Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Electronic Gene Ontology annotations created by ARBA machine learning models
The Arabidopsis CLAVATA2 gene encodes a receptor-like protein required for the stability of the CLAVATA1 receptor-like kinase.
A genome-wide functional investigation into the roles of receptor-like proteins in Arabidopsis.
Analysis of interactions among the CLAVATA3 receptors reveals a direct interaction between CLAVATA2 and CORYNE in Arabidopsis.
Stem cell signaling in Arabidopsis requires CRN to localize CLV2 to the plasma membrane.
CLAVATA2 forms a distinct CLE-binding receptor complex regulating Arabidopsis stem cell specification.
Membrane distributions of two ligand-binding receptor complexes in the CLAVATA pathway.
CLAVATA signaling pathway receptors of Arabidopsis regulate cell proliferation in fruit organ formation as well as in meristems.
Shared and distinct functions of the pseudokinase CORYNE (CRN) in shoot and root stem cell maintenance of Arabidopsis.
Phosphate Starvation-Dependent Iron Mobilization Induces CLE14 Expression to Trigger Root Meristem Differentiation through CLV2/PEPR2 Signaling.
Perception of root-active CLE peptides requires CORYNE function in the phloem vasculature.
CLAVATA2, a regulator of meristem and organ development in Arabidopsis.
The 14-amino acid CLV3, CLE19, and CLE40 peptides trigger consumption of the root meristem in Arabidopsis through a CLAVATA2-dependent pathway.
The receptor kinase CORYNE of Arabidopsis transmits the stem cell-limiting signal CLAVATA3 independently of CLAVATA1.
Nematode CLE signaling in Arabidopsis requires CLAVATA2 and CORYNE.
Reevaluation of the CLV3-receptor interaction in the shoot apical meristem: dissection of the CLV3 signaling pathway from a direct ligand-binding point of view.
A group of receptor kinases are essential for CLAVATA signalling to maintain stem cell homeostasis.