CDK4 antibody 11026-1-AP from Proteintech Group Inc

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Cancer cell international
November 19 2022

Fig 1: Cell proliferation was enhanced and G1 phase arrest occurred in 3D culture system A Cell colony formation in each group on day 1, 3, 5 and 7 (scale bar 100 µm). B, C Comparison of plating efficiency and colony diameter of CNE-1 cells cultured in three systems (n = 3, *P < 0.05). D The flow cytometry histogram of CNE-1 cells. The cell cycle distribution of CNE-1 cells in 3D groups arrested at G1 phase. E Western blot analysis of Cyclin E1, Cyclin D1 and CDk4 in three groups
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Redox biology
December 01 2022

Fig 2: Transduction with SARS-CoV-2 proteins increases apoptosis and causes cell cycle arrest in BEAS-2B cells.A) Representative immunoblots and densitometry showing upregulated expression of AIF and CDK4, 96 hours following transduction with 3 different SARS-CoV-2 proteins (vs GFP control). Only transduction with M protein downregulates CDK4. **P < 0.01; NS, not significant; n = 3/group.B) Representative images and mean data showing that heterologous expression of each of the three selected SARS-CoV-2 proteins increase the expression of AIF relative to the mitochondrial reporter protein, TOMM20, in BEAS-2B cells at 96 hours. Cells were stained with AIF mouse monoclonal antibody (green). Cells were also stained with TOMM20 rabbit polyclonal antibody (red). Ex/Em: 556/560-580 nm ***P < 0.001; n = 5–7/group.C) Lentiviral transduction of A549 cells with SARS-CoV-2 proteins, Nsp7, Nsp9 & M increase apoptosis, defined as cells that are annexin V positive and propidium iodide (PI) negative, relative to the GFP control. ***P < 0.001; n = 3/group.D) Lentiviral transduction of A549 cells with SARS-CoV-2 M protein causes cell cycle arrest in G1/G0, relative to GFP controls and other SARS-CoV-2 proteins. ***P < 0.001; NS; not significant; n = 3/group.E) BEAS-2B cells were loaded with mPTP staining dye-AM (Abcam ab239704; flow cytometry kit). CoCl2 was used to quench the cytosolic fluorescence, maintaining only the mitochondrial signal. Histograms demonstrate reduced mPTP activity (as the result of the mPTP opening) in M-transfected cells (light gray) versus control (dotted histogram). mPTP activity was not affected in Nsp9-transfected cells (dark gray) compared to control. The bar graph shows the fold change comparison in mPTP activity and confirms that that M-transfected cells had significantly reduced mPTP activity (open mPTP) versus control (p = 0.019; parametric one-way ANOVA). mPTP activity was calculated as MFI(CoCl2) – MFI (CoCl2+Ionomycin); MFI – median fluorescence intensity. MFI = mean fluorescent intensity. *P < 0.05; NS; not significant; n = 4/group.
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Molecular therapy. Nucleic acids
March 06 2020

Fig 3: Effects of FBRP on Expression Levels of Candidate Targets Involved in PI3K/AKT/NF-?B Signaling in Liver Tissues of DEN-Induced HCC Rats(A) Western blots of the candidate targets of FBRP against HCC involved in PI3K/AKT/NF-?B signaling. (B–M) Relative protein expression levels of (B) p-PI3K, (C) p-AKT, (D) IK?B, (E) p-IK?B, (F) the ratio of p-IK?B to IK?B, (G) NF-?B (p65), (H) p-NF-?B (p65), (I) the ratio of NF-?B (p65) to p-NF-?B (p65), (J) CCND1, (K) CCNE1, (L) CDK2, and (M) CDK4 in different groups are shown. Data are expressed as the mean ± SD. #p < 0.05, ##p < 0.01, ###p < 0.001, comparison with the normal group; @p < 0.05, @@p < 0.01, @@@p < 0.001, comparison with the DEN-12w group; *p < 0.05, **p < 0.01, ***p < 0.001, comparison with the DEN-15w group; $p < 0.05, $$p < 0.01, $$$p < 0.001, comparison with the DEN-18w group.
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Acta pharmaceutica Sinica. B
August 01 2022

Fig 4: NAT10 regulates cycle distribution and promotes cellular proliferation in MM cells. (A) Volcano plots showed genes with upregulated (red) and downregulated (blue) expression upon NAT10 overexpression. (B) Venn diagram of two pairs of MM cells with common upregulated or downregulated genes. (C) Pathway enrichment analysis of RNA-seq data revealed that NAT10 was correlated to cell proliferation and cell cycle. (D, E) Flow cytometry analysis displayed that NAT10 overexpression increased G2/M phase fraction (D) and siNAT10 decreased G2/M phase fraction (E) in MM cells (n = 3). (F, G) Western blotting assays indicated that NAT10 upregulated CDK4 and CDK6 expression (F) and siNAT10 decreased CDK4 and CDK6 expression (G) in MM cells. (H) Western blotting analysis confirmed that siNAT10 promoted apoptotic protein expression. All data are displayed as mean ± SD; *P < 0.05, **P < 0.01, ***P < 0.001.
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Drug delivery
December 01 2022

