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anti-Human Calreticulin Antibodies:
anti-Mouse (Murine) Calreticulin Antibodies:
anti-Rat (Rattus) Calreticulin Antibodies:
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Cow (Bovine) Polyclonal Calreticulin Primary Antibody for BP, DB - ABIN153063
Placantonakis, Cicirata, Welsh: A dominant negative mutation of neuronal connexin 36 that blocks intercellular permeability. in Brain research. Molecular brain research 2002
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Polyclonal Calreticulin Primary Antibody for IHC (fro), IF - ABIN540420
Zhou, Tanaka, Sekiguchi, He, Yasuoka, Itoh, Kawahara, Abe: ATP-sensitive K+-channel subunits on the mitochondria and endoplasmic reticulum of rat cardiomyocytes. in The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society 2005
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Chicken Polyclonal Calreticulin Primary Antibody for ICC, FACS - ABIN361835
Antoniou, Ford, Pilley, Blake, Powis: Interactions formed by individually expressed TAP1 and TAP2 polypeptide subunits. in Immunology 2002
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Human Polyclonal Calreticulin Primary Antibody for ICC, IF - ABIN269297
Leslie, Watkins, Kim, Brouwer: Differential inhibition of rat and human Na+-dependent taurocholate cotransporting polypeptide (NTCP/SLC10A1)by bosentan: a mechanism for species differences in hepatotoxicity. in The Journal of pharmacology and experimental therapeutics 2007
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Human Polyclonal Calreticulin Primary Antibody for WB - ABIN2801959
McCauliffe, Lux, Lieu, Sanz, Hanke, Newkirk, Bachinski, Itoh, Siciliano, Reichlin: Molecular cloning, expression, and chromosome 19 localization of a human Ro/SS-A autoantigen. in The Journal of clinical investigation 1990
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Human Polyclonal Calreticulin Primary Antibody for FACS, IF (p) - ABIN759731
Chen, Wu, Xu, Xu: Calreticulin Binds to Fas Ligand and Inhibits Neuronal Cell Apoptosis Induced by Ischemia-Reperfusion Injury. in BioMed research international 2015
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Human Polyclonal Calreticulin Primary Antibody for ELISA, WB - ABIN969575
Harada, Okiyoneda, Hashimoto, Ueno, Nakamura, Yamahira, Sugahara, Shuto, Wada, Suico, Kai: Calreticulin negatively regulates the cell surface expression of cystic fibrosis transmembrane conductance regulator. in The Journal of biological chemistry 2006
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Polyclonal Calreticulin Primary Antibody for WB - ABIN540421
Llewellyn, Johnson, Eggleton: Calreticulin comes of age. in Trends in cell biology 2000
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Human Monoclonal Calreticulin Primary Antibody for IF, IHC - ABIN965739
Tan, Chen, Li, Mabuchi, Bouvier: The calcium- and zinc-responsive regions of calreticulin reside strictly in the N-/C-domain. in Biochimica et biophysica acta 2006
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JAK2, CALR, MPL and ASXL1 mutational status correlates with distinct histological features in Philadelphia chromosome-negative myeloproliferative neoplasms
Insights into the mechanism of the pathogenic mutant CALR-MPL interaction in myeloproliferative neoplasms.
study confirms the clinical significance of driver mutational status and JAK2(mut) load in MPNs; in addition, unravels a novel clinical association between high CALR(mut) load and a more proliferative phenotype in ET
This study explored the relationship between mutations in the Janus kinase 2 gene ( JAK2), MPL, and the calreticulin gene ( CALR) in Uygur and Han Chinese patients with BCR-ABL fusion gene-negative myeloproliferative neoplasms.
The CALR exon 9 mutations are targets for specific T cells.
unwanted cells such as aging neutrophils and living cancer cells are susceptible to "labeling" by secreted calreticulin (CRT) from macrophages, enabling their clearance through programmed cell removal.
Patients with CALR mutation had significantly higher concentration of PDGF-BB and lower concentration of SDF-1alpha than patients with JAK2V617F mutation. High concentration of PDGF-BB and low concentration of SDF-1alpha in patients with CALR(+) ET may indicate a contribution of these chemokines in disturbed Ca2+ metabolism in platelets.
These results implicate miR-455 regulated hydrogen sulfide protection of lung epithelial cells against hypoxia-induced apoptosis by stimulating Calr
Calreticulin has a dual nature, and it has been found to be up-regulated or down-regulated in several types of cancer serving as either oncogene or anti-oncogene.
Study propose that leukocytes infiltration via the binding of CRT to ITGAs is necessary for the onset and development of the ulcerative colitis and the inhibition of this interaction may be a novel therapeutic strategy for the treatment of inflammatory bowel diseases.
Triplex probe-based TaqMan qPCR is an accurate and sensitive method for screening essential thrombocythemia or primary myelofibrosis patients with type I and II mutations in CALR.
