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Mouse Anti-CAV1 Recombinant Antibody (CAP331) (CBMAB-AP830LY)

Summary

Host Animal
Mouse
Specificity
Human, Mouse, Rat
Clone
CAP331
Antibody Isotype
IgG1
Application
WB

Basic Information

Immunogen
A synthetic peptide (conjugated with KLH) corresponding to the C-terminal of mouse Caveolin-1.
Specificity
Human, Mouse, Rat
Antibody Isotype
IgG1
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

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

Format
Liquid
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freezethaw cycles.

Target

Full Name
Caveolin 1
Introduction
The scaffolding protein encoded by this gene is the main component of the caveolae plasma membranes found in most cell types. The protein links integrin subunits to the tyrosine kinase FYN, an initiating step in coupling integrins to the Ras-ERK pathway and promoting cell cycle progression. The gene is a tumor suppressor gene candidate and a negative regulator of the Ras-p42/44 mitogen-activated kinase cascade. Caveolin 1 and caveolin 2 are located next to each other on chromosome 7 and express colocalizing proteins that form a stable hetero-oligomeric complex. Mutations in this gene have been associated with Berardinelli-Seip congenital lipodystrophy. Alternatively spliced transcripts encode alpha and beta isoforms of caveolin 1.[provided by RefSeq, Mar 2010]
Entrez Gene ID
Human857
Mouse12389
Rat25404
UniProt ID
HumanQ03135
MouseP49817
RatP41350
Alternative Names
Caveolin 1; Caveolin 1, Caveolae Protein, 22kDa; Caveolin 1, Caveolae Protein, 22kD; Cell Growth-Inhibiting Protein 32; Caveolin-1; MSTP085; BSCL3;
Function
May act as a scaffolding protein within caveolar membranes (PubMed:11751885).
Forms a stable heterooligomeric complex with CAV2 that targets to lipid rafts and drives caveolae formation. Mediates the recruitment of CAVIN proteins (CAVIN1/2/3/4) to the caveolae (PubMed:19262564).
Interacts directly with G-protein alpha subunits and can functionally regulate their activity (By similarity).
Involved in the costimulatory signal essential for T-cell receptor (TCR)-mediated T-cell activation. Its binding to DPP4 induces T-cell proliferation and NF-kappa-B activation in a T-cell receptor/CD3-dependent manner (PubMed:17287217).
Recruits CTNNB1 to caveolar membranes and may regulate CTNNB1-mediated signaling through the Wnt pathway (By similarity).
Negatively regulates TGFB1-mediated activation of SMAD2/3 by mediating the internalization of TGFBR1 from membrane rafts leading to its subsequent degradation (PubMed:25893292).
Biological Process
Angiogenesis Source: Ensembl
Angiotensin-activated signaling pathway involved in heart process Source: BHF-UCL
Apoptotic signaling pathway Source: UniProtKB
Basement membrane organization Source: Ensembl
Beta-catenin destruction complex disassembly Source: Reactome
Calcium ion homeostasis Source: BHF-UCL
Calcium ion transport Source: BHF-UCL
Caveola assembly Source: BHF-UCL
Caveolin-mediated endocytosis Source: UniProtKB
Cell differentiation Source: GO_Central
Cellular calcium ion homeostasis Source: BHF-UCL
Cellular response to exogenous dsRNA Source: UniProtKB
Cellular response to hyperoxia Source: UniProtKB
Cellular response to peptide hormone stimulus Source: BHF-UCL
Cellular response to starvation Source: BHF-UCL
Cellular response to transforming growth factor beta stimulus Source: Ensembl
Cholesterol homeostasis Source: BHF-UCL
Cholesterol transport Source: HGNC-UCL
Inactivation of MAPK activity Source: BHF-UCL
Insulin receptor internalization Source: Ensembl
Lactation Source: Ensembl
Leukocyte migration Source: Reactome
Lipid storage Source: BHF-UCL
Maintenance of protein location in cell Source: BHF-UCL
Mammary gland development Source: BHF-UCL
Mammary gland involution Source: BHF-UCL
Membrane depolarization Source: BHF-UCL
Negative regulation of anoikis Source: UniProtKB
Negative regulation of BMP signaling pathway Source: BHF-UCL
Negative regulation of canonical Wnt signaling pathway Source: UniProtKB
Negative regulation of cytokine-mediated signaling pathway Source: Ensembl
Negative regulation of endothelial cell proliferation Source: BHF-UCL
Negative regulation of epithelial cell differentiation Source: BHF-UCL
Negative regulation of inward rectifier potassium channel activity Source: BHF-UCL
Negative regulation of MAPK cascade Source: BHF-UCL
Negative regulation of necroptotic process Source: Ensembl
Negative regulation of nitric oxide biosynthetic process Source: BHF-UCL
Negative regulation of nitric-oxide synthase activity Source: Ensembl
Negative regulation of peptidyl-serine phosphorylation Source: BHF-UCL
Negative regulation of peptidyl-tyrosine autophosphorylation Source: BHF-UCL
Negative regulation of pinocytosis Source: UniProtKB
Negative regulation of potassium ion transmembrane transport Source: BHF-UCL
Negative regulation of protein binding Source: BHF-UCL
Negative regulation of protein tyrosine kinase activity Source: BHF-UCL
Negative regulation of protein ubiquitination Source: UniProtKB
Negative regulation of receptor signaling pathway via JAK-STAT Source: BHF-UCL
Negative regulation of transcription by RNA polymerase II Source: UniProtKB
Negative regulation of transforming growth factor beta receptor signaling pathway Source: UniProtKB