Fig 5: Lewis lung cancer cells (LLC) activated ND-DOX-loaded platelets to release ND-DOX which entered and damaged the cancer cells. (A) Microscopy of co-cultured Lewis cells and platelets loaded with ND-DOX or DOX. Arrow marked were platelet aggregates. (B) TEM observation of ND-DOX-loaded platelets in fresh culture medium or cancer cell-conditioned culture medium. Arrow marked were pseudopodia from activated platelets. (C) Aggregation of platelets and ND-DOX-loaded platelets in the presence and absence of the cancer cells. Assay was dynamic light scattering assay. (D,E) Surface expression of P-selectin in platelets and ND-DOX-loaded platelets in the presence and absence of the cancer cells. (F) Unloading of ND-DOX by ND-DOX-loaded platelets after 2-hr co-culture with cancer cells. Detection was by flow cytometry. (G) Cancer cell uptake of ND-DOX released from ND-DOX-loaded platelets in co-culture for 2 hr. Detection was by flow cytometry. (H) Fluorescent microscopy of ND-DOX-loaded platelets and cancer cells after 2-hr co-culture. (I) Viability of cancer cells after 12-hr co-culture with empty platelets, ND-DOX-loaded platelets or DOX-loaded-platelets. ND-DOX and DOX treatments were given as controls. (J) Expression of PCNA and CDK4 in cancer cells after 12-hr co-culture with empty platelets, ND-DOX-loaded platelets or DOX-loaded-platelets. ND-DOX and DOX treatments were given as controls. (K) Apoptosis of cancer cells after 12-hr co-culture with empty platelets, ND-DOX-loaded platelets or DOX-loaded-platelets. ND-DOX and DOX treatments were given as controls. Apoptosis was detected by annexin-v staining and flow cytometry. Geometric means were used to quantify the mean fluorescence intensity (MFI) of flow cytometry. Values were means ± SD (n = 3, *p < .05). Representative flow cytometry raw data were shown in Figure S2 of the supporting information. Plt@ND-DOX refers to platelets loaded with ND-DOX; Plt@DOX refers to platelets loaded with DOX.

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Proteintech Group Inc for
CDK4 antibody

Description

The CDK4 antibody from Proteintech is a rabbit polyclonal antibody to a recombinant protein of CDK4. This antibody recognizes recombinant protein antigen. The CDK4 antibody has been validated for the following applications: WB, RIP, IP, IHC, IF, FC, CoIP, ELISA analysis

Product Specs
ItemCDK4 antibody
CompanyProteintech Group Inc
Price Pricing Info Supplier Page View Company Product Page
Catalog Number11026-1-AP
ApplicationsWB, RIP, IP, IHC, IF, FC, CoIP, ELISA
IsotypeIgG
Quantity20ul
ClonalityPolyclonal
ReactivityHuman, Rat
FormatPBS with 0.02% sodium azide and 50% glycerol pH 7.3
Antibody Typeprimary antibodies
Conjugate/TagUnconjugated
HostRabbit
PurityAntigen affinity purification
ImmunogenRecombinant Protein
Research AreaBinding Proteins, Cell Cycle, Cytoskeleton/Scaffold Proteins, Metabolism, Signal transduction
TargetCDK4
NCBI Full Gene Namecyclin dependent kinase 4
NCBI Gene AliasesCMM3, PSK-J3

Specifications/Features

20ul available

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Proteintech Group Inc

5500 Pearl Street, Suite 400

Rosemont,, Illinois 60018

United States

Phone: 1-888-478-4522

Email: proteintech@ptglab.com

Company Profile

Website: http://www.ptglab.com

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(5) Emodin promotes hepatic stellate cell senescence and alleviates liver fibrosis via a nuclear receptor (Nur77)-mediated epigenetic regulation of glutaminase 1British journal of pharmacologyOctober 1, 2023Chen L, Liang B, Xia S, Wang F, Li Z, Shao J, Zhang Z, Chen A, Zheng S, Zhang F.

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(7) Methamphetamine exposure drives cell cycle exit and aberrant differentiation in rat hippocampal-derived neurospheresFrontiers in PharmacologySeptember 19, 2023Shaomin Wang, Liang Wang, Qian Bu, Qian Wei, Linhong Jiang, Yanping Dai, Ni Zhang, Weihong Kuang, Yinglan Zhao, Xiaobo Cenlisted in the following: rabbit anti-CDK2 (1:4000; 22060-1-AP; Proteintech), rabbit anti-CDK4 (1:8000; 11026-1-AP; Proteintech), rabbit anti-CDK6 (1:4000; 19117-1-AP; Proteintech), rabbit anti-Cyclin E1 (1:1000; ab33911;

(8) LTe2 induces cell apoptosis in multiple myeloma by suppressing AKT phosphorylation at Thr308 and Ser473Frontiers in OncologySeptember 14, 2023Yuanjiao Zhang, Jiacheng Qian, Mingmei Jiang, Shu Yang, Lianxin Zhou, Qin Zhang, Liping Lin, Ye YangProteintech), Cleaved Caspase-3 (9661S, Cell Signaling Technology), β-actin (60008-1-Ig, Proteintech), CDK4 (11026-1-AP, Proteintech), CDK6 (14052-1-AP, Proteintech), CyclinD1 (55506T, Cell Signaling Technology), AKT (9272s,

