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FANCE encodes the complementation group E subunit of the multimeric Fanconi anemia (FA) nuclear complex composed of proteins encoded by over ten Fanconi anemia complementation (FANC) group genes: FANCA, FANCB, FANCC, FANCD1 (also called BRCA2), FANCD2. Zusätzlich bieten wir Ihnen Fanconi Anemia, Complementation Group E Proteine (2) und viele weitere Produktgruppen zu diesem Protein an.
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Human Polyclonal FANCE Primary Antibody für ELISA, IHC - ABIN4310515
Barroso, Pita, Arias, Menendez, Zamora, Blanco, Benitez, Ribas: The Fanconi anemia family of genes and its correlation with breast cancer susceptibility and breast cancer features. in Breast cancer research and treatment 2009
A novel alternative splicing event of the FANCE gene has been characterized. FANCEDelta4 cannot support the activation of the FANC-BRCA pathway and DNA repair.
a phenylalanine located at the highly conserved extreme C terminus, referred to as Phe-522, is a critical residue for mediating the monoubiquitination of the FANCD2 (zeige FANCD2 Antikörper)-FANCI (zeige FANCI Antikörper) complex.
FANCE protein is part of the FA nuclear complex, binding FANCC & FAN (zeige PALB2 Antikörper)CD2. It is required for the nuclear accumulation of FANCC and provides a bridge between the FA complex and FANCD2. FANCC mutants do not bind FANCE or prevent chromosome breakage.
This Fanconi anemia protein (zeige FANCF Antikörper) promotes the nuclear accumulation of FANCC (zeige FANCC Antikörper).
FANCC (zeige FANCC Antikörper), FANCE, and FANCD2 (zeige FANCD2 Antikörper) form a ternary complex in the Fanconi anemia (zeige PALB2 Antikörper) DNA damage response pathway
nuclear accumulation of FANCE does not rely solely on its nuclear localization signal motifs, but also on FANCC (zeige FANCC Antikörper)
Chk1 (zeige CHEK1 Antikörper)-mediated phosphorylation of FANCE is required for a function independent of FANCD2 (zeige FANCD2 Antikörper) monoubiquitination.
Disease-associated mutations disrupt the FANCE-FANCD2 (zeige FANCD2 Antikörper) interaction, providing structural insight into the molecular mechanisms of Fanconi Anaemia pathogenesis.
Results provide evidence that fance protein plays an important, but not absolutely essential, role in the initial developmental expansion of the male germ line.
Primary ovarian insufficiency is induced by Fance mutation in a mouse model.
The fact that defects in the human ortholog result in Fanconi anemia (zeige PALB2 Antikörper) disease suggests that this protein has a critical function and is likely evolutionarily conserved.
The Fanconi anemia complementation group (FANC) currently includes FANCA, FANCB, FANCC, FANCD1 (also called BRCA2), FANCD2, FANCE, FANCF, FANCG, FANCI, FANCJ (also called BRIP1), FANCL, FANCM and FANCN (also called PALB2). The previously defined group FANCH is the same as FANCA. Fanconi anemia is a genetically heterogeneous recessive disorder characterized by cytogenetic instability, hypersensitivity to DNA crosslinking agents, increased chromosomal breakage, and defective DNA repair. The members of the Fanconi anemia complementation group do not share sequence similarity\; they are related by their assembly into a common nuclear protein complex. This gene encodes the protein for complementation group E.
Fanconi anemia, complementation group E
, Fanconi anemia E
, Fanconi anemia group E protein
, fanconi anemia group E protein-like
, Fanconi anemia group E protein-like