C57BL/6-Nrp1em1Cruh/H
Status | Available to order |
EMMA ID | EM:11988 |
International strain name | C57BL/6-Nrp1em1Cruh/H |
Alternative name | Nrp1 D320K |
Strain type | Endonuclease-mediated |
Allele/Transgene symbol | Nrp1em1Cruh |
Gene/Transgene symbol | Nrp1 |
Information from provider
Provider | Christiana Ruhrberg |
Provider affiliation | UCL Institute of Ophthalmology, University College London |
Genetic information | CRISPR/Cas9 technology introduced a lysine to aspartate substitution at amino acid 320 (D320K) which is predicted to abrogate VEGF164 binding to NRP1. |
Phenotypic information | Homozygous:Nrp1-D320K/D320K mice have significantly reduced VEGF164-induced permeability.Heterozygous:-- |
References |
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Homozygous fertile | not known |
Homozygous viable | yes |
Homozygous matings required | no |
Immunocompromised | no |
Information from EMMA
Archiving centre | Mary Lyon Centre at MRC Harwell, Oxford, United Kingdom |
Disease and phenotype information
IMPC phenotypes (gene matching)
MGI phenotypes (gene matching)
- abnormal vascular development / MGI
- abnormal pulmonary artery morphology / MGI
- abnormal corpus callosum morphology / MGI
- abnormal hippocampus morphology / MGI
- abnormal facial motor nucleus morphology / MGI
- abnormal dorsal root ganglion morphology / MGI
- abnormal cranial nerve morphology / MGI
- abnormal trigeminal nerve morphology / MGI
- abnormal facial nerve morphology / MGI
- abnormal vestibulocochlear nerve morphology / MGI
- abnormal spinal nerve morphology / MGI
- decreased body size / MGI
- disorganized yolk sac vascular plexus / MGI
- postnatal growth retardation / MGI
- postnatal lethality / MGI
- premature death / MGI
- abnormal dendritic cell physiology / MGI
- abnormal T cell physiology / MGI
- persistent truncus arteriosis / MGI
- abnormal pharyngeal arch artery morphology / MGI
- abnormal retinal vasculature morphology / MGI
- abnormal axon guidance / MGI
- dilated heart atrium / MGI
- decreased tumor growth/size / MGI
- nervous system phenotype / MGI
- vascular smooth muscle hypoplasia / MGI
- transposition of great arteries / MGI
- abnormal coronary artery morphology / MGI
- right aortic arch / MGI
- double aortic arch / MGI
- abnormal dorsal aorta morphology / MGI
- abnormal brain vasculature morphology / MGI
- cardiovascular system phenotype / MGI
- vision/eye phenotype / MGI
- decreased angiogenesis / MGI
- abnormal neuronal migration / MGI
- abnormal fourth pharyngeal arch artery morphology / MGI
- abnormal sixth pharyngeal arch artery morphology / MGI
- abnormal third pharyngeal arch artery morphology / MGI
- abnormal induced retinal neovascularization / MGI
- abnormal retinal blood vessel morphology / MGI
- abnormal retinal blood vessel pattern / MGI
- abnormal first pharyngeal arch artery morphology / MGI
- abnormal second pharyngeal arch artery morphology / MGI
- abnormal aortic arch and aortic arch branch attachment / MGI
- abnormal coronary vessel morphology / MGI
- postnatal lethality, incomplete penetrance / MGI
- embryonic lethality, complete penetrance / MGI
- embryonic lethality during organogenesis, complete penetrance / MGI
Literature references
- VEGF165-induced vascular permeability requires NRP1 for ABL-mediated SRC family kinase activation.;Fantin Alessandro, Lampropoulou Anastasia, Senatore Valentina, Brash James T, Prahst Claudia, Lange Clemens A, Liyanage Sidath E, Raimondi Claudio, Bainbridge James W, Augustin Hellmut G, Ruhrberg Christiana, ;2017;The Journal of experimental medicine;214;1049-1064; 28289053
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