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anti-Human KDELR1 Antibodies:
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KDELR (show KDELR Antibodies) protein mediated the intracellular trafficking of Japanese encephalitis virus particles.
A Golgi-based KDELR (show KDELR Antibodies)-dependent signalling pathway controls invadopodia-dependent extracellular matrix degradation.
We propose a model whereby in analogy to previous findings (e.g., the RAS-RAF (show RAF1 Antibodies) signalling pathway), PHB (show PHB Antibodies) can act as a signalling scaffold protein (show HOMER1 Antibodies) to assist in KDELR (show KDELR Antibodies)-dependent Src (show SRC Antibodies) activation
It discuss the particular role of KDEL receptor (show KDELR Antibodies) signaling in the regulation of important pathways involved in the maintenance of the homeostasis of the transport apparatus, and in particular, of the Golgi complex.
KDEL receptor (show KDELR Antibodies) activates CREB1 (show CREB1 Antibodies) and other transcription factors that upregulate transport-related genes
These findings reveal an unexpected GPCR-like mode of action of the KDEL-R and shed light on a core molecular control mechanism of intra-Golgi traffic.
our data provide evidence that KDELR (show KDELR Antibodies), as a novel inducer of autophagy, participates in the degradation of misfolded neurodegenerative disease-related proteins.
Cystinosin (show CTNS Antibodies), MPDU1 (show MPDU1 Antibodies), SWEETs and KDELR (show KDELR Antibodies) belong to a well-defined protein family with putative function of cargo receptors.
the KDEL receptor (show KDELR Antibodies) participates in the ER stress response not only by its retrieval ability but also by modulating MAP kinase (show MAPK1 Antibodies) signaling
Src (show SRC Antibodies) relocated the KDEL receptor (show KDELR Antibodies) (KDEL-R) from the Golgi apparatus to the endoplasmic reticulum
In a mouse line having nonfunctional KDELR1, polyclonal naive T cells show excessive integrated stress responses, which are rescued by strong TCR-mediated signaling
present a recessive mouse missense allele of the prototypical mammalian KDEL receptor (show KDELR Antibodies), KDEL ER protein retention receptor 1 (KDELR1). Kdelr1 homozygous mutants were mildly lymphopenic, as were mice with a CRISPR/Cas9-engineered frameshift allele
dilated cardiomyopathy found in the mutant KDEL receptor (show KDELR Antibodies) transgenic mice is associated with ER stress
Retention of resident soluble proteins in the lumen of the endoplasmic reticulum (ER) is achieved in both yeast and animal cells by their continual retrieval from the cis-Golgi, or a pre-Golgi compartment. Sorting of these proteins is dependent on a C-terminal tetrapeptide signal, usually lys-asp-glu-leu (KDEL) in animal cells, and his-asp-glu-leu (HDEL) in S. cerevisiae. This process is mediated by a receptor that recognizes, and binds the tetrapeptide-containing protein, and returns it to the ER. In yeast, the sorting receptor encoded by a single gene, ERD2, which is a seven-transmembrane protein. Unlike yeast, several human homologs of the ERD2 gene, constituting the KDEL receptor gene family, have been described. The protein encoded by this gene was the first member of the family to be identified, and it encodes a protein structurally and functionally similar to the yeast ERD2 gene product.
ER lumen protein retaining receptor 1
, KDEL endoplasmic reticulum protein retention receptor 1
, KDEL receptor 1
, putative MAPK-activating protein PM23