anti-Engrailed Homeobox 2 (EN2) Antibodies

Mouse (Murine) Engrailed Homeobox 2 (EN2) interaction partners

1. This study demonstrated that Ketogenic diet exposure during the juvenile period increases social behaviors and forebrain neural activation in adult Engrailed 2 null mice.

2. Study showed that BDNF (show BDNF Antibodies) signaling through its low-affinity receptor p75 (show NGFR Antibodies) is compromised in the forebrain of En2-/- mice; BDNF (show BDNF Antibodies) signaling deficits might be involved in the neurodevelopmental alterations observed in the En2-/- forebrain

3. En2 deletion reduces monoamine innervation of target forebrain structures, affecting forebrain structural growth, postnatal neurogenesis and related behavior.

4. confirm the early neurotransmitter deficit with a late compensatory recovery in En2 KO-mice further suggesting that this experimental animal may be considered a good predictive model for the human disease

5. The homeoprotein Engrailed is not only a survival factor for mesencephalic dopaminergic (mDA) neurons during development, but continues to exert neuroprotective and physiological functions in adult mDA neurons. [Review]

6. En2-/- hippocampus, neurofibromin (show NF1 Antibodies)-dependent pathways converging on SynI (show SYN1 Antibodies) phosphorylation might underlie hippocampal-dependent learning deficits observed in En2-/- mice.

7. This study demonistrated that engrailed 2 knock-out mice show impaired spatial learning with hippocampal dysreulation.

8. EN2 levels are increased in affected individuals with an A-C/G-T genotype, supporting EN2 as an autism spectrum disorder susceptibility gene.

9. This study showed that the Engrailed proteins are present in postnatal GABAergic neurons of the mouse hippocampus and cerebral cortex, and adult En2(-/-) mice show reduced expression of GABAergic marker mRNAs in these areas.

10. En1 (show EN1 Antibodies) is the predominant functional En paralog in maturing 5-HT (show DDC Antibodies) neurons, although a small contribution from En2 was reproducibly detected

Human Engrailed Homeobox 2 (EN2) interaction partners

1. The critical role of miR212 in inhibiting prostate tumor growth was verified in xenograft models of prostate cancer. These findings highlighted the role of miR212 in PCa (show FLVCR1 Antibodies) progression. More importantly, we speculate that EN-2 is a direct target gene of miR212.

2. We identified a novel heterozygous missense variant (c.425C>G, p.Pro142Arg) in the Engrailed 2 (EN2) gene in two patients. The G variant has never been reported in public databases and was absent in 100 Thai patients with ASD (show ARSD Antibodies) and 435 Thai controls. A case-control study showed that the G allele of c.425C>G was significantly associated with ASD (show ARSD Antibodies)

3. EN2 is negatively regulated by miR (show MLXIP Antibodies)-605, and down-regulation of miR (show MLXIP Antibodies)-605 promotes the proliferation and invasion of prostate cancer (PCa (show FLVCR1 Antibodies)) cells by up-regulating EN2, which leads to PCa (show FLVCR1 Antibodies) development and progression

4. Our data suggest that the functional interaction of miR (show MLXIP Antibodies)-33a and EN-2 is involved in tumorigenesis of prostate cancer

5. the results demonstrated that EN2 might play an anti-oncogenic role in oncogenesis and development of CCRCC, thereby maintaining the normal growth of human renal tubular epithelial cells.

6. EN2 may be a candidate oncogene in bladder cancer by activating the PI3K/Akt pathway and inhibiting PTEN.

7. Engrailed-2 (EN-2) is a developmentally regulated homeobox (show Lbx1 Antibodies) gene that is essential for Purkinje cell maturation and normal cerebellar development and patterning.

8. The mean EN2 levels in prostate cancer patients were 3.76-fold higher than those in non-prostate patients after prostate massage.

9. The exact role of EN2 expression in renal carcinoma (show TSC2 Antibodies) carcinogenesis requires further investigation.

10. En2 identified as a new regulator of T-cell differentiation whose disruption induces a malignant T-cell fate in chronic myelogenous leukemia progression.