anti-Dead End Homolog 1 (Zebrafish) (DND1) Antikörper

Mouse (Murine) Dead End Homolog 1 (Zebrafish) (DND1) Interaktionspartner

1. DND1 binds a UU(A/U) trinucleotide motif predominantly in the 3' untranslated regions of mRNA, and destabilizes target mRNAs through direct recruitment of the CCR4-NOT deadenylase complex.

2. DND1 interacts with NANOS2 to load unique RNAs into the CCR4-NOTdeaden complex; this interaction is mediated by the zinc finger domain of NANOS2, which is essential for its association with target RNAs; DND1 is an essential partner for NANOS2 that leads to the degradation of specific RNAs in male germ cell development

3. Dnd1 heterozygotes, lower oxygen availability was associated with metabolic differences

4. APOBEC3G inhibits DND1 function to regulate microRNA activity.

5. results show that Dnd1 is essential for normal allelic inheritance and that Dnd1Ter has a novel combination of functions that significantly increase risk for both testicular and intestinal cancer

6. DND1 is the first protein known to have an RNA recognition motif directly implicated as a heritable cause of spontaneous tumorigenesis

7. DND1-alpha isoform to be necessary for germ cell viability and its loss in Ter mice results in germ cell depletion, germ cell tumor development and partial embryonic lethality in the 129 strain.

8. Trans-generational epistasis between Dnd1Ter and other modifier genes controls susceptibility to testicular germ cell tumors.

9. The role of dead-end in germ-cell tumor development.

10. The interaction of DND1 and APOBEC3 could be one mechanism for maintaining viability of germ cells and for preventing germ cell tumor development

11. when Dnd1(Ter/Ter) XX germ cells developed in a testicular environment they gave rise to the same neoplastic clusters as mutant XY germ cells in a testis.

Human Dead End Homolog 1 (Zebrafish) (DND1) Interaktionspartner

1. Mechanistically, Dnd1 could bind to 3'-UTR of LATS2, the key kinase of Hippo pathway, thus elevating LATS2 mRNA stability and its expression, subsequently leading to phosphorylation of YAP and its cytoplasmic retention.

2. Dnd1 facilitates apoptosis by increasing the expression of Bim via its competitive combining with miR-221 in Bim-3'UTR.

3. RBM38 and DND1 are repressed in primary acute myeloid leukemia, neutrophil differentiation is dependent on increased expression of both proteins, and they have a role in regulating p21(CIP1) expression during acute promyelocytic leukemia differentiation

4. APOBEC3G inhibits DND1 function to regulate microRNA activity.

5. The increased sensitivity of transformed keratinocytes to miR-21's effects occurs in part through downregulation of the RNA-binding protein DND1 during the transformation process.

6. Results suggest that DND1 may impose another level of translational regulation to modulate expression of critical factors in ES cells.

7. We conclude that germline DND1 mutations are unlikely to contribute significantly to human testicular germ cell tumor susceptibility

8. Cloning of zebrafish dnd1 and identification of human DND1 by database analysis.

9. Unravels a novel role of Dnd1 in protecting certain mRNAs from miRNA-mediated repression.

10. MiR-24 up-regulation reduced the expression of RNA-binding protein dead end 1 (DND1). Knockdown of miR-24 led to enhanced expression of DND1.

11. The variant, p. Glu86Ala, found in only one case of testiciular germ cell tumor, is within a known functional domain of DND1 and is highly conserved through evolution; mutations in DND1 make, at most, a very small contribution to TGCT susceptibility