| CSB and SMARCAL1 compete for RPA32 at stalled forks and differentially control the fate of stalled forks in BRCA2-deficient cells. | CSB and SMARCAL1 compete for RPA32 at stalled forks and differentially control the fate of stalled forks in BRCA2-deficient cells.
Batenburg NL, Sowa DJ, Walker JR, Andres SN, Zhu XD., Free PMC Article | 06/10/2024 |
| Oncogenic functions and therapeutic potentials of targeted inhibition of SMARCAL1 in small cell lung cancer. | Oncogenic functions and therapeutic potentials of targeted inhibition of SMARCAL1 in small cell lung cancer.
Sun BB, Wang GZ, Han SC, Yang FY, Guo H, Liu J, Liu YT, Zhou GB. | 06/8/2024 |
| Cancer-associated SMARCAL1 loss-of-function mutations promote alternative lengthening of telomeres and tumorigenesis in telomerase-negative glioblastoma cells. | Cancer-associated SMARCAL1 loss-of-function mutations promote alternative lengthening of telomeres and tumorigenesis in telomerase-negative glioblastoma cells.
Liu H, Xu C, Diplas BH, Brown A, Strickland LM, Yao H, Ling J, McLendon RE, Keir ST, Ashley DM, He Y, Waitkus MS., Free PMC Article | 09/7/2023 |
| Different Phenotypes of Schimke Immuno-Osseous Dysplasia (SIOD) in Two Sisters with the Same Mutation in the SMARCAL1 Gene. | Different Phenotypes of Schimke Immuno-Osseous Dysplasia (SIOD) in Two Sisters with the Same Mutation in the SMARCAL1 Gene.
Castellano-Martinez A, Acuñas-Soto S, Varga-Martinez R, Rodriguez-Gonzalez M, Mora-Lopez F, Iriarte-Gahete M, Roldan-Cano V. | 09/10/2022 |
| SMARCAL1 loss and alternative lengthening of telomeres (ALT) are enriched in giant cell glioblastoma. | SMARCAL1 loss and alternative lengthening of telomeres (ALT) are enriched in giant cell glioblastoma.
Brosnan-Cashman JA, Davis CM, Diplas BH, Meeker AK, Rodriguez FJ, Heaphy CM. | 03/19/2022 |
| A patient with Silver-Russell syndrome with multilocus imprinting disturbance, and Schimke immuno-osseous dysplasia unmasked by uniparental isodisomy of chromosome 2. | A patient with Silver-Russell syndrome with multilocus imprinting disturbance, and Schimke immuno-osseous dysplasia unmasked by uniparental isodisomy of chromosome 2.
Hara-Isono K, Matsubara K, Hamada R, Shimada S, Yamaguchi T, Wakui K, Miyazaki O, Muroya K, Kurosawa K, Fukami M, Ogata T, Kosho T, Kagami M. | 02/12/2022 |
| SMARCAL1, the annealing helicase and the transcriptional co-regulator. | SMARCAL1, the annealing helicase and the transcriptional co-regulator.
Bansal R, Hussain S, Chanana UB, Bisht D, Goel I, Muthuswami R. | 12/4/2021 |
| Time for remodeling: SNF2-family DNA translocases in replication fork metabolism and human disease. | Time for remodeling: SNF2-family DNA translocases in replication fork metabolism and human disease.
Joseph SA, Taglialatela A, Leuzzi G, Huang JW, Cuella-Martin R, Ciccia A., Free PMC Article | 04/3/2021 |
| SMARCAL1-deficient induced pluripotent stem cells maintain active DNA damage response beyond differentiation. | Inducible SMARCAL1 knockdown in iPSC reveals a link between replication stress and altered expression of master differentiation genes.
Pugliese GM, Salaris F, Palermo V, Marabitti V, Morina N, Rosa A, Franchitto A, Pichierri P., Free PMC Article | 05/30/2020 |
| EXD2 deficiency leads to fork collapse, hypersensitivity to replication inhibitors, and genomic instability. Impeding fork regression by inactivation of SMARCAL1 or removal of RECQ1's inhibition in EXD2(-/-) cells restores efficient fork restart and genome stability. Moreover, purified EXD2 efficiently processes substrates mimicking regressed forks. | EXD2 Protects Stressed Replication Forks and Is Required for Cell Viability in the Absence of BRCA1/2.
Nieminuszczy J, Broderick R, Bellani MA, Smethurst E, Schwab RA, Cherdyntseva V, Evmorfopoulou T, Lin YL, Minczuk M, Pasero P, Gagos S, Seidman MM, Niedzwiedz W., Free PMC Article | 01/18/2020 |
| Downregulation of SMARCAL1 and BRG1 results in downregulation of ATM and ATR and therefore, mitotic abnormalities. | Regulation of ATM and ATR by SMARCAL1 and BRG1.
Sethy R, Rakesh R, Patne K, Arya V, Sharma T, Haokip DT, Kumari R, Muthuswami R. | 06/1/2019 |
| Mcm10 is a potent DNA strand-annealing protein that inhibits fork regression by SMARCAL1. | Mcm10 has potent strand-annealing activity and limits translocase-mediated fork regression.
Mayle R, Langston L, Molloy KR, Zhang D, Chait BT, O'Donnell ME., Free PMC Article | 03/16/2019 |
| A large number of SNF2 family, DNA and ATP-dependent motor proteins are needed during transcription, DNA replication, and DNA repair to manipulate protein-DNA interactions and change DNA structure. SMARCAL1, ZRANB3, and HLTF are three related members of this family with specialized functions that maintain genome stability during DNA replication. [review] | Functions of SMARCAL1, ZRANB3, and HLTF in maintaining genome stability.