Comprehensive genomic characterization identified distinct genetic subgroups and provided a classification of myeloproliferative neoplasms on the basis of causal biologic mechanisms. Mutations in JAK2, CALR, or MPL being the sole abnormality in 45% of the patients.
The prevalence of CALR mutation in JAK2V617F-negative essential thrombocythemia in this study is 35.7%. HRM is an effective method of detecting CALR mutation and is a more advantageous method of screening for CALR mutation.
MPL and CALR genotypes show a similar clinical picture at essential thrombocythaemia diagnosis. In CALR genotype features of prefibrotic myelofibrosis are common.
explored CRT reactivity of 14 different recombinant monoclonal antibodies (mAbs) derived from CLL patients carrying BCRs from various different stereotyped subsets
The novel mutations occurred and changed the amino acid sequence of the C domain amino acid residues of CALR, which will interfere with the calcium-binding capacity of the molecule. The CALR mutations will improve our understanding of the pathophysiology of myeloproliferative neoplasms.
Our study shows that JAK2V617F leads to abnormal expression of numerous proteins at the membrane of circulating PV red blood cells, with overexpression of CALR and persistence of CANX
In 94.9% of PV, 85.5% ET and 85.2% PMF, authors found mutations in JAK2, MPL or CALR. 74.9% carried JAK2V617F, 12.3% CALR mutations, 2.1% MPL mutations and 10.7% were triple negative.
these data support the model that CALR-mutated essential thrombocythemia could be considered as a distinct disease entity from JAK2V617F-positive myeloproliferative neoplasms
This phenotypic diversity is further emphasized by the following report of a patient with an isolated erythrocytosis, persistent for nearly twelve years, associated with a CALR exon 9 mutation
Endoplasmic reticulum Ca(2+) status and loss of calreticulin important determinants of the basal sensitivity of the sterol sensing mechanism .
Homozygous CALR(del/del) mice developed extreme thrombocytosis accompanied by features of Myelofibrosis, including leukocytosis, reduced hematocrit, splenomegaly, and increased bone marrow reticulin. this provides a powerful model for dissection the pathogenesis of CALR-mutant essential thrombocythemia and primary myelofibrosis.
Calr specifically at myoendothelial junction at holes in the internal elastic lamina may act in a non-ER dependent manner to regulate arteriolar heterocellular communication and blood pressure.
role for NR5A2 and its SUMOylation on the transcriptional regulation of the calreticulin gene in a model of renal fibrosis
Calreticulin is required for TGF-beta mediated epithelial-mesenchymal transition and cardiomyogenesis from mESCs.
CALR mutation analysis can thus be a useful additional diagnostic tool to achieve an accurate diagnosis for patients with ET who lack JAK2V617F and MPLW515 mutations
CRT inhibition significantly blunted APN's anti-oxidative action (evidenced by gp91(phox) expression and superoxide generation). However, CRT inhibition did not attenuate AMPK phosphorylation by APN administration in NCM. Therefore, these novel findings strongly indicate that APN exerts cardioprotective effects against I/R injury partially via CRT mediated anti-apoptotic and anti-oxidative actions.
we show that the homologous mouse CALR del52, ins5 and del61 mutants also activate thrombopoietin receptor signaling via JAK-STAT pathway
study provides a model showing that the C-terminal of mutant CALR activated JAK-STAT signaling specifically downstream of MPL 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 inhibited Fas/FasL-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 activation.
Thrombopoietin receptor activation by myeloproliferative neoplasm associated calreticulin mutants.
These studies reveal central roles for ATP and calcium binding as regulators of calreticulin-substrate interactions and as key determinants of PLC dynamics.
study demonstrates for the first time that LRH-1 has a CRT-dependent NES which is not only required for cytoplasmic trafficking, but also essential for correct protein folding to avoid misfolding-induced aggregation.
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
Here the authors identify porcine calreticulin expressed by swine intestinal cells as a host-specific receptor for Salmonella Choleraesuis FimH adhesin, suggesting that such an interaction may contribute to Salmonella Choleraesuis host specificity.
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.
Found in extracellular matrix where it may play an important role in mineralization.
the lectin site of CRT is the main target for gentamicin binding
These findings suggest that protein kinase C is involved in the regulation of CRT function.
Nkx2.5 signaling via activation of Nkx2.5-Calr-p53 signaling pathway results in cardiac dysfunction and hyperglycemia-induced cardiomyopathy.
These findings showed that mutant CALR activates jak-stat signaling through an mpl-dependent mechanism to mediate pathogenic thrombopoiesis in zebrafish, and illustrated that the signaling machinery related to mutant CALR tumorigenesis are conserved between human and zebrafish.
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.
, Sicca syndrome antigen A (autoantigen Ro; calreticulin)
, endoplasmic reticulum resident protein 60
, pot pourri
, calcium-binding protein 3
, Endoplasmic reticulum resident protein 60
, calreticulin, like 2