Browse our anti-SRY (Sex Determining Region Y)-Box 11 (SOX11) Antibodies

Human SRY (Sex Determining Region Y)-Box 11 (SOX11) interaction partners

1. CircCEP128 functions as a ceRNA for miR-145-5p, which could up regulate SOX11 and further promote cell proliferation and inhibit cell apoptosis of bladder cancer.

2. SOX11 promoter methylation plus AFP showed a sensitivity of 85% in discriminating hepatocellular carcinoma from chronic hepatitis B.

3. Data demonstrate a key role for SOX11 in normal kidney development and may suggest that variants in this gene predispose to CAKUT.

4. miR-223 was found to be negatively correlated with the mRNA level of SOX11 in clinical samples. Our work demonstrates for the first time that miR-223 is repressed and correlated with high-risk clinical features in MCL, which provides a potential molecule to target to optimize MCL management.

5. SOX11 hypermethylation was associated with adverse clinicopathological characteristics of prostate cancer

6. Our results confirm high specificity of SOX11 expression as a molecular marker for minimal residual disease in mantle cell lymphoma

7. Both SOX11 and TFE3 were overexpressed in solid-pseudopapillary neoplasms (SPNs) and may be involved in the pathogenesis.

8. Studied the association between miR-211-5p and SOX11 in regards to proliferation, viability, and invasion of human thyroid cancer (TC) cells. Found miR-211-5p was upregulated and SOX11 was downregulated in TC tissues and cell lines, and found By inhibiting SOX11, miR-211- 5p suppressed the proliferation and invasion of the TC cells.

9. REVIEW: addresses the implication of SOX11 overexpression and frequent genetic lesions, cooperating with cyclin D1 underlying the pathogenesis of mantle cell lymphoma

10. our work casts new light on the biology of mantle cell lymphoma (MCL), revealing the role of SOX11 exerting a functional effect through the repression of BCL6 transcription in MCL cells

11. Study showed for the first time that HIG-2 and SOX11 mutually co-regulate each other, and that HIG-2 and SOX11 knock-down promote increased proliferation in a non-synergistic manner in primary mantle cell lymphoma cells.

12. Solid pseudopapillary neoplasms (SPNs) showed positive staining for SRY-related high-mobility group box 11 (SOX-11), transcription factor E3 (TFE3) and beta-catenin on cell blocks.

13. SOX11 (sex determining region Y-box 11) was inversely expressed with miR-223-3p in ovarian cancer (OC) cell lines and tissue specimens. miR-223-3p mimic decreased SOX11 expression. Overexpressing SOX11 inhibited ovarian cancer cell proliferation and invasion, which indicated that miR-223-3p regulated OC cell proliferation and invasion through targeting SOX11 expression.

14. Our studies demonstrate that SOX11 is a critical regulator of multiple basal-like breast cancer phenotypes, including growth, migration, invasion, and expression of signature basal-like breast cancer genes

15. findings suggest that SOX11 is a potential biomarker for ductal carcinoma in situ lesions containing cells harbouring distinct biological features that are likely to progress to invasive breast cancer.

16. SOX11 antigen can be reliably detected in decalcified tissue bone marrow tissue from mantle cell lymphoma patients.

17. results suggest that SOX11 promotes MCL homing and invasion and increases CAM-DR through the direct regulation of CXCR4 and FAK expression and FAK/PI3K/AKT pathway activation, contributing to a more aggressive phenotype.

18. In this study we screened the transcriptional profiles of 70 MCL patients for SOXC cluster and miR17, miR18a, miR19b and miR92a, from the miR-17-92 cluster. Gene expression analysis showed higher SOX11 and SOX12 levels compared to SOX4 (P

19. Analysis of 28 other patients with CHARGE showed no SOX11 copy number changes or pathogenic sequence variants. To our knowledge, this child's chromosomal abnormality is unique and represents the first co-occurrence of duplication 2p25 and clinical features of CHARGE syndrome

20. SOX11 immunohistochemistry could be a useful adjunct in distinguishing secondary cutaneous mantle cell lymphoma from primary cutaneous B-cell lymphomas.

