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Mouse Anti-CDK4 Recombinant Antibody (CBFYC-1600) (CBMAB-C1659-FY)


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Published Data
CBMAB-C1659-FY-1
Mouse Anti-CDK4 Recombinant Antibody (CBFYC-1600) (CBMAB-C1659-FY) in WB
Western blot analysis of OSCC cell lines for various stemness markers (Lt) and immune modulators (Rt). ...View More
Chang, K. W., Lin, C. E., Tu, H. F., Chung, H. Y., Chen, Y. F., & Lin, S. C. (2020). Establishment of a p53 null murine oral carcinoma cell line and the identification of genetic alterations associated with this carcinoma. International Journal of Molecular Sciences, 21(24), 9354.
Distributed under Open Access license CC BY 4.0, without modification.

Summary

Host Animal
Mouse
Specificity
Human, Mouse, Rat
Clone
CBFYC-1600
Antibody Isotype
IgG1, κ
Application
WB, IP, IF

Basic Information

Immunogen
Amino acids 270-290 of Cdk4 of human.
Host Species
Mouse
Specificity
Human, Mouse, Rat
Antibody Isotype
IgG1, κ
Clonality
Monoclonal Antibody
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.
ApplicationNote
WB1:100-1:1,000
IP1-2 µg per 100-500 µg of total protein (1 ml of cell lysate)
IF(ICC)1:50-1:500

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Buffer
PBS, 0.1% gelatin
Preservative
< 0.1% sodium azide
Concentration
0.2 mg/ml
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at-20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
Cyclin Dependent Kinase 4
Introduction
CDK4 exists, in part, as a multi-protein complex with a D-type cyclin, proliferating cell nuclear antigen and a protein, p21 (refs 7–9)
Entrez Gene ID
1019
UniProt ID
P11802
Alternative Names
Cyclin Dependent Kinase 4; Cell Division Protein Kinase 4; EC 2.7.11.22; PSK-J3; Cyclin-Dependent Kinase 4; EC 2.7.11; CMM3
Function
Ser/Thr-kinase component of cyclin D-CDK4 (DC) complexes that phosphorylate and inhibit members of the retinoblastoma (RB) protein family including RB1 and regulate the cell-cycle during G1/S transition. Phosphorylation of RB1 allows dissociation of the transcription factor E2F from the RB/E2F complexes and the subsequent transcription of E2F target genes which are responsible for the progression through the G1 phase. Hypophosphorylates RB1 in early G1 phase. Cyclin D-CDK4 complexes are major integrators of various mitogenenic and antimitogenic signals. Also phosphorylates SMAD3 in a cell-cycle-dependent manner and represses its transcriptional activity. Component of the ternary complex, cyclin D/CDK4/CDKN1B, required for nuclear translocation and activity of the cyclin D-CDK4 complex.
Biological Process
Adipose tissue development Source: Ensembl
Animal organ regeneration Source: Ensembl
Cell division Source: UniProtKB-KW
Cellular response to insulin stimulus Source: Ensembl
Cellular response to interleukin-4 Source: Ensembl
Cellular response to ionomycin Source: Ensembl
Cellular response to lipopolysaccharide Source: Ensembl
Cellular response to phorbol 13-acetate 12-myristate Source: Ensembl
Circadian rhythm Source: Ensembl
G1/S transition of mitotic cell cycle Source: BHF-UCL
Granulocyte differentiation Source: Reactome
Lens development in camera-type eye Source: Ensembl
Negative regulation of cell cycle arrest Source: UniProtKB
Negative regulation of G1/S transition of mitotic cell cycle Source: Reactome
Positive regulation of apoptotic process Source: Ensembl
Positive regulation of cell cycle Source: Reactome
Positive regulation of cell population proliferation Source: BHF-UCL
Positive regulation of cell size Source: Ensembl
Positive regulation of fibroblast proliferation Source: BHF-UCL
Positive regulation of G2/M transition of mitotic cell cycle Source: UniProtKB
Positive regulation of translation Source: Ensembl
Protein phosphorylation Source: BHF-UCL
Regulation of cell cycle Source: GO_Central
Regulation of gene expression Source: BHF-UCL
Regulation of insulin receptor signaling pathway Source: Ensembl
Regulation of lipid biosynthetic process Source: Ensembl
Regulation of lipid catabolic process Source: Ensembl
Regulation of multicellular organism growth Source: Ensembl
Regulation of transcription initiation from RNA polymerase II promoter Source: Reactome
Response to drug Source: UniProtKB
Response to hyperoxia Source: Ensembl
Response to lead ion Source: Ensembl
Response to testosterone Source: Ensembl
Response to toxic substance Source: Ensembl
Signal transduction Source: Ensembl
Cellular Location
Nucleus; Nucleus membrane; Cytoplasm. Cytoplasmic when non-complexed. Forms a cyclin D-CDK4 complex in the cytoplasm as cells progress through G1 phase. The complex accumulates on the nuclear membrane and enters the nucleus on transition from G1 to S phase. Also present in nucleoli and heterochromatin lumps. Colocalizes with RB1 after release into the nucleus.
Involvement in disease
Melanoma, cutaneous malignant 3 (CMM3): A malignant neoplasm of melanocytes, arising de novo or from a pre-existing benign nevus, which occurs most often in the skin but also may involve other sites.
PTM
Phosphorylation at Thr-172 is required for enzymatic activity. Phosphorylated, in vitro, at this site by CCNH-CDK7, but, in vivo, appears to be phosphorylated by a proline-directed kinase. In the cyclin D-CDK4-CDKN1B complex, this phosphorylation and consequent CDK4 enzyme activity, is dependent on the tyrosine phosphorylation state of CDKN1B. Thus, in proliferating cells, CDK4 within the complex is phosphorylated on Thr-172 in the T-loop. In resting cells, phosphorylation on Thr-172 is prevented by the non-tyrosine-phosphorylated form of CDKN1B.
More Infomation

