Browse our anti-SMARCE1 (SMARCE1) Antibodies

Human SWI/SNF Related, Matrix Associated, Actin Dependent Regulator of Chromatin, Subfamily E, Member 1 (SMARCE1) interaction partners

1. A de novo splicing mutation in SMARCE1 was identified in a patient with Angelman-like syndrome.

2. Study showed, for the first time, that SMARCE1 immunostaining is a highly sensitive biomarker for clear cell meningioma, useful as a routine diagnostic biomarker.

3. High SMARCE1 expression is associated with eventual relapse and metastasis in breast cancer.

4. miR-29a promotes hepatitis B virus (HBV) replication and expression through regulating SMARCE1 in HBV-infected HepG2.2.15 cells.

5. the malignancy risk in schwannomatosis is not well defined but may include an increased risk of malignant peripheral nerve sheath tumor in SMARCB1 Imaging protocols are also proposed for SMARCB1 and LZTR1 schwannomatosis and SMARCE1-related meningioma predisposition.

6. BAF57, BAF60a and SNF5 might act as novel pro-senescence factors in both normal and tumor human skin cells

7. We report here three additional individuals with clinical features consistent with CSS and alterations in SMARCE1, one of which is novel. The probands all exhibited dysmorphic facial features, moderate developmental and cognitive delay, poor growth, and hypoplastic digital nails/phalanges, including digits not typically affected in the other genes associated with CSS.

8. SMARCE1 mutational hits, including novel SMARCE1 mutations, were found in six of eight tested patients with clear cell meningioma

9. SMARCE1 plays an essential role in breast cancer metastasis by protecting cells against anoikis through the HIF1A/PTK2 pathway.

10. An exhaustive analysis of the BAF57 molecular and biochemical properties, cellular functions, loss-of-function phenotypes in living organisms and pathological manifestations in cases of human mutations. [review]

11. a family with a pediatric CCM patient and an adult CCM patient and several asymptomatic relatives carrying a germline SMARCE1 mutation.

12. Addition of the EGFR inhibitor gefitinib restores the sensitivity of SMARCE1-knockdown cells to MET and ALK inhibitors in NSCLCs. Our findings link SMARCE1 to EGFR oncogenic signaling and suggest targeted treatment options for SMARCE1-deficient tumors.

13. The results suggested that BAF57 is involved in ovarian cancer cell growth and sensitivity to anticancer agents, and that BAF57 may be a target for ovarian cancer therapy.

14. BAF complex gene SMARCE1 is mutated in Coffin-Siris syndrome patients.

15. Genotype-phenotype correlation of Coffin-Siris syndrome caused by mutations in SmarCE1 gene.

16. Since both TTF1 and SMARCE1 are involved in chromatin remodeling, our results imply an epigenetic regulatory mechanism for T-cell recruitment that invites deciphering.

17. these results demonstrate that loss of SMARCE1 is relevant to cranial as well as spinal meningiomas

18. Data indicate that BAF57 deregulation predisposes to metastasis.

19. Our findings identify multiple-spinal-meningioma disease as a new discrete entity and establish a key role for the SWI/SNF complex in the pathogenesis of both meningiomas and tumors with clear-cell histology.

20. mutations in BAF57 could impinge on several oncogenic signaling pathways contributing to the origin and/or development of breast cancer.

Mouse (Murine) SWI/SNF Related, Matrix Associated, Actin Dependent Regulator of Chromatin, Subfamily E, Member 1 (SMARCE1) interaction partners

1. These results reveal a novel function of BAF57 as an essential regulator of T cell activation.

2. The N terminus of Brdt is involved in the recognition of Smarce1 as well as in the reorganization of hyperacetylated round spermatid chromatin.

3. suggest a novel mechanism for transcriptional repression by TSHZ3 in which TSHZ3 and BAF57 cooperate to modulate MyoD activity on the Myog promoter to regulate skeletal muscle differentiation.

4. Data show that neuregulin-1 (NRG) inhibition is followed by a decrease in NSC proliferation and of neuronal or oligodendroglial differentiation, and that Nrg-1 physically interacts with BRM and BAF57.

5. Reciprocal regulation of CD4/CD8 expression by SWI/SNF-like BAF complexes.

6. The ER interacts with BAF57, which is stimulated by estrogen and requires both a functional hormone-binding domain & the DNA-binding region of the ER. The p160 family of coactivators interacts with BAF57. Their potentiation of transcription depends on it.

7. Smarce1 (Baf27)is a critical modulator of the androgen neceptor (AR) that is capable of altering AR activity, coactivator function, and AR-dependent proliferation.

8. BAF complex uses BAF57 to remodel the endogenous, H1-containing chromatin at the CD4 silencer, which facilitates the binding of Runx1, a key repressor of CD4 transcription.