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抗Mouse (Murine) 抗体:
抗Rat (Rattus) 抗体:
These human and mouse studies indicate that loss of NUP155 function causes atrial fibrillation by altering mRNA and protein transport and link the nuclear pore complex to cardiovascular disease.
The interaction of Nup53 (显示 NUP35 抗体) and Nup155 has a crucial role in nuclear pore complex formation.
In vivo depletion of Nup155 led to failure of nuclear lamina formation and defects in chromosome segregation at anaphase.
The Nup155-mediated localization was required for HDAC4 (显示 HDAC4 抗体)'s effect on gene expression.
The Nup155 depletion massively alters nuclear envelope structure, causing a dramatic decrease in Nuclear pore complexes numbers and the improper targeting of membrane proteins to the inner nuclear membrane.
Nucleoporins are the main components of the nuclear pore complex (NPC) of eukaryotic cells. They are involved in the bidirectional trafficking of molecules, especially mRNAs and proteins, between the nucleus and the cytoplasm. The protein encoded by this gene does not contain the typical FG repeat sequences found in most vertebrate nucleoporins. Two protein isoforms are encoded by transcript variants of this gene.
, nuclear pore protein
, nuclear pore complex protein Nup155-like
, 155 kDa nucleoporin
, nuclear pore complex protein Nup155
, nucleoporin Nup155
, nucleoporin 155kD