Finn, R. S., Liu, Y., Zhu, Z., Martin, M., Rugo, H. S., Diéras, V., ... & Slamon, D. J. (2020). Biomarker analyses of response to cyclin-dependent kinase 4/6 inhibition and endocrine therapy in women with treatment-naive metastatic breast cancer. Clinical Cancer Research, 26(1), 110-121.

Wang, P. F., Qiu, H. Y., He, Y., & Zhu, H. L. (2020). Cyclin-dependent kinase 4/6 inhibitors for cancer therapy: a patent review (2015–2019). Expert Opinion on Therapeutic Patents, 30(10), 795-805.

Spring, L. M., Wander, S. A., Andre, F., Moy, B., Turner, N. C., & Bardia, A. (2020). Cyclin-dependent kinase 4 and 6 inhibitors for hormone receptor-positive breast cancer: past, present, and future. The Lancet, 395(10226), 817-827.

Zheng, J., Wu, J., Wang, C., Zhuang, S., Chen, J., & Ye, F. (2020). Combination cyclin-dependent kinase 4/6 inhibitors and endocrine therapy versus endocrine monotherapy for hormonal receptor-positive, human epidermal growth factor receptor 2-negative advanced breast cancer: A systematic review and meta-analysis. PloS one, 15(6), e0233571.

Guiley, K. Z., Stevenson, J. W., Lou, K., Barkovich, K. J., Kumarasamy, V., Wijeratne, T. U., ... & Rubin, S. M. (2019). p27 allosterically activates cyclin-dependent kinase 4 and antagonizes palbociclib inhibition. Science, 366(6471).

Thill, M., & Schmidt, M. (2018). Management of adverse events during cyclin-dependent kinase 4/6 (CDK4/6) inhibitor-based treatment in breast cancer. Therapeutic advances in medical oncology, 10, 1758835918793326.

Zhou, Y., Shen, J. K., Yu, Z., Hornicek, F. J., Kan, Q., & Duan, Z. (2018). Expression and therapeutic implications of cyclin-dependent kinase 4 (CDK4) in osteosarcoma. Biochimica et Biophysica Acta (BBA)-Molecular Basis of Disease, 1864(5), 1573-1582.

Battisti, N. M. L., De Glas, N., Sedrak, M. S., Loh, K. P., Liposits, G., Soto-Perez-de-Celis, E., ... & Ring, A. (2018). Use of cyclin-dependent kinase 4/6 (CDK4/6) inhibitors in older patients with ER-positive HER2-negative breast cancer: Young International Society of Geriatric Oncology review paper. Therapeutic advances in medical oncology, 10, 1758835918809610.

Tripathy, D., Bardia, A., & Sellers, W. R. (2017). Ribociclib (LEE011): mechanism of action and clinical impact of this selective cyclin-dependent kinase 4/6 inhibitor in various solid tumors. Clinical Cancer Research, 23(13), 3251-3262.

Kwapisz, D. (2017). Cyclin-dependent kinase 4/6 inhibitors in breast cancer: palbociclib, ribociclib, and abemaciclib. Breast cancer research and treatment, 166(1), 41-54.

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For research use only. Not intended for any clinical use.

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