rhoa ras homolog family member A
Phenotypes manually curated with terms from the Xenopus phenotype ontology covering anatomical, gene ontology, and neurobehavioral phenotypes.
|increased thickness of the blastocoel roof (2 sources), abnormal animal cap morphology (1 source), abnormal blastocoel roof morphology (1 source), abnormal cell division (1 source), abnormal cell morphology (1 source), abnormal epithelial cell (1 source), abnormally anterioralized embryo (1 source), abnormally decreased number of filamentous actin in the blastocoel roof (1 source), abnormally delayed closure of blastopore (1 source), abnormally increased number of filamentous actin in the blastocoel roof (1 source), abnormally localised head (1 source), absent upper blastopore lip (1 source), duplicated anterior-posterior axis (1 source), duplicated head (1 source), increased cell population proliferation in epithelium (1 source), increased pigmentation in the animal hemisphere (1 source)|
Gene expression phenotype annotations where the gene of interest has been disrupted (manipulated) or is the gene assayed (assayed). Computed annotations are derived from differential expression analysis from Xenbase processed GEO data with the criteria of a TPM >= 1, FDR <= 0.05 and an absolute LogFC >= 2.
|Manual annotations: rhoa manipulated (3 sources)|
These are short form descriptions of experiments using reagents targeting the gene of interest.
|Xla Wt + Tg(Hsa.rhoaQ63L:GFP (4 sources), Xla Wt + rhoa (3 sources), Xla Wt + rhoa (3 sources), Xla Wt + dnHsa.rhoa (2 sources), Xla Wt + rhoa + dnbmpr1a (1 source), Xla Wt + dnrhoa (1 source)|
|Monarch Ortholog Phenotypes
These phenotypes are associated with this gene with a has phenotype relation via Monarch.
Mouse (15 sources):
abnormal brain development,
abnormal midbrain development,
abnormal neural tube ventricular layer morphology,
abnormal neuron proliferation,
abnormal neuronal precursor proliferation,
embryonic lethality, complete penetrance,
increased T cell proliferation,
increased T follicular helper cell number,
increased midbrain size,
increased neuronal precursor cell number,
increased regulatory T cell number, increased spinal cord apoptosis, nervous system phenotype, no abnormal phenotype detected, premature neuronal precursor differentiation[+]