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Molecular and Cellular Biology|December 28, 2020
Rothmund-Thomson Syndrome-Like RECQL4 Truncating Mutations Cause a Haploinsufficient Low-Bone-Mass Phenotype in MiceWilson Castillo-Tandazo, Ann E Frazier, Natalie A Sims, et al.Blood Advances|August 31, 2021
Genome-wide screening identifies cell-cycle control as a synthetic lethal pathway with SRSF2P95H mutationJane Jialu Xu, Alistair M Chalk, Iva Nikolic, et al.Experimental Hematology|November 9, 2018
Modeling human RNA spliceosome mutations in the mouse: not all mice were created equalJane Jialu Xu, Monique F Smeets, Shuh Ying Tan, et al.Leukemia|October 21, 2022
Srsf2P95H/+ co-operates with loss of TET2 to promote myeloid bias and initiate a chronic myelomonocytic leukemia-like disease in miceJane Jialu Xu, Alistair M Chalk, Meaghan Wall, et al.Plos Genetics|July 6, 2019
ATP-dependent helicase activity is dispensable for the physiological functions of Recql4Wilson Castillo-Tandazo, Monique F Smeets, Vincent Murphy, et al.FEBS Letters|January 31, 2025
Characteristics of the Kelch domain containing (KLHDC) subfamily and relationships with diseasesCourtney Pilcher, Paula Armina V Buco, Jia Q Truong, et al.The Journal of Clinical Investigation|June 25, 2014
The Rothmund-Thomson syndrome helicase RECQL4 is essential for hematopoiesisMonique F Smeets, Elisabetta DeLuca, Meaghan Wall, et al.Scientific Reports|October 22, 2015
Ciliary neurotrophic factor has intrinsic and extrinsic roles in regulating B cell differentiation and bone structureMaria Askmyr, Kirby E White, Tanja Jovic, et al.EMBO Reports|March 11, 2026
Minute amounts of helicase-deficient truncated RECQL4 are sufficient for DNA replicationPaula Armina V Buco, Wilson Castillo-Tandazo, Alistair M Chalk, et al.Plos Genetics|April 11, 2015
The DNA helicase recql4 is required for normal osteoblast expansion and osteosarcoma formationAlvin J M Ng, Mannu K Walia, Monique F Smeets, et al.Pageof 2