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Transglutaminase 5

Tg x, Transglutaminase 5, TGM5
This gene encodes a member of the transglutaminase family. The encoded protein catalyzes formation of protein cross-links between glutamine and lysine residues, often resulting in stabilization of protein assemblies. This reaction is calcium dependent. Mutations in this gene have been associated with acral peeling skin syndrome. [provided by RefSeq, Oct 2009] (from NCBI)
Top mentioned proteins: PI3K, Transglutaminase, Akt, CAN, HAD
Papers on Tg x
Acral peeling skin syndrome associated with a novel CSTA gene mutation.
Batta et al., London, United Kingdom. In Clin Exp Dermatol, Jan 2016
UNASSIGNED: Acral peeling skin syndrome (APSS) is a rare autosomal recessive condition, characterized by asymptomatic peeling of the skin of the hands and feet, often linked to mutations in the gene TGM5.
De novo mutations from sporadic schizophrenia cases highlight important signaling genes in an independent sample.
Malaspina et al., New York City, United States. In Schizophr Res, Aug 2015
First, whole exome sequencing was conducted to identify disruptive de novo mutations in 14 complete parent-offspring trios with sporadic schizophrenia from Jerusalem, which identified 5 sporadic cases with de novo gene mutations in 5 different genes (PTPRG, TGM5, SLC39A13, BTK, CDKN3).
Activation of phosphatidylinositol 3-kinase β by the platelet collagen receptors integrin α2β1 and GPVI: The role of Pyk2 and c-Cbl.
Torti et al., Pavia, Italy. In Biochim Biophys Acta, Aug 2015
Moreover, GPVI-induced intracellular Ca2+ increase and pleckstrin phosphorylation were also strongly inhibited in human platelets treated with the PI3Kβ inhibitor TGX-221.
Phosphoinositide 3-kinase β, phosphoinositide 3-kinase δ, and phosphoinositide 3-kinase γ mediate the anti-inflammatory effects of magnesium sulfate.
Huang et al., Taipei, Taiwan. In J Surg Res, Aug 2015
MATERIALS AND METHODS: PI3K isoform investigation: macrophages (RAW264.7 cells) were treated with endotoxin, endotoxin plus MgSO₄, or endotoxin plus MgSO₄ plus the selective inhibitor of PI3Kα (PIK-75), PI3Kβ (TGX-221), PI3Kδ (IC-87114), or PI3Kγ (AS-252424).
Exploring the isoform selectivity of TGX-221 related pyrido[1,2-a]pyrimidinone-based Class IA PI 3-kinase inhibitors: synthesis, biological evaluation and molecular modelling.
Rewcastle et al., Auckland, New Zealand. In Bioorg Med Chem, Aug 2015
A novel series of TGX-221 analogues was prepared and tested for their potency against the p110α, p110β, and p110δ isoforms of the PI3K enzyme, and in two cellular assays.
[Toxicogenomics and its application in safety evaluation of traditional Chinese medicine].
Fan et al., In Zhongguo Zhong Yao Za Zhi, Jul 2015
Toxicogenomics (TGx) refers to a set of technologies that assess genome-wide responses after toxic agent exposure.
Profound blockade of T cell activation requires concomitant inhibition of different class I PI3K isoforms.
Del Cañizo et al., Salamanca, Spain. In Immunol Res, Jun 2015
In particular, we have analyzed proliferation, expression of activation and differentiation markers, apoptosis induction, cytokine secretion and Akt phosphorylation in T cells stimulated in vitro with anti-CD3 and anti-CD28 monoclonal antibodies and cultured with either one of these compounds: p110β-specific inhibitor TGX-221, p110δ-specific inhibitor IC-87114, p110γ inhibitor AS-242525 or pan-class I PI3K inhibitor BKM120.
Class IA Phosphatidylinositol 3-Kinase Isoform p110α Mediates Vascular Remodeling.
Rosenkranz et al., Köln, Germany. In Arterioscler Thromb Vasc Biol, Jun 2015
To analyze their significance for receptor tyrosine kinases-dependent cellular responses, we used targeted gene knockdown and isoform-specific small molecule inhibitors of p110α (PIK-75), p110β (TGX-221), and p110δ (IC-87114), respectively.
Oncogenic activation of the PI3-kinase p110β isoform via the tumor-derived PIK3Cβ(D1067V) kinase domain mutation.
