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alpha-Integrin expression and function modulates presentation of cell surface calreticulin (show CALR Proteins).
Although CALR (show CALR Proteins) mutations resulted in protein instability and proteosomal degradation, mutant CALR (show CALR Proteins) was able to enhance megakaryopoiesis and pro-platelet production from human CD34 (show CD34 Proteins)(+) progenitors.
Studies show that all CALR (show CALR Proteins) 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 (show CALR Proteins) constitutively activates MPL (show MPL Proteins) to induce cellular transformation. The interaction between the mutant CALR (show CALR Proteins) and MPL (show MPL Proteins) is achieved by the conformational change in the C-terminal allowing N-domain binding to MPL (show MPL Proteins). [review]
C-CALR (show CALR Proteins) in response to Ca2 (show CA2 Proteins)+ 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 Proteins) signaling in proliferation mode, contributing to erythrocytosis in PV.
Mannan-binding lectin (MBL (show MBL2 Proteins)) bound to T cells through interaction between the collagen-like region of MBL (show MBL2 Proteins) and calreticulin (CRT (show CALR Proteins)) expressed on the T-cell surface.
CRT exposure represents a novel powerful prognostic biomarker for patients with acute myeloid leukemia (show BCL11A Proteins).
In absence of CALR (show CALR Proteins), immature MPO (show MPO Proteins) 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 Proteins), CALR (show CALR Proteins), and MPL (show MPL Proteins) genes in myeloproliferative neoplasms suggest that CALR (show CALR Proteins) and MPL (show MPL Proteins) should be analyzed not only in JAK2 (show JAK2 Proteins)-negative patients but also in low V617F mutation patients.
CALR (show CALR Proteins)-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)
study provides a model showing that the C-terminal of mutant CALR (show CALR Proteins) activated JAK (show JAK3 Proteins)-STAT (show STAT1 Proteins) signaling specifically downstream of MPL (show MPL Proteins) and may have a central role in CALR (show CALR Proteins)-induced myeloproliferative neoplasms
the results of this investigation provide the first molecular insights into the phospholipid binding site of calreticulin (show CALR Proteins) as a key anchor point for the cell surface expression of calreticulin (show CALR Proteins) on apoptotic cells
a profound impairment in calreticulin (show CALR Proteins) 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 (show CALR Proteins) within the endoplasmic reticulum.
This essential role of calreticulin (show CALR Proteins) 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 (show CALR Proteins) 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 (show FAS Proteins)/FasL (show FASL Proteins)-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 (show CALR Proteins) in female reproduction and demonstrate that compromised CALR (show CALR Proteins) function leads to ovarian insufficiency and female infertility.
Calreticulin (show CALR Proteins) mediates vascular smooth muscle cell responses to injury through the regulation of collagen deposition and neointima formation.
CALR (show CALR Proteins) mutants are sufficient to induce thrombocytosis through MPL (show MPL Proteins) activation.
Thrombopoietin receptor (show MPL Proteins) activation by myeloproliferative neoplasm associated calreticulin (show CALR Proteins) mutants.
GSK3ss down-regulates the creatine transporter CreaT, an effect reversed by treatment with the antidepressant Lithium and by co-expression of PKB/Akt (show AKT1 Proteins).
Mammalian target of rapamycin (mTOR (show FRAP1 Proteins)) stimulates the creatine transporter SLC6A8 through mechanisms at least partially shared by the serum and glucocorticoid-inducible kinase SGK1 (show SGK1 Proteins).
The observations suggest that SGK1 (show SGK1 Proteins) regulates the creatine transporter SLC6A8 at least partially through phosphorylation and activation of PIKfyve (show PIKFYVE Proteins).
The protein encoded by this gene is a plasma membrane protein whose function is to transport creatine into and out of cells. Defects in this gene can result in X-linked creatine deficiency syndrome. Multiple transcript variants encoding different isoforms have been found for this gene.
solute carrier family 6 (neurotransmitter transporter, creatine), member 8
, Sodium- and chloride-dependent creatine transporter 1
, sodium- and chloride-dependent creatine transporter 1-like
, Sicca syndrome antigen A (autoantigen Ro; calreticulin)
, endoplasmic reticulum resident protein 60
, sodium- and chloride-dependent creatine transporter 1
, choline transporter
, creatine transporter 1
, solute carrier family 6 member 8
, creatine transporter, solute carrier family 6, member 8
, solute carrier family 6, member 8
, creatine transporter SLC6A8