Mouse (Murine) SRY (Sex Determining Region Y)-Box 11 (SOX11) interaction partners

1. Data demonstrate a key role for SOX11 in normal kidney development and may suggest that variants in this gene predispose to CAKUT.

2. SOX11 represents a useful prognostic marker in mantle cell lymphoma.

3. Sox11 can induce substantial axon regeneration. Transcriptome profiling indicated that Sox11 activates genes involved in cytoskeletal remodeling and axon growth. Remarkably, alpha-RGCs, which preferentially regenerate following treatments such as Pten deletion, were killed by Sox11 overexpression. Thus, Sox11 promotes regeneration of non-alpha-RGCs, which are refractory to Pten deletion-induced regeneration.

4. These findings indicate that suppression of dendritic morphogenesis by Sox11 during radial migration is crucial for the formation of the cerebral cortex.

5. Following elevation of the palatal shelves (E14.5), Sox2, Sox11 and Sox21 expression was present in the midline epithelial seam. We thus identify dynamic spatio-temporal expression of Sox gene family during the process of palatogenesis

6. Sox11 directly regulates the expression of Fgf9; ablation of the Sox11 gene results in clefting of the secondary palate resembling the Pierre Robin sequence.

7. SOXC proteins act cell- and non-cell-autonomously in perichondrocytes and chondrocytes to establish noncanonical WNT signaling crosstalk essential for growth plate induction and control

8. Sox11 and Sox4 are not redundant in promoting neuronal differentiation in the cortex, but rather act in overlapping and discrete populations of neurons

9. Fetal Sox11 disruption lead to hypoplastic lungs, ventricular septation defects, abdominal defects, skeletal malformations, decreased birth weight and postnatal lethality.

10. regulates osteogenesis

11. These data identify Sox11 as a key transcription factor that can confer an elevated innate regenerative capacity to CNS neurons.

12. Sox11 expression was high in fetal.

13. Sox4 and Sox11 are required for proper development of cardiac neural crest cells.

14. The expression of Sox11 is increased in the injured spinal cord. Sox11 expression is located in ependymal cells lining the central canal and in newly-generated neurons in the injured spinal cord.

15. Sox11 is required for both embryonic and adult neurogenesis

16. Sox11 plays a crucial role in the proliferation and survival of mesenchymal and osteoblast precursors by Tead2, and osteogenic differentiation by regulating Runx2 and Osterix.

17. Data indicate that a complete loss of retinal ganglion cells (RGCs) was observed in Sox4/Sox11-null retinas, suggesting the two genes play similar roles in the development of RGCs.

18. TANK is expressed in DRG neurons. TANK is increased by peripheral nerve injury. the regulation of TANK expression is, at least in part, controlled by the injury-associated transcription factor Sox11.

19. This work implicates SOX11 as a potential regulator of GDF5 expression in joint maintenance and suggests a possible role in the pathogenesis of osteoarthritis

20. Data suggest that levels of Sox11 decline in developing retina; levels of histone H3-acetylation and H3-lysine 4 trimethylation at Sox11 gene locus decline during retinal development but increase markedly in adult retina.

Zebrafish SRY (Sex Determining Region Y)-Box 11 (SOX11) interaction partners

1. This study demonstrated that SOX11a strongly expressed in retinal ganglion cells (RGCs), and knockdown of Sox11a inhibited RGC axon regrowth in retinal explants.

2. Sox11a/b knockdown in zebrafish causes brain abnormalities, potentially explaining the brain phenotype of Coffin-Siris syndrome in humans.

3. our study reveals a novel role for Sox11 in controlling Hedgehog signaling, and suggests that SOX11 variants contribute to pediatric eye disorders.

4. the duplicated zebrafish sox11a and -b loci were used to test the duplication, degeneration, complementation model of genome evolution through whole genome duplication.