Recombinant Anti-KRIT1 antibody [EPR16560] (ab196025)
Key features and details
- Produced recombinantly (animal-free) for high batch-to-batch consistency and long term security of supply
- Rabbit monoclonal [EPR16560] to KRIT1
- Suitable for: WB, ICC/IF
- Reacts with: Mouse, Human
Related conjugates and formulations
Overview
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Product name
Anti-KRIT1 antibody [EPR16560]
See all KRIT1 primary antibodies -
Description
Rabbit monoclonal [EPR16560] to KRIT1 -
Host species
Rabbit -
Tested applications
Suitable for: WB, ICC/IFmore details -
Species reactivity
Reacts with: Mouse, Human -
Immunogen
Recombinant fragment. This information is proprietary to Abcam and/or its suppliers.
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Positive control
- Human fetal brain and Mouse brain lysates; SH-SY5Y, Raji, NIH/3T3 and HUVEC cell lysates; HUVEC cells.
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General notes
This product is a recombinant monoclonal antibody, which offers several advantages including:
- - High batch-to-batch consistency and reproducibility
- - Improved sensitivity and specificity
- - Long-term security of supply
- - Animal-free production
Our RabMAb® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMAb® patents.
Properties
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Form
Liquid -
Storage instructions
Shipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term. Avoid freeze / thaw cycle. -
Storage buffer
pH: 7.2
Preservative: 0.01% Sodium azide
Constituents: 59% PBS, 40% Glycerol (glycerin, glycerine), 0.05% BSA -
Concentration information loading...
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Purity
Protein A purified -
Clonality
Monoclonal -
Clone number
EPR16560 -
Isotype
IgG -
Research areas
Associated products
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Alternative Versions
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Compatible Secondaries
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Isotype control
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Recombinant Protein
Applications
The Abpromise guarantee
Our Abpromise guarantee covers the use of ab196025 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Application | Abreviews | Notes |
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WB | (2) |
1/1000. Detects a band of approximately 84 kDa (predicted molecular weight: 84 kDa).
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ICC/IF |
1/100.
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Notes |
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WB
1/1000. Detects a band of approximately 84 kDa (predicted molecular weight: 84 kDa). |
ICC/IF
1/100. |
Target
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Function
Negative regulator of angiogenesis. Inhibits endothelial proliferation, apoptosis, migration, lumen formation and sprouting angiogenesis in primary endothelial cells. Promotes AKT phosphorylation in a NOTCH-dependent and independent manner, and inhibits EKR1/2 phosphorylation indirectly through activation of the DELTA-NOTCH cascade. Acts in concert with CDH5 to establish and maintain correct endothelial cell polarity and vascular lumen and these effects are mediated by recruitment and activation of the Par polarity complex and RAP1B. Required for the localization of phosphorylated PRKCZ, PARD3, TIAM1 and RAP1B to the cell junction. Plays an important role in the maintenance of the intracellular reactive oxygen species (ROS) homeostasis to prevent oxidative cellular damage. Regulates the homeostasis of intracellular ROS through an antioxidant pathway involving FOXO1 and SOD2. Facilitates the down-regulation of cyclin D1 levels required for cell transition from proliferative growth to quiescence by preventing the accumulation of intracellular ROS through the modulation of FOXO1 and SOD2 levels. -
Tissue specificity
Low levels in brain. Very weak expression found in heart and muscle. -
Involvement in disease
Defects in KRIT1 are the cause of cerebral cavernous malformations type 1 (CCM1) [MIM:116860]. Cerebral cavernous malformations (CCMs) are congenital vascular anomalies of the central nervous system that can result in hemorrhagic stroke, seizures, recurrent headaches, and focal neurologic deficits. CCMs have an incidence of 0.1%-0.5% in the general population and usually present clinically during the 3rd to 5th decade of life. The lesions are characterized by grossly enlarged blood vessels consisting of a single layer of endothelium and without any intervening neural tissue, ranging in diameter from a few millimeters to several centimeters. -
Sequence similarities
Contains 4 ANK repeats.
Contains 1 FERM domain. -
Cellular localization
Membrane. Cell junction. KRIT1 and CDH5 reciprocally regulate their localization to endothelial cell-cell junctions. - Information by UniProt
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Database links
- Entrez Gene: 889 Human
- Entrez Gene: 79264 Mouse
- Omim: 604214 Human
- SwissProt: O00522 Human
- SwissProt: Q6S5J6 Mouse
- Unigene: 531987 Human
- Unigene: 32368 Mouse
- Unigene: 482273 Mouse
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Alternative names
- Ankyrin repeat containing protein Krit1 antibody
- CAM antibody
- CCM 1 antibody
see all
Images
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All lanes : Anti-KRIT1 antibody [EPR16560] (ab196025) at 1/5000 dilution
Lane 1 : Human fetal brain lysate
Lane 2 : SH-SY5Y (Human neuroblastoma from bone marrow cells) cell lysate
Lane 3 : Raji (Human Burkitt's lymphoma cell line) cell lysate
Lysates/proteins at 20 µg per lane.