Negative regulation of tyrosine phosphorylation of STAT protein Source: Ensembl
Nitric oxide homeostasis Source: BHF-UCL
Positive regulation of calcium ion transport into cytosol Source: BHF-UCL
Positive regulation of canonical Wnt signaling pathway Source: BHF-UCL
Positive regulation of catalytic activity Source: BHF-UCL
Positive regulation of cell adhesion molecule production Source: UniProtKB
Positive regulation of cell migration Source: BHF-UCL
Positive regulation of cholesterol efflux Source: ARUK-UCL
Positive regulation of cold-induced thermogenesis Source: YuBioLab
Positive regulation of ER-associated ubiquitin-dependent protein catabolic process Source: ParkinsonsUK-UCL
Positive regulation of extrinsic apoptotic signaling pathway Source: UniProtKB
Positive regulation of gap junction assembly Source: BHF-UCL
Positive regulation of gene expression Source: Ensembl
Positive regulation of intrinsic apoptotic signaling pathway Source: UniProtKB
Positive regulation of NF-kappaB transcription factor activity Source: ARUK-UCL
Positive regulation of peptidyl-serine phosphorylation Source: BHF-UCL
Positive regulation of protein binding Source: ParkinsonsUK-UCL
Positive regulation of protein ubiquitination Source: ParkinsonsUK-UCL
Positive regulation of toll-like receptor 3 signaling pathway Source: UniProtKB
Positive regulation of vasoconstriction Source: BHF-UCL
Posttranscriptional regulation of gene expression Source: Ensembl
Protein localization Source: BHF-UCL
Protein localization to basolateral plasma membrane Source: BHF-UCL
Protein localization to plasma membrane raft Source: BHF-UCL
Protein transport Source: Ensembl
Receptor internalization Source: UniProtKB
Receptor internalization involved in canonical Wnt signaling pathway Source: BHF-UCL
Receptor-mediated endocytosis of virus by host cell Source: CACAO
Regulation of blood coagulation Source: BHF-UCL
Regulation of cardiac muscle cell action potential involved in regulation of contraction Source: BHF-UCL
Regulation of cell communication by electrical coupling involved in cardiac conduction Source: BHF-UCL
Regulation of cytosolic calcium ion concentration Source: BHF-UCL
Regulation of entry of bacterium into host cell Source: AgBase
Regulation of fatty acid metabolic process Source: BHF-UCL
Regulation of heart rate by cardiac conduction Source: BHF-UCL
Regulation of membrane repolarization during action potential Source: BHF-UCL
Regulation of nitric-oxide synthase activity Source: Reactome
Regulation of peptidase activity Source: BHF-UCL
Regulation of ruffle assembly Source: AgBase
Regulation of smooth muscle contraction Source: BHF-UCL
Regulation of the force of heart contraction by chemical signal Source: Ensembl
Regulation of ventricular cardiac muscle cell action potential Source: BHF-UCL
Response to bacterium Source: AgBase
Response to calcium ion Source: BHF-UCL
Response to estrogen Source: MGI
Response to hypoxia Source: BHF-UCL
Response to ischemia Source: Ensembl
Response to progesterone Source: MGI
Skeletal muscle tissue development Source: BHF-UCL
T cell costimulation Source: UniProtKB
Triglyceride metabolic process Source: BHF-UCL
Vasculogenesis Source: BHF-UCL
Vasoconstriction Source: Ensembl
Vesicle organization Source: BHF-UCL
Cellular Location
Cell membrane; Golgi apparatus membrane; Trans-Golgi network; Caveola; Membrane raft. Colocalized with DPP4 in membrane rafts. Potential hairpin-like structure in the membrane. Membrane protein of caveolae.
Involvement in disease
Congenital generalized lipodystrophy 3 (CGL3): An autosomal recessive disorder characterized by a near complete absence of adipose tissue, extreme insulin resistance, hypertriglyceridemia, hepatic steatosis and early onset of diabetes.
Pulmonary hypertension, primary, 3 (PPH3): A rare disorder characterized by plexiform lesions of proliferating endothelial cells in pulmonary arterioles. The lesions lead to elevated pulmonary arterial pression, right ventricular failure, and death. The disease can occur from infancy throughout life and it has a mean age at onset of 36 years. Penetrance is reduced. Although familial pulmonary hypertension is rare, cases secondary to known etiologies are more common and include those associated with the appetite-suppressant drugs.
Lipodystrophy, familial partial, 7 (FPLD7): A form of partial lipodystrophy, a disorder characterized by abnormal subcutaneous fat distribution. Affected individuals manifest a gradual loss of subcutaneous adipose tissue in various parts of the body, accompanied by an accumulation of adipose tissue in the face and neck in some cases causing a double chin, fat neck, or cushingoid appearance. FPLD7 is an autosomal dominant form with a variable phenotype. Some patients manifest congenital cataracts and neurodegeneration leading to cerebellar and spinal cord dysfunction.
Topology
Cytoplasmic: 2-104
Helical: 105-125
Cytoplasmic: 126-178
PTM
Ubiquitinated. Undergo monoubiquitination and multi- and/or polyubiquitination (PubMed:21822278). Monoubiquitination of N-terminal lysines promotes integration in a ternary complex with UBXN6 and VCP which promotes oligomeric CAV1 targeting to lysosomes for degradation (PubMed:23335559).
The initiator methionine for isoform 2 is removed during or just after translation. The new N-terminal amino acid is then N-acetylated.
Phosphorylated at Tyr-14 by ABL1 in response to oxidative stress.

