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Calreticulin plays a key role in olfactory system function, possibly by establishing its overall sensitivity to odorants.
Calreticulin mediates hypersensitivity to diethylether and resistance to isoflurane in association with low expression of the gene.
These results collectively indicate that calreticulin is the first molecule to be identified as a marker for phagocytosis of apoptotic cells by Drosophila phagocytes
Although CALR mutations resulted in protein instability and proteosomal degradation, mutant CALR was able to enhance megakaryopoiesis and pro-platelet production from human CD34 (show CD34 ELISA Kits)(+) progenitors.
Studies show that all CALR mutations generate frameshift mutation in the exon 9, which encodes the C-terminus end conferring a common mutant-specific sequence in all mutants. Mutant CALR constitutively activates MPL (show MPL ELISA Kits) to induce cellular transformation. The interaction between the mutant CALR and MPL (show MPL ELISA Kits) is achieved by the conformational change in the C-terminal allowing N-domain binding to MPL (show MPL ELISA Kits). [review]
C-CALR in response to Ca2 (show CA2 ELISA Kits)+ undergoes conformational changes that trigger its function to export GR from the nucleus, resetting the stress response of normal erythroid cells. Impairment of this function in JAK2V617F-positive erythroid cells maintains EPO-R (show EPOR ELISA Kits) signaling in proliferation mode, contributing to erythrocytosis in PV.
Mannan-binding lectin (MBL (show MBL2 ELISA Kits)) bound to T cells through interaction between the collagen-like region of MBL (show MBL2 ELISA Kits) and calreticulin (CRT) expressed on the T-cell surface.
CRT (show SLC6A8 ELISA Kits) exposure represents a novel powerful prognostic biomarker for patients with acute myeloid leukemia (show BCL11A ELISA Kits).
In absence of CALR, immature MPO (show MPO ELISA Kits) protein precursors are degraded in the proteasome.
In patients with HD, a panel using calretinin and peripherin with or without MAP-2 may be most helpful in identifying transition zones
Coexisting mutations of the JAK2 (show JAK2 ELISA Kits), CALR, and MPL (show MPL ELISA Kits) genes in myeloproliferative neoplasms suggest that CALR and MPL (show MPL ELISA Kits) should be analyzed not only in JAK2 (show JAK2 ELISA Kits)-negative patients but also in low V617F mutation patients.
CALR-mutated essential thrombocythemia (ET) patients harbored a higher mutant load at progenitor level than JAK2V617F-positive ET (HSCs: 39.9% vs 7.5% p<0.001, hematopoietic stem cells)
Results indicate that NGF (show NGFB ELISA Kits) inhibited CRT (show SLC6A8 ELISA Kits) translocation induced by mitoxantrone. NGF (show NGFB ELISA Kits) effect on CRT (show SLC6A8 ELISA Kits) translocation could have consequences in immunotherapy, potentially lessening the effectiveness of this type of treatment.
These findings suggest that protein kinase C (show PKC ELISA Kits) is involved in the regulation of CRT function.
study provides a model showing that the C-terminal of mutant CALR activated JAK (show JAK3 ELISA Kits)-STAT (show STAT1 ELISA Kits) signaling specifically downstream of MPL (show MPL ELISA Kits) and may have a central role in CALR-induced myeloproliferative neoplasms
the results of this investigation provide the first molecular insights into the phospholipid binding site of calreticulin as a key anchor point for the cell surface expression of calreticulin on apoptotic cells
a profound impairment in calreticulin function when its lectin site was inactivated. Remarkably, inactivation of the polypeptide binding site had little impact. These findings indicate that the lectin-based mode of client interaction is the predominant contributor to the chaperone functions of calreticulin within the endoplasmic reticulum.
This essential role of calreticulin in nucleocytoplasmic communication competency ties its regulatory action with proficiency of cardiac myofibrillogenesis essential for proper cardiac development.
Study provides evidence that chronic stress activates calreticulin and might be one of the pathological mechanisms underlying the motor coordination and motor learning dysfunctions seen in social defeat mice.
This study for the first time revealed that increased CRT (show SLC6A8 ELISA Kits) inhibited Fas (show FAS ELISA Kits)/FasL (show FASL ELISA Kits)-mediated neuronal cell apoptosis during the early stage of ischemic stroke, suggesting it to be a potential protector activated soon after ischemia-reperfusion injury
The findings highlight the importance of CALR in female reproduction and demonstrate that compromised CALR function leads to ovarian insufficiency and female infertility.
Calreticulin mediates vascular smooth muscle cell responses to injury through the regulation of collagen deposition and neointima formation.
CALR mutants are sufficient to induce thrombocytosis through MPL (show MPL ELISA Kits) activation.
Thrombopoietin receptor (show MPL ELISA Kits) activation by myeloproliferative neoplasm associated calreticulin mutants.
the lectin site of CRT is the main target for gentamicin binding
Calreticulin is confined to subplasmalemmal vesicles partially overlapping with cortical granule contents. Its exocytosis after the oocyte activation seems to participate in the membrane block to polyspermy in pigs.
Calreticulin was widely expressed in pig tissues and its transcripts were downregulated during maturation, especially at 44 hr, and were undetectable at the blastocyst stage.
Calreticulin is a multifunctional protein that acts as a major Ca(2+)-binding (storage) protein in the lumen of the endoplasmic reticulum. It is also found in the nucleus, suggesting that it may have a role in transcription regulation. Calreticulin binds to the synthetic peptide KLGFFKR, which is almost identical to an amino acid sequence in the DNA-binding domain of the superfamily of nuclear receptors. Calreticulin binds to antibodies in certain sera of systemic lupus and Sjogren patients which contain anti-Ro/SSA antibodies, it is highly conserved among species, and it is located in the endoplasmic and sarcoplasmic reticulum where it may bind calcium. The amino terminus of calreticulin interacts with the DNA-binding domain of the glucocorticoid receptor and prevents the receptor from binding to its specific glucocorticoid response element. Calreticulin can inhibit the binding of androgen receptor to its hormone-responsive DNA element and can inhibit androgen receptor and retinoic acid receptor transcriptional activities in vivo, as well as retinoic acid-induced neuronal differentiation. Thus, calreticulin can act as an important modulator of the regulation of gene transcription by nuclear hormone receptors. Systemic lupus erythematosus is associated with increased autoantibody titers against calreticulin but calreticulin is not a Ro/SS-A antigen. Earlier papers referred to calreticulin as an Ro/SS-A antigen but this was later disproven. Increased autoantibody titer against human calreticulin is found in infants with complete congenital heart block of both the IgG and IgM classes.
, pot pourri
, ER-resident chaperone calreticulin
, Sicca syndrome antigen A (autoantigen Ro; calreticulin)
, endoplasmic reticulum resident protein 60
, calcium-binding protein 3
, Endoplasmic reticulum resident protein 60