashioka M, Oka M, Hirouchi M, Ohkuma S.phosphor-CREB (Ser133) (rabbit polyclonal anti-p-CREB, #4276), and PKARI-a (rabbit polyclonal anti-PKA, #5675) were purchased from Cell Signaling Techonology, Inc. (Boston, MA, USA). Mouse anti-b-actin (sc-47778)

(16) Secreted PLA2 induces proliferation in astrocytoma through the EGF receptor: another inflammation-cancer linkNeuro-OncologyOctober 1, 2010Marita Hernandez, RubÃ©n Martin, Miriam Daniela Garcia-Cubillas, Patricia Maeso-Hernandez, MarÃa Luisa NietoTriggering of degranulation in mast cells by exogenous type II phospholipase A2. J Immunol. 1993; 151:5675 –5684. 43. Schlessinger J. Cell signaling by receptor tyrosine kinases. Cell. 2000;103:211 –225. 44.

Be the First to Write a Review!

eLife

eLife

Elife

Elife

PKA RI-alpha (D54D9) Rabbit mAb from Cell Signaling Technology

Cell Signaling Technology

Citations (16)

Reviews

PKA RI-alpha (D54D9) Rabbit mAb from Cell Signaling Technology

About Biocompare

Advertise with Us

Specialized Search Tools

Site Map