Bivona et al., San Francisco, United States. In Oncogene, Jun 2015
Pharmacologic inhibition of PIK3Cβ with TGX-221 (isoform-selective p110β inhibitor) specifically suppressed growth in patient-derived renal-cell carcinoma cells with endogenous PIK3Cβ(D1067V) and in NIH-3T3 and human EGFR-mutant lung adenocarcinoma cells engineered to express this mutant PI3K.
[Distributions and air-sea fluxes of dissolved nitrous oxide in the Yangtze River estuary and its adjacent marine area in spring and summer].
Ren et al., In Huan Jing Ke Xue, 2014
The annual emissions of N2O from the Yangtze River estuary and its adjacent marine area were estimated to be 0.6 x 10(-2) Tg x a(-1) (LM86), 1.1 x 10(-2) Tg x a(-1) (W92) and 2.0 x 10(-2) Tg x a(-1) (RC01).
Inhibitors of pan-PI3K Signaling Synergize with BRAF or MEK Inhibitors to Prevent BRAF-Mutant Melanoma Cell Growth.
Jamieson et al., Auckland, New Zealand. In Front Oncol, 2014
Here, a panel of nine low-passage human metastatic melanoma cell lines with BRAF mutations was tested in cell proliferation and protein expression assays for sensitivity to inhibitors of MEK (selumetinib) and BRAF (vemurafenib) as single agents and in combination with inhibitors of pan-PI3K (ZSTK474), pan-PI3K/mTOR (BEZ235), individual PI3K isoforms (p110α, A66; p110β, TGX-221; p110γ, AS-252424; p110δ, idelalisib), or mTORC1/2 (KU-0063794).
Inhibition of class IA PI3K enzymes in non-small cell lung cancer cells uncovers functional compensation among isoforms.
Black et al., Lexington, United States. In Cancer Biol Ther, 2014
We found that class IA PI3K enzymes were expressed in all cell lines tested, but treatment of NSCLC lines with isoform-selective inhibitors (A66, TGX-221, CAL-101 and IC488743) had little effect on cell proliferation or prolonged inhibition of AKT activity.
Hypercalciuria in a child with acral peeling skin syndrome: a case report.
Śmigiel et al., Wrocław, Poland. In Acta Dermatovenerol Croat, 2014
No mutation was present in TGM5 and CSTA genes, but the typical clinical picture and the biopsy from flaccid blisters on the feet confirmed the acral peeling skin syndrome (APSS).
A recurrent mutation in the TGM5 gene in European patients with acral peeling skin syndrome.
van Geel et al., In J Dermatol Sci, 2012
analysis of a recurrent mutation in the TGM5 gene in European patients with acral peeling skin syndrome
Changes in soil organic carbon of terrestrial ecosystems in China: a mini-review.
Yu et al., Beijing, China. In Sci China Life Sci, 2010
Datasets from the literature suggest that SOC stocks in forest, grassland, shrubland and cropland increased between the early 1980s and the early 2000s, amounting to (71+/-19) Tg x a(-1).
Acral peeling skin syndrome with TGM5 gene mutations may resemble epidermolysis bullosa simplex in young individuals.
Has et al., In J Invest Dermatol, 2010
Acral peeling skin syndrome with TGM5 gene mutations may resemble epidermolysis bullosa simplex in young individuals.
A missense mutation in TGM5 causes acral peeling skin syndrome in a Tunisian family.
Fischer et al., In J Invest Dermatol, 2009
A missense mutation in TGM5 causes acral peeling skin syndrome in a Tunisian family.
Inactive and highly active, proteolytically processed transglutaminase-5 in epithelial cells.
Melino et al., Roma, Italy. In J Invest Dermatol, 2008
TG5 full-length enzyme has very low enzymatic activity, while the 53-kDa proteolytically processed form is highly active.
Advances in development of phosphatidylinositol 3-kinase inhibitors.
Yamori et al., Tokyo, Japan. In Curr Med Chem, 2008
While PI3Kbeta, delta and gamma isoform-specific PI3K inhibitors (TGX-221, IC87114 and AS-605240) have been developed for therapy of coronary heart disease, asthma, and glomerulonephritis, respectively, a promising PI3Kalpha specific inhibitor is not yet available.
A homozygous missense mutation in TGM5 abolishes epidermal transglutaminase 5 activity and causes acral peeling skin syndrome.
McLean et al., Dundee, United Kingdom. In Am J Hum Genet, 2005
A homozygous missense mutation in TGM5 abolishes epidermal TGM5 activity and causes acral peeling skin syndrome.
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