Associated Papers
Mutations to transcription factor MAX allosterically increase DNA selectivity by altering folding and binding pathways.
Hastings R et al.
Nature Communications, 2025
39805837 (PubMed )
Supplement: 41467_2024_55672_MOESM7_ESM.pdf
Genotype and clinical phenotype characteristics of MAX germline mutation-associated pheochromocytoma/paraganglioma syndrome.
Lian B et al.
Frontiers in Endocrinology, 2024
Bilateral Pheochromocytoma with Germline MAX Variant without Family History.
Hata S et al.
Clinics and Practice, 2022
35645312 (PubMed )
Supplement: clinpract-12-00035-s001.zip › clinpract-1702561-supplementary.pdf
MYCN and MAX alterations in Wilms tumor and identification of novel N-MYC interaction partners as biomarker candidates.
Jiménez Martín O et al.
Cancer Cell International, 2021
MAX Mutations in Endometrial Cancer: Clinicopathologic Associations and Recurrent MAX p.His28Arg Functional Characterization.
Walker CJ et al.
Journal of the National Cancer Institute, 2018
Functional and in silico assessment of MAX variants of unknown significance.
Comino-Méndez I et al.
Journal of Molecular Medicine (berlin, Germany), 2015
MAX mutations cause hereditary and sporadic pheochromocytoma and paraganglioma.
Burnichon N et al.
Clinical Cancer Research : an Official Journal of the American Association for Cancer Research, 2012
Select a paper to view details