Secondary
All lanes : Goat Anti-Rabbit IgG, (H+L), Peroxidase conjugated at 1/1000 dilution
Predicted band size: 84 kDa
Observed band size: 84 kDaBlocking/Dilution buffer: 5% NFDM/TBST.
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All lanes : Anti-KRIT1 antibody [EPR16560] (ab196025) at 1/1000 dilution
Lane 1 : Mouse brain lysate
Lane 2 : NIH/3T3 (Mouse embyro fibroblast cells) cell lysate
Lysates/proteins at 10 µg per lane.
Secondary
All lanes : Goat Anti-Rabbit IgG, (H+L), Peroxidase conjugated at 1/1000 dilution
Predicted band size: 84 kDa
Observed band size: 84 kDaBlocking/Dilution buffer: 5% NFDM/TBST.
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Anti-KRIT1 antibody [EPR16560] (ab196025) at 1/5000 dilution + HUVEC (Human umbilical vein endothelial cell line) whole cell lysate at 10 µg
Secondary
Goat Anti-Rabbit IgG, (H+L), Peroxidase conjugated at 1/1000 dilution
Predicted band size: 84 kDa
Observed band size: 84 kDaBlocking/Dilution buffer: 5% NFDM/TBST.
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Immunofluorescent analysis of 4% paraformaldehyde-fixed, 0.1% Triton X-100 permeabilized HUVEC (Human umbilical vein endothelial cell line) cells labeling KRIT1 with ab196025 at 1/100 dilution, followed by Goat anti-rabbit IgG (Alexa Fluor® 488) (ab150077) secondary antibody at 1/500 dilution (green). Cytoplasm staining on HUVEC cell line is observed. The nuclear counter stain is DAPI (blue). Tubulin is detected with ab7291 (anti-Tubulin mouse mAb) at 1/1000 dilution and ab150120 (AlexaFluor®594 Goat anti-Mouse secondary) at 1/500 dilution (red).
The negative controls are as follows:
-ve control 1: ab196025 at 1/100 dilution followed by ab150120 (AlexaFluor®594 Goat anti-Mouse secondary) at 1/500 dilution.
-ve control 2: ab7291 (anti-Tubulin mouse mAb) at 1/1000 dilution followed by ab150077 (Alexa Fluor®488 Goat Anti-Rabbit IgG H&L) at 1/500 dilution.
Protocols
Datasheets and documents
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SDS download
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Datasheet download
Certificate of Compliance
References (7)
ab196025 has been referenced in 7 publications.
- Delle Monache S & Retta SF Generation of CCM Phenotype by a Human Microvascular Endothelial Model. Methods Mol Biol 2152:131-137 (2020). PubMed: 32524549
- Goitre L et al. Production of KRIT1-knockout and KRIT1-knockin Mouse Embryonic Fibroblasts as Cellular Models of CCM Disease. Methods Mol Biol 2152:151-167 (2020). PubMed: 32524551
- Parchur AK et al. NIR-II window tracking of hyperglycemia induced intracerebral hemorrhage in cerebral cavernous malformation deficient mice. Biomater Sci 8:5133-5144 (2020). PubMed: 32821891
- Cianfruglia L et al. KRIT1 Loss-Of-Function Associated with Cerebral Cavernous Malformation Disease Leads to Enhanced S-Glutathionylation of Distinct Structural and Regulatory Proteins. Antioxidants (Basel) 8:N/A (2019). PubMed: 30658464
- La Sala L et al. Glucose-sensing microRNA-21 disrupts ROS homeostasis and impairs antioxidant responses in cellular glucose variability. Cardiovasc Diabetol 17:105 (2018). PubMed: 30037352
- De Luca E et al. Multifunctional Platinum@BSA-Rapamycin Nanocarriers for the Combinatorial Therapy of Cerebral Cavernous Malformation. ACS Omega 3:15389-15398 (2018). PubMed: 30556006
- Nardella G et al. A single-center study on 140 patients with cerebral cavernous malformations: 28 new pathogenic variants and functional characterization of a PDCD10 large deletion. Hum Mutat 39:1885-1900 (2018). PubMed: 30161288