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anti-Rat (Rattus) SLC6A8 Antibodies:
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These findings showed that mutant CALR (show CALR Antibodies) activates jak (show JAK3 Antibodies)-stat (show STAT1 Antibodies) signaling through an mpl (show MPL Antibodies)-dependent mechanism to mediate pathogenic thrombopoiesis in zebrafish, and illustrated that the signaling machinery related to mutant CALR (show CALR Antibodies) tumorigenesis are conserved between human and zebrafish.
The present work suggests that Ca(2 (show CA2 Antibodies)+)-dependent regulation is caused by different conformations of a long proline-rich loop that changes the accessibility to the peptide/lectin-binding site. Our results indicate that the binding of Ca(2 (show CA2 Antibodies)+) to calreticulin (show CALR Antibodies) may thus not only just be a question of Ca(2 (show CA2 Antibodies)+) storage but is likely to have an impact on the chaperone activity.
CRT regulates TGF-beta1 (show TGFB1 Antibodies)-induced-EMT (show ITK Antibodies) through modulating Smad (show SMAD1 Antibodies) signaling
Our results showed that a wide range of different CALR mutations are associated with a distinct ET clinical phenotype that is associated with the male gender, younger age at diagnosis, higher platelet and lower leukocyte and erythrocyte counts and lower hemoglobin level, and a milder clinical course.
alpha-Integrin expression and function modulates presentation of cell surface calreticulin (show CALR Antibodies).
Although CALR (show CALR Antibodies) mutations resulted in protein instability and proteosomal degradation, mutant CALR (show CALR Antibodies) was able to enhance megakaryopoiesis and pro-platelet production from human CD34 (show CD34 Antibodies)(+) progenitors.
Studies show that all CALR (show CALR Antibodies) 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 Antibodies) constitutively activates MPL (show MPL Antibodies) to induce cellular transformation. The interaction between the mutant CALR (show CALR Antibodies) and MPL (show MPL Antibodies) is achieved by the conformational change in the C-terminal allowing N-domain binding to MPL (show MPL Antibodies). [review]
C-CALR (show CALR Antibodies) in response to Ca2 (show CA2 Antibodies)+ 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 Antibodies) signaling in proliferation mode, contributing to erythrocytosis in PV.
Mannan-binding lectin (MBL (show MBL2 Antibodies)) bound to T cells through interaction between the collagen-like region of MBL (show MBL2 Antibodies) and calreticulin (CRT (show CALR Antibodies)) expressed on the T-cell surface.
CRT exposure represents a novel powerful prognostic biomarker for patients with acute myeloid leukemia (show BCL11A Antibodies).
study provides a model showing that the C-terminal of mutant CALR (show CALR Antibodies) activated JAK (show JAK3 Antibodies)-STAT (show STAT1 Antibodies) signaling specifically downstream of MPL (show MPL Antibodies) and may have a central role in CALR (show CALR Antibodies)-induced myeloproliferative neoplasms
the results of this investigation provide the first molecular insights into the phospholipid binding site of calreticulin (show CALR Antibodies) as a key anchor point for the cell surface expression of calreticulin (show CALR Antibodies) on apoptotic cells
a profound impairment in calreticulin (show CALR Antibodies) 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 Antibodies) within the endoplasmic reticulum.
This essential role of calreticulin (show CALR Antibodies) 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 Antibodies) 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 Antibodies)/FasL (show FASL Antibodies)-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 Antibodies) in female reproduction and demonstrate that compromised CALR (show CALR Antibodies) function leads to ovarian insufficiency and female infertility.
Calreticulin (show CALR Antibodies) mediates vascular smooth muscle cell responses to injury through the regulation of collagen deposition and neointima formation.
CALR (show CALR Antibodies) mutants are sufficient to induce thrombocytosis through MPL (show MPL Antibodies) activation.
Thrombopoietin receptor (show MPL Antibodies) activation by myeloproliferative neoplasm associated calreticulin (show CALR Antibodies) 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 Antibodies).
Mammalian target of rapamycin (mTOR (show FRAP1 Antibodies)) stimulates the creatine transporter SLC6A8 through mechanisms at least partially shared by the serum and glucocorticoid-inducible kinase SGK1 (show SGK1 Antibodies).
The observations suggest that SGK1 (show SGK1 Antibodies) regulates the creatine transporter SLC6A8 at least partially through phosphorylation and activation of PIKfyve (show PIKFYVE Antibodies).
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.
, creatine transporter 1
, sodium- and chloride-dependent creatine transporter 1
, solute carrier family 6 member 8
, solute carrier family 6 (neurotransmitter transporter, creatine), member 8
, Sodium- and chloride-dependent creatine transporter 1
, sodium- and chloride-dependent creatine transporter 1-like
, choline transporter
, creatine transporter, solute carrier family 6, member 8
, solute carrier family 6, member 8
, creatine transporter SLC6A8