Poole LA, Cortez D., Free PMC Article | 12/16/2017 |
| The main roles of SMARCAL1 in DNA repair, telomere maintenance and replication fork stability in response to DNA replication stress are reviewed. | The role of SMARCAL1 in replication fork stability and telomere maintenance.
Lugli N, Sotiriou SK, Halazonetis TD. | 11/18/2017 |
| BRG1 and SMARCAL1, members of the ATP-dependent chromatin remodelling family, are shown to co-regulate the transcription of DROSHA, DGCR8, and DICER in response to double-strand DNA breaks. | BRG1 and SMARCAL1 transcriptionally co-regulate DROSHA, DGCR8 and DICER in response to doxorubicin-induced DNA damage.
Patne K, Rakesh R, Arya V, Chanana UB, Sethy R, Swer PB, Muthuswami R. | 11/4/2017 |
| depletion of SMARCAL1, a SNF2-family DNA translocase that remodels stalled forks, restores replication fork stability and reduces the formation of replication stress-induced DNA breaks and chromosomal aberrations in BRCA1/2-deficient cells. In addition to SMARCAL1, other SNF2-family fork remodelers, including ZRANB3 and HLTF, cause nascent DNA degradation and genomic instability | Restoration of Replication Fork Stability in BRCA1- and BRCA2-Deficient Cells by Inactivation of SNF2-Family Fork Remodelers.
Taglialatela A, Alvarez S, Leuzzi G, Sannino V, Ranjha L, Huang JW, Madubata C, Anand R, Levy B, Rabadan R, Cejka P, Costanzo V, Ciccia A., Free PMC Article | 10/28/2017 |
| our data reveal the critical function of the DNA replication stress response and, specifically, Smarcal1 in hematopoietic cell survival and tumor development. Our results also provide important insight into the immunodeficiency observed in individuals with mutations in SMARCAL1 by suggesting that it is an HSPC defect. | Defective replication stress response inhibits lymphomagenesis and impairs lymphocyte reconstitution.
Puccetti MV, Fischer MA, Arrate MP, Boyd KL, Duszynski RJ, Bétous R, Cortez D, Eischen CM., Free PMC Article | 09/9/2017 |
| the mechanism of SMARCAL1 function in maintaining genome stability | SMARCAL1 and telomeres: Replicating the troublesome ends.
Poole LA, Cortez D., Free PMC Article | 05/20/2017 |
| deficiency of a SMARCAL1 ortholog altering the chromatin structure of a gene | Chromatin changes in SMARCAL1 deficiency: A hypothesis for the gene expression alterations of Schimke immuno-osseous dysplasia.
Morimoto M, Choi K, Boerkoel CF, Cho KS., Free PMC Article | 05/13/2017 |
| Results provide evidence that BRG1 and SMARCAL1 regulate each other. BRG1 binds to the SMARCAL1 promoter, while SMARCAL1 binds to the brg1 promoter. During DNA damage, the occupancy of SMARCAL1 on the brg1 promoter increases coinciding with an increase in BRG1 occupancy on the SMARCAL1 promoter, leading to increased brg1 and SMARCAL1 transcripts respectively. | Transcriptional Regulation of Atp-Dependent Chromatin Remodeling Factors: Smarcal1 and Brg1 Mutually Co-Regulate Each Other.
Haokip DT, Goel I, Arya V, Sharma T, Kumari R, Priya R, Singh M, Muthuswami R., Free PMC Article | 01/14/2017 |
| the replication stress response protein SMARCAL1 is a critical regulator of alternative lengthening of telomeres activity. | SMARCAL1 Resolves Replication Stress at ALT Telomeres.
Cox KE, Maréchal A, Flynn RL., Free PMC Article | 11/5/2016 |
| SMARCAL1 negatively regulates c-myc transcription by altering the conformation of its promoter region during differentiation. | SMARCAL1 Negatively Regulates C-Myc Transcription By Altering The Conformation Of The Promoter Region.
Sharma T, Bansal R, Haokip DT, Goel I, Muthuswami R., Free PMC Article | 10/22/2016 |
| Mutations in human SMARCAL1 that result in loss in ATPase activity lead to increased replication stress and therefore possibly manifestation of Schimke immuno-osseous dysplasia. | Ligand-induced conformation changes drive ATP hydrolysis and function in SMARCAL1.
Gupta M, Mazumder M, Dhatchinamoorthy K, Nongkhlaw M, Haokip DT, Gourinath S, Komath SS, Muthuswami R. | 04/30/2016 |
| results provide the first identification, to our knowledge, of an endogenous source of replication stress that requires SMARCAL1 for resolution and define differences between members of this class of replication fork-repair enzymes. | SMARCAL1 maintains telomere integrity during DNA replication.
Poole LA, Zhao R, Glick GG, Lovejoy CA, Eischen CM, Cortez D., Free PMC Article | 04/16/2016 |
| The results suggest that Smarcal1 enhances nonhomologous end-joining repair, presumably by interacting with RPA at unwound single-strand sequences and then facilitating annealing at double-strand-break ends. | Smarcal1 promotes double-strand-break repair by nonhomologous end-joining.
Keka IS, Mohiuddin, Maede Y, Rahman MM, Sakuma T, Honma M, Yamamoto T, Takeda S, Sasanuma H., Free PMC Article | 10/24/2015 |