Anti-GPR177/WLS antibody

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GPR177 also known as Wntless (WLS) is a protein that facilitates the transport of Wnt proteins. Wnt proteins are signaling molecules vital for various developmental processes. GPR177/WLS with an approximate mass of 50 kDa is expressed in multiple tissues particularly during early developmental stages. Its role involves the binding and shuttling of Wnt proteins from the Golgi apparatus to the cell surface making it essential for Wnt protein secretion and function.

Biological function summary

GPR177 plays a significant role in the Wnt signaling pathway. This pathway is a fundamental regulator of cellular processes such as proliferation and differentiation. GPR177 is necessary for the proper functioning of this pathway as it forms part of a larger protein complex responsible for Wnt ligand secretion. This complex includes other key proteins like the Evi and Wnt family proteins ensuring the efficient delivery and extracellular presentation of Wnt molecules.

Pathways

The involvement of GPR177 in the Wnt signaling highly influences developmental processes and cellular homeostasis given its pivotal connections to the canonical Wnt/β-catenin pathway and the non-canonical Wnt pathway. GPR177 collaborates specifically with proteins like β-catenin in the canonical pathway where it impacts gene transcription upon Wnt signaling activation. It also associates with signaling components of non-canonical pathways affecting planar cell polarity and calcium signaling which are essential for organismal development and maintenance.

Dysregulation in GPR177 function can contribute to abnormal Wnt signaling linking it to disorders such as cancer and osteoporosis. Abnormal expression or mutation of GPR177 affects the balance of Wnt signaling thereby promoting oncogenic processes in certain cancers by altering β-catenin levels. Moreover impaired Wnt signaling due to GPR177 dysfunction affects bone metabolism connecting it to osteoporosis. Alterations in Wnt pathway components including Frizzled receptors further influence these disease pathways demonstrating the broad impact of GPR177 misregulation.