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these results indicate the Appa (show APP Proteins)-RFP (show MKRN1 Proteins) and Aplp2 fusion proteins are likely secreted from the central nervous system and accumulate in the embryonic veins independent of blood flow.
This paper demonstrates an important role for APLP2 in refractive development in mice and humans, suggesting a high level of evolutionary conservation of the signaling pathways underlying refractive eye development.
Data show that amyloid precursor-like protein 2 (APLP2) expression is elevated in pancreatic cancer metastases.
We conclude that PCSK9 (show PCSK9 Proteins) enhances the degradation of the LDLR (show LDLR Proteins) independently of either APLP2 or sortilin (show SORT1 Proteins) both ex vivo and in mice.
APLP1 (show APLP1 Proteins) and APLP2, behave similarly to APP (show APP Proteins) in that they both associate with assembled NMDA receptors in the endoplasmic reticulum
our discoveries establish a role for APLP2 in the growth of pancreatic cancer cells and show that inhibitors preventing APLP2 cleavage reduce the viability of pancreatic cancer cells.
amyloid precursor protein-like (show APP Proteins) protein-2, but not amyloid precursor protein (show APP Proteins), is involved in mediating postendocytic delivery of PCSK9 (show PCSK9 Proteins) to lysosomes and is therefore important for PCSK9 (show PCSK9 Proteins) function
Aberrant enhancement of YWK-II/APLP2 by nuclear export of Bat3 (show BAT3 Proteins) may play a role in cancer development by inhibiting cell apoptosis.
APP (show APP Proteins) and its mammalian homologs, amyloid precursor-like proteins APLP1 (show APLP1 Proteins) and APLP2, participate under physiological conditions via trans-cellular dimerization in synaptogenesis.
APLP-2 (and APLP1 (show APLP1 Proteins)) are capable of activating gene transcription via binding to Mint3 (show APBA3 Proteins).
Regulation of major histocompatibility complex class I molecule expression on cancer cells by amyloid precursor-like protein 2.
APLP2 couples retina development and synaptic genes and present the first evidence that APLP2 expression may be linked to synaptic disease.
These data support the notion that APP (show APP Proteins) and APLP2 facilitate transmitter release, likely through the interaction with the neurotransmitter release machinery.
Study provides compelling evidence for an essential role of both APP (show APP Proteins) and APLP2 for neuronal and synaptic morphology as well as hippocampal function and suggest an acute and specific function of endogenous APPsalpha to facilitate synaptic plasticity
The study investigates the subcellular distribution patterns of the metal ions Cu, Zn, Fe, and Ca in individual neurons derived from APP (show APP Proteins) and APLP2 knockout mice brains to further define their role in metal homeostasis.
This study further highlights the distinct and essential role of APLP2 at NMJ synapses that cannot be compensated by APP (show APP Proteins).
Amyloid precursor protein (APP)/APP-like (show APP Proteins) protein 2 (APLP2) expression is required to initiate endosome-nucleus-autophagosome
The study investigated copper, iron, zinc and manganese levels in APP (show APP Proteins) and APLP-2 single knockout mice as well as homozygous:hemizygous knockout mice at 3, 12 and 18 plus months of age.
Data reveal that APLP2 is specifically required for proper cell cycle exit of neuronal progenitors, and thus has a distinct role in priming cortical progenitors for neuronal differentiation.
APLP2 and the intracellular domain of APP (show APP Proteins) are not essential for coherent activity patterns in the hippocampus, but have subtle effects on synaptic plasticity and fine-tuning of network oscillations.
This gene encodes amyloid precursor- like protein 2 (APLP2), which is a member of the APP (amyloid precursor protein) family including APP, APLP1 and APLP2. This protein is ubiquitously expressed. It contains heparin-, copper- and zinc- binding domains at the N-terminus, BPTI/Kunitz inhibitor and E2 domains in the middle region, and transmembrane and intracellular domains at the C-terminus. This protein interacts with major histocompatibility complex (MHC) class I molecules. The synergy of this protein and the APP is required to mediate neuromuscular transmission, spatial learning and synaptic plasticity. This protein has been implicated in the pathogenesis of Alzheimer's disease. Multiple alternatively spliced transcript variants encoding different isoforms have been identified.
amyloid beta (A4) precursor-like protein 2
, amyloid-beta-like protein B
, DIP13 beta
, adaptor protein, phosphotyrosine interaction, PH domain and leucine zipper containing 2
, suppression of tumorigenicity 14
, amyloid-like protein 2
, DCC-interacting protein 13-beta-like
, amyloid-like protein 2-like
, amyloid-beta-like protein A
, CDEI box-binding protein
, amyloid precursor protein homolog HSD-2
, Amyloid protein precursor-like protein 2
, amyloid beta (A4) precursor-like protein 2-like
, sperm membrane protein (YWK-II)
, sperm membrane protein YWK-II