Ariotti, N., Wu, Y., Okano, S., Gambin, Y., Follett, J., Rae, J., ... & Parton, R. G. (2021). An inverted CAV1 (caveolin 1) topology defines novel autophagy-dependent exosome secretion from prostate cancer cells. Autophagy, 17(9), 2200-2216.

Concas, M. P., Cocca, M., Catamo, E., Gasparini, P., & Robino, A. (2021). Eating disinhibition and food liking are influenced by variants in CAV1 (caveolin 1) gene. Food Quality and Preference, 104447.

Zhang, X., Ramírez, C. M., Aryal, B., Madrigal-Matute, J., Liu, X., Diaz, A., ... & Fernández-Hernando, C. (2020). Cav-1 (Caveolin-1) deficiency increases autophagy in the endothelium and attenuates vascular inflammation and atherosclerosis. Arteriosclerosis, thrombosis, and vascular biology, 40(6), 1510-1522.

Simón, L., Campos, A., Leyton, L., & Quest, A. F. (2020). Caveolin-1 function at the plasma membrane and in intracellular compartments in cancer. Cancer and Metastasis Reviews, 39, 435-453.

Qian, X. L., Pan, Y. H., Huang, Q. Y., Shi, Y. B., Huang, Q. Y., Hu, Z. Z., & Xiong, L. X. (2019). Caveolin-1: a multifaceted driver of breast cancer progression and its application in clinical treatment. OncoTargets and therapy, 12, 1539.

Ramírez, C. M., Zhang, X., Bandyopadhyay, C., Rotllan, N., Sugiyama, M. G., Aryal, B., ... & Fernández-Hernando, C. (2019). Caveolin-1 regulates atherogenesis by attenuating low-density lipoprotein transcytosis and vascular inflammation independently of endothelial nitric oxide synthase activation. Circulation, 140(3), 225-239.

Oliveira, S. D., Chen, J., Castellon, M., Mao, M., Raj, J. U., Comhair, S., ... & Minshall, R. D. (2019). Injury-Induced Shedding of Extracellular Vesicles Depletes Endothelial Cells of Cav-1 (Caveolin-1) and Enables TGF-β (Transforming Growth Factor-β)–Dependent Pulmonary Arterial Hypertension. Arteriosclerosis, thrombosis, and vascular biology, 39(6), 1191-1202.

Campos, A., Burgos-Ravanal, R., González, M. F., Huilcaman, R., Lobos González, L., & Quest, A. F. G. (2019). Cell intrinsic and extrinsic mechanisms of caveolin-1-enhanced metastasis. Biomolecules, 9(8), 314.

Chen, Z., DS Oliveira, S., Zimnicka, A. M., Jiang, Y., Sharma, T., Chen, S., ... & Minshall, R. D. (2018). Reciprocal regulation of eNOS and caveolin-1 functions in endothelial cells. Molecular biology of the cell, 29(10), 1190-1202.

Chung, J. W., Kim, D. H., Oh, M. J., Cho, Y. H., Kim, E. H., Moon, G. J., ... & Bang, O. Y. (2018). Cav-1 (Caveolin-1) and arterial remodeling in adult moyamoya disease. Stroke, 49(11), 2597-2604.

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

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