(9) HECW2 promotes the progression and chemoresistance of colorectal cancer via AKT/mTOR signaling activation by mediating the ubiquitin-proteasome degradation of lamin B1Journal of CancerSeptember 4, 2023Fang Li, Li Wang, Yujue Wang, Hui Shen, Qianrui Kou, Changjun Shen, Xiangrong Xu, Yunqing Zhang, Jing Zhang(Proteintech, 10375-2-AP, 1:2000), anti-MMP2 (Proteintech, 10373-2-AP, 1:2000), anti-CDK4 (Proteintech, 11026-1-AP, 1:3000), anti-Cyclin D1 (Proteintech, 26939-1-AP, 1:3000), anti-lamin B1 (Proteintech, 12987-1-AP,

(10) Inhibition of VCP modulates NF-κB signaling pathway to suppress multiple myeloma cell proliferation and osteoclast differentiationAging (Albany NY)August 30, 2023Rongfang Wei, Yuhao Cao, Hongjie Wu, Xin Liu, Mingmei Jiang, Xian Luo, Zhendong Deng, Ze Wang, Mengying Ke, Yongqiang Zhu, et al.PARP (9542S, Cell Signaling Technology), Cleaved Caspase-3 (9661S, Cell Signaling Technology), CDK4 (11026-1-AP, Proteintech), CDK6 (14052-1-AP, Proteintech), Histone H3 (17168-1-AP, Proteintech), CD63 (216130, Abcam,

(11) PHF23 promotes NSCLC proliferation, metastasis, and chemoresistance via stabilization of ACTN4 and activation of the ERK pathwayCell death & diseaseAugust 25, 2023Cheng M, Cao H, Yao P, Guan J, Wu P, Ji H, Jiang S, Yuan Y, Fu L, Zheng Q, et al.E1,Proteintech,11554-1-AP,Rabbit,1:1000 MMP9,Proteintech,10375-2-AP,Rabbit,1:1000 CDK4,Proteintech,11026-1-AP,Rabbit,1:1000 CDK6,Proteintech,14052-1-AP,Rabbit,1:1000 E-cadherin,Proteintech,20874-1-AP,Rabbit,1:5000 N-cadherin,Proteintech,22018-1-AP,Rabbit,1:2000 ERK1/2,Proteintech,11257-1-AP,Rabbit,1:1000 Phospho-JUN

(12) Histone acetylation by HBO1 (KAT7) activates Wnt/β-catenin signaling to promote leukemogenesis in B-cell acute lymphoblastic leukemiaCell death & diseaseAugust 4, 2023Wang H, Qiu Y, Zhang H, Chang N, Hu Y, Chen J, Hu R, Liao P, Li Z, Yang Y, et al.(13751–1-AP), Histone H4 (16047–1-AP), BCL2 (12789–1-AP), P21 (10355–1-AP), Cyclin D1 (60186–1-Ig), CDK4 (11026–1-AP), LaminB1 (66095–1-Ig), β-catenin (51067–2-AP), c-MYC (10828–1-AP) and MMP7 (10374–2-AP) were obtained

(13) Sanggenon C inhibits cell proliferation and induces apoptosis by regulating the MIB1/DAPK1 axis in glioblastomaMedComm (2020)August 1, 2023Chang H, Hou J, Shao Y, Xu M, Weng X, Du Y, Shi J, Zhang L, Cui H.HY‐17364) was purchased from MedChemExpress (NJ, USA). Anti‐CDK2 (Cat# 10122‐1‐AP), anti‐CDK4 (Cat# 11026‐1‐AP), anti‐CyclinE1 (Cat# 11554‐1‐AP), anti‐MIB1 (Cat# 11893‐1‐AP), anti‐Tubulin (Cat# 11224‐1‐AP), anti‐HA

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(18) Analysis and validation of the potential of the MYO1E gene in pancreatic adenocarcinoma based on a bioinformatics approachOncology lettersJuly 1, 2023Liu S, Liu P, Fei X, Zhu C, Hou J, Wang X, Pan Y.

(19) HDAC inhibitor chidamide overcomes drug resistance in chronic myeloid leukemia with the T315i mutation through the Akt-autophagy pathwayHuman cellJuly 1, 2023Yin L, Zhang Q, Xie S, Cheng Z, Li R, Zhu H, Yu Q, Yuan H, Wang C, Peng H, et al.

(20) The Natural Alkaloid (-)-N-Hydroxyapiosporamide Suppresses Colorectal Tumor Progression as an NF-κB Pathway Inhibitor by Targeting the TAK1-TRAF6 ComplexJournal of natural productsJune 23, 2023Feng L, Shang RR, Wang XJ, Li L, Li X, Gong YX, Shi LY, Wang JW, Qian ZY, Tan NH, et al.