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Human Monoclonal HERPUD1 Primary Antibody for IHC (p), IP - ABIN564201
Lass, Kujawa, McConnell, Paton, Paton, Wójcik: Decreased ER-associated degradation of alpha-TCR induced by Grp78 depletion with the SubAB cytotoxin. in The international journal of biochemistry & cell biology 2008
Show all 3 Pubmed References
Human Polyclonal HERPUD1 Primary Antibody for ELISA, WB - ABIN564199
Hong, Kim, Kim, Lee, Shin, Son, Han, Sung, Kwon: Apoptosis induction of 2'-hydroxycinnamaldehyde as a proteasome inhibitor is associated with ER stress and mitochondrial perturbation in cancer cells. in Biochemical pharmacology 2007
This study showed that Herp stability was regulated by synoviolin through lysine ubiquitination-independent proteasomal degradation.
HERP plays an important role in the regulation of host innate immunity in response to ER stress during the infection of RNA viruses.
results indicated that low expression of miR (show MLXIP Antibodies)-9-3p results in a high level of Herpud1, which may protect against apoptosis in glioma
Thus, our findings indicated that NQO1 (show NQO1 Antibodies) could stabilize Herp protein expression via indirect regulation of synoviolin.
The authors found that the CREB3 (show CREB3 Antibodies)/Herp pathway limited the increase in cytosolic Ca2 (show CA2 Antibodies)+ concentration and apoptosis early in poliovirus infection and this may reduce the extent of poliovirus-induced damage to the central nervous system during poliomyelitis.
HERPUD1 SNPs are highly associated with polypoidal choroidal vasculopathy.
concluded that the HERPUD1-mediated cytoprotective effect against oxidative stress depends on the ITPR and Ca(2 (show CA2 Antibodies)+) transfer from the endoplasmic reticulum to mitochondria
The results indicate that Nrf1 (show NFE2L1 Antibodies) is a transcriptional activator of Herpud1 expression during ER stress, and they suggest Nrf1 (show NFE2L1 Antibodies) is a key player in the regulation of the ER stress response in cells.
Herp operates as a relevant factor in the defense against glucose starvation by modulating autophagy levels.
Together with histological grade, increased co-expression of MIF (show AMH Antibodies) and MMP9 (show MMP9 Antibodies) in tumor might be a valuable predictor for recurrence, especially for benign meningiomas
Herpud1 is necessary for adequate insulin-induced glucose uptake due to its role in Ca(2+)/calcineurin regulation in L6 myotubes.
Herp may regulate the cell cycle and hormone secretions in mouse granulosa cells
Herp lentiviral shRNA vectors had been successfully constructed; knockdown Herp inhibited ER stress and had a different effect on inflammatory responses in RAW 264.7 macrophages depending on whether they were exposed to tunicamycin or thapsigargin
Herp localizes to the endoplasmic reticulum-derived quality control compartment (ERQC) and recruits HRD1, which targets to endoplasmic reticulum associated degradation the substrate presented by the OS-9 lectin at the ERQC.
A deficiency of Herp, an endoplasmic reticulum stress protein, suppresses atherosclerosis in ApoE (show APOE Antibodies) knockout mice by attenuating inflammatory responses.
Data conclude that Herpud1 regulates insulin (show INS Antibodies) secretion via control of Nnt (show NNT Antibodies) expression.
Derlin-1 (show DERL1 Antibodies) deficiency is embryonic lethal, Derlin-3 (show DERL3 Antibodies) deficiency appears normal, and Herp deficiency is intolerant to glucose load and ischemia in mice
increased NADH levels resulting from ENOX2 (show ENOX2 Antibodies) inhibition result in decreased prosurvival sphingosine-1-phosphate and increased proapoptotic ceramide, both of which may be important to initiation of the ENOX2 (show ENOX2 Antibodies) inhibitor-induced apoptotic cascade.
upregulation by Wnt-1 (show WNT1 Antibodies)
The accumulation of unfolded proteins in the endoplasmic reticulum (ER) triggers the ER stress response. This response includes the inhibition of translation to prevent further accumulation of unfolded proteins, the increased expression of proteins involved in polypeptide folding, known as the unfolded protein response (UPR), and the destruction of misfolded proteins by the ER-associated protein degradation (ERAD) system. This gene may play a role in both UPR and ERAD. Its expression is induced by UPR and it has an ER stress response element in its promoter region while the encoded protein has an N-terminal ubiquitin-like domain which may interact with the ERAD system. This protein has been shown to interact with presenilin proteins and to increase the level of amyloid-beta protein following its overexpression. Alternative splicing of this gene produces multiple transcript variants encoding different isoforms. The full-length nature of all transcript variants has not been determined.
homocysteine-inducible, endoplasmic reticulum stress-inducible, ubiquitin-like domain member 1
, homocysteine-responsive endoplasmic reticulum-resident ubiquitin-like domain member 1 protein
, homocysteine-inducible endoplasmic reticulum stress-inducible ubiquitin-like domain member 1 protein
, methyl methanesulfonate (MMF)-inducible fragment protein 1