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


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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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