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anti-Mouse (Murine) GEN1 Antikörper:
anti-Human GEN1 Antikörper:
anti-Rat (Rattus) GEN1 Antikörper:
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Study found that a Gen1 mutation alone did not affect DNA repair or meiotic recombination in mice; it caused synthetic lethality when combined with Eme1 mutations at an early embryonic stage. Also, combination of Gen1 and Eme1 mutations makes embryonic fibroblasts more sensitive to DNA damage & mice less capable of meiotic recombination. These results indicate that Gen1 and Eme1 are functionally redundant in mice.
The results suggest that GEN1 may play an important role in the development of mammary gland.
GEN1 efficiently cleaves both single and double Holliday junctions contained within large recombination intermediates. Moreover, we find that GEN1 exhibits a weak sequence preference for incision between two G residues that reside in a T-rich region of DNA.
Data suggest that dimeric GEN1 binds with high affinity/selectivity to Holliday junctions, introducing two symmetrical hydrolytic cleavages of phosphodiester backbone; at present, less is known about SLX1-SLX4-MUS81-EME1 resolving enzyme complex. (GEN1 = Holliday junction 5' flap endonuclease; SLX = structure-specific endonuclease subunit; MUS81 = MUS81 endonuclease; EME1 = essential meiotic endonuclease 1) [REVIEW]
human GEN1 protein promotes Holliday junction resolution by a mechanism that is analogous to that exhibited by the prototypic HJ resolvase E. coli RuvC.
GEN1 is controlled by nuclear exclusion, driven by a nuclear export signal that restricts GEN1 actions to mitosis. Spatial control of GEN1 contributes to genome stability by avoiding competition with non-crossover promoting repair pathways.
GEN1 activity cannot be substituted for the SLX4 (zeige BTBD12 Antikörper)-associated nucleases, and one of the HJ resolvase activities, either of those associated with SLX4 (zeige BTBD12 Antikörper) or with GEN1, is required for cell viability, even in the presence of BLM (zeige BLM Antikörper).
Data show that three structure-selective endonucleases, SLX1-SLX4 (zeige BTBD12 Antikörper), MUS81 (zeige MUS81 Antikörper)-EME1, and GEN1, define two pathways of Holliday junctions (HJs) resolution in HeLa cells.
Study observed centrosome defects in the absence of XRCC3 (zeige XRCC3 Antikörper). While RAD51B (zeige Rad51B Antikörper) and RAD51C (zeige RAD51C Antikörper) act early in homologous recombination, XRCC3 (zeige XRCC3 Antikörper) functions jointly with GEN1 later in the pathway at the stage of Holliday junction resolution.
Our findings provide novel insight into the biological functions of GEN1 by uncovering an important role of GEN1 in the regulation of centrosome integrity.
Data indicate that although it also plays a key role in double-strand DNA break repair, GEN1 does not make an appreciable contribution to breast cancer susceptibility by acting as a high- or intermediate-penetrance breast cancer predisposition gene.
Study shows that, like E coli Holliday junction (HJ)resolvase RuvC, GEN1 binds specifically to HJs and resolves them by a dual incision mechanism in which nicks are introduced in the pair of continuous strands within the lifetime of the GEN1-HJ complex.
Endonuclease which resolves Holliday junctions by the introduction of symmetrically related cuts across the junction point, to produce nicked duplex products in which the nicks can be readily ligated. Four-way DNA intermediates, also known as Holliday junctions, are formed during homologous recombination and DNA repair, and their resolution is necessary for proper chromosome segregation.
Gen homolog 1, endonuclease
, flap endonuclease GEN homolog 1
, Gen endonuclease homolog 1
, Holliday junction resolvase