Sentences with phrase «b subunit»

In contrast, the retrograde transport of the Shiga toxin B subunit between the plasma membrane and the Golgi complex is partly inhibited in cells overexpressing the Rab6 - binding domain of Rab6IP2.

PP2A is composed of the structural A and catalytic C subunits, and a regulatory B subunit.

The presence of GluR - B subunits in heteromeric GluRs determined the I - V behavior of the resulting channels.

When the PP2A catalytic C subunit associates with the A and B subunits several protein isoforms, namely holoenzymes, are produced with distinct activity and substrate specificity.

The cytosolic catalytic domain consists of 3 A subunits and 3 B subunits, which bind and hydrolyze ATP, as well as regulatory accessory subunits.

Not exact matches

It contains five metal clusters of which clusters B, B ′, and a subunit - bridging, surface - exposed cluster D are cubane - type [4Fe - 4S] clusters.

The gene, called gyrase B, codes for a variable subunit of the DNA gyrase protein, which helps DNA coil and uncoil.

Twelve percent encoded mitochondrial proteins such as succinate dehydrogenase complex, subunit B, iron sulfur (Ip)(τ statistic = — 0.76, P = 2.2 × 10 — 7), and ubiquinol — cytochrome c reductase subunit (τ statistic = — 0.65, P = 7.4 × 10 — 6)(Figure 1), and 6 % encoded lysosomal proteins (Supplemental Table 2, http://www.jci.org/cgi/content/full/112/12/1796/DC1).

Examples of adipose tissue transcripts whose expression correlated with body mass include (a) Csf1r and (b) CD68 antigen (Cd68), which correlated positively with body mass, (c) succinate dehydrogenase complex, subunit B, iron sulfur (Ip)(Sdhb), and (d) ubiquinol — cytochrome c reductase subunit (Uqcr), which correlated negatively with body massb) CD68 antigen (Cd68), which correlated positively with body mass, (c) succinate dehydrogenase complex, subunit B, iron sulfur (Ip)(Sdhb), and (d) ubiquinol — cytochrome c reductase subunit (Uqcr), which correlated negatively with body massB, iron sulfur (Ip)(Sdhb), and (d) ubiquinol — cytochrome c reductase subunit (Uqcr), which correlated negatively with body mass.

Although several proteins have been demonstrated to be targets of Cbl - b, including the TCR itself, much of the inhibition attributable to Cbl - b results from ubiquitination of the p85α subunit of PI (3) K (21, 22).

Cbl - b targets the p85α subunit of PI (3) K for degradation, resulting in termination of substrate activation downstream of phosphatidylinositol 3,4,5 - triphosphate (21).

Abbreviations: AGL = glycogen debranching enzyme; GSK3A / B = glycogen synthase kinase 3 α / β; GYS2 = glycogen synthase 2; PYGL = glycogen phosphorylase, liver form; PCK1 / 2 = phosphoenolpyruvate carboxykinase 1/2; FBP1 / 2 = fructose -1,6-bisphosphatase 1/2; G6PC = glucose -6-phosphatase; G6PD = glucose -6-phosphate 1 - dehydrogenase; GLUT - 2 = glucose transporter 2; INSR = insulin receptor; IRS1 / 2 = insulin receptor substrate 1/2; PIK3CA / B / D = PI3 - kinase subunit α / β / δ; and AKT1 = protein kinase B - α.

DGKζ, a lipid kinase, phosphorylates the second messenger DAG, terminating DAG - mediated activation of RasGRP1 and PKC - θ, whereas Cbl - b, an E3 ubiquitin ligase, facilitates ubiquitination and subsequent degradation of the p85 subunit of PI (3) K. Previous studies have evaluated numerous aspects of T cell biology in the two models (16 — 18, 25, 38), but the signaling and functional effects of DKGζ deficiency and Cbl - b deficiency in T cells had not been directly compared.

We describe here that in cells derived from human monocytes, i.e., macrophages and dendritic cells, the B - subunit was internalized in a receptor - dependent manner, but retrograde transport to the biosynthetic / secretory pathway did not occur and part of the internalized protein was degraded in lysosomes.

In agreement with this hypothesis we found that in HeLa cells, the B - subunit resisted extraction by Triton X-100 until its arrival in the target compartments of the retrograde pathway, i.e., the Golgi apparatus and the endoplasmic reticulum.

These differences correlated with the observation that the B - subunit associated with Triton X-100-resistant membranes in HeLa cells, but not in monocyte - derived cells, suggesting that retrograde targeting to the biosynthetic / secretory pathway required association with specialized microdomains of biological membranes.

The B - subunit of the bacterial Shiga toxin (STxB), which is nontoxic and has low immunogenicity, can be used for tumor targeting of breast, colon, and pancreatic cancer.

We have validated the glycosphingolipid - binding non-toxic B - subunit of Shiga toxin as a delivery tool for cancer immunotherapy, and are currently building therapeutic vaccine prototypes for breast and head - and - neck cancers.

His basic studies have allowed him to validate the B - subunit of Shiga toxin (STxB) as a «pilot» for the delivery of therapeutic compounds to precise intracellular locations of dendritic and tumor cells (10 patent families, 5 of which are delivered in the US, Europe and other countries).

We here show that after oral or i.v. injections in mice, the B - subunit targets spontaneous digestive Gb3 - expressing adenocarcinomas.

With respect to UNC - 7S co-localization, this indicated that UNC - 9 could potentially contribute subunits to hemichannels in the motor neurons, in AVB, or in both, and UNC - 9 may play a role in the formation of ectopic gap junctions noted in unc - 7 (e5)(between AVA and B class motor neurons).

We postulated that UNC - 7S might rescue forward locomotion by providing a gap junction subunit in AVB hemichannels that form channels with B class motor neurons.

The observation that the cholera toxin B (CtxB) subunit, a multivalent counter-receptor that binds with high affinity and specificity to GM1 (8), produced the same effects as the Treg product Gal - 1 served to emphasize the pivotal role of GM1 cross-linking in Teff suppression (7).

Protection against Shiga toxin - producing Escherichia coli infection by transcutaneous immunization with Shiga Toxin subunit B. Zhu C, Yu J, Yang Z, Davis K, Rios H, Wang B, Glenn G, Boedeker EC.