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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Adenosine monophosphate deaminase 1

Smad1, AMP Deaminase, Mad1, GlyRs
Adenosine monophosphate deaminase 1 catalyzes the deamination of AMP to IMP in skeletal muscle and plays an important role in the purine nucleotide cycle. Two other genes have been identified, AMPD2 and AMPD3, for the liver- and erythocyte-specific isoforms, respectively. Deficiency of the muscle-specific enzyme is apparently a common cause of exercise-induced myopathy and probably the most common cause of metabolic myopathy in the human. Alternatively spliced transcript variants encoding different isoforms have been identified in this gene.[provided by RefSeq, Feb 2010] (from NCBI)
Top mentioned proteins: CAN, ACID, V1a, Rdl, HAD
Papers using Smad1 antibodies
Characterization of connexin31.1-deficient mice reveals impaired placental development
Asashima Makoto et al., In In Vitro Cellular & Developmental Biology. Animal, 2006
... The primary antibodies used are as follows: anti-α-tubulin (Sigma, 1:1,000), anti-Smad1/5/8 (Santa Cruz Biotechnology, Santa Cruz, CA, 1:1,000), ...
Serotonin 5-HT2C receptor homodimer biogenesis in the endoplasmic reticulum
Yan B et al., In Cell Death & Disease, 2005
... Smad1/5/8/9 antibody (ab72504) was from Abcam (Cambridge, MA, USA) ...
The Lens Organizes the Anterior Segment: Specification of Neural Crest Cell Differentiation in the Avian Eye
Beebe David C et al., In BMC Cell Biology, 1999
... Antibody to phosphorylated Smad1 (pSmad1) was obtained from Upstate Biotechnology, anti-pSmad1/5/8, anti-pSmad2 and anti-β-tubulin were from Cell Signaling Technology (Danvers, MA), anti-Smad4, ...
Misexpression of chick Vg1 in the marginal zone induces primitive streak formation
Dodd Jane et al., In Neural Development, 1996
... ]); rabbit α-Smad1/5/8 (N18; Santa Cruz Biotechnology, Santa Cruz, CA, USA), ...
Selective antagonism by PPADS at P2X-purinoceptors in rabbit isolated blood vessels
Yamada Yoshihiko et al., In The Journal of Cell Biology, 1993
... Antibodies for P-Rb, CaM, CaMKII, P-CaMKII, CN, p53, Akt, p-Akt, Smad1, and P-Smad1/5 were obtained from Cell Signaling Technology; Rb, P-NFATc1, and ...
Papers on Smad1
KCC2 knockdown impairs glycinergic synapse maturation in cultured spinal cord neurons.
Kuhse et al., Heidelberg, Germany. In Histochem Cell Biol, Feb 2016
UNASSIGNED: Synaptic inhibition in the spinal cord is mediated mainly by strychnine-sensitive glycine (GlyRs) and by γ-aminobutyric acid type A receptors (GABAAR).
Bone Morphogenic Protein 4-Smad-Induced Upregulation of Platelet-Derived Growth Factor AA Impairs Endothelial Function.
Huang et al., Hong Kong, Hong Kong. In Arterioscler Thromb Vasc Biol, Feb 2016
SMAD4-shRNA lentivirus, SMAD1-shRNA, and SMAD5 shRNA adenovirus were used for knockdown in human endothelial cells.
BMP Sustains Embryonic Stem Cell Self-Renewal through Distinct Functions of Different Krüppel-like Factors.
Miyazono et al., Uppsala, Sweden. In Stem Cell Reports, Feb 2016
SMAD1 and SMAD5, which transduce BMP signals, recognize enhancer regions together with KLF4 and KLF5 in naive mESCs.
Regulation of impaired angiogenesis in diabetic dermal wound healing by microRNA-26a.
Feinberg et al., Boston, United States. In J Mol Cell Cardiol, Feb 2016
Mechanistically, inhibition of miR-26a increased its target gene SMAD1 in ECs nine days post-wounding of diabetic mice.
PINK1 expression increases during brain development and stem cell differentiation, and affects the development of GFAP-positive astrocytes.
Joe et al., Suwŏn, South Korea. In Mol Brain, Dec 2015
Interestingly, during differentiation of KO NSCs there were no defects in mitochondrial function, and there were not changes in signaling molecules such as SMAD1/5/8, STAT3, and HES1 involved in differentiation of NSCs into astrocytes.
Ethanol effects on glycinergic transmission: From molecular pharmacology to behavior responses.
Aguayo et al., Concepción, Chile. In Pharmacol Res, Nov 2015
GlyRs are relevant for the effects of ethanol because they are found in the spinal cord and brain stem where they primarily express the α1 subunit.
Structure-function relationships in mammalian histidine-proline-rich glycoprotein.
Raggi et al., Pisa, Italy. In Biochimie, Nov 2015
This observation provides a structural basis to the function of HPRG as an intracellular zinc chaperone which has been suggested by the involvement of the protein in the maintenance of the quaternary structure of skeletal muscle AMP deaminase (AMPD).
CMT2D neuropathy is linked to the neomorphic binding activity of glycyl-tRNA synthetase.
Yang et al., Los Angeles, United States. In Nature, Nov 2015
A subtype of these diseases--CMT type 2D (CMT2D)--is caused by dominant mutations in GARS, encoding the ubiquitously expressed enzyme glycyl-transfer RNA (tRNA) synthetase (GlyRS).
Inhibition of AMP deaminase as therapeutic target in cardiovascular pathology.
Smolenski et al., Gdańsk, Poland. In Pharmacol Rep, Aug 2015
AMP deaminase (AMPD; EC catalyzes hydrolysis of the amino group from the adenine ring of AMP resulting in production of inosine 5'-monophosphate (IMP) and ammonia.
Inhibitory SMADs: potential regulators of ovarian function.
Li, College Station, United States. In Biol Reprod, Feb 2015
SMAD proteins are canonical TGFB signaling components consisting of receptor-regulated SMADs (SMAD1/2/3/5/9), a common SMAD (SMAD4), and inhibitory SMADs (SMAD6/7).
An emerging role for the miR-26 family in cardiovascular disease.
Feinberg et al., Boston, United States. In Trends Cardiovasc Med, 2014
Recent evidence supports a central role for the miR-26 family in cardiovascular disease by controlling critical signaling pathways, such as BMP/SMAD1 signaling, and targets relevant to endothelial cell growth, angiogenesis, and LV function post-MI.
Recurrent somatic mutations in ACVR1 in pediatric midline high-grade astrocytoma.
Kieran et al., Montréal, Canada. In Nat Genet, 2014
Hyperactivation of the bone morphogenetic protein (BMP)-ACVR1 developmental pathway in mHGAs harboring ACVR1 mutations led to increased levels of phosphorylated SMAD1, SMAD5 and SMAD8 and upregulation of BMP downstream early-response genes in tumor cells.
TGF-β2 dictates disseminated tumour cell fate in target organs through TGF-β-RIII and p38α/β signalling.
Aguirre-Ghiso et al., United States. In Nat Cell Biol, 2013
TGF-β2-induced dormancy required TGF-β receptor-I (TGF-β-RI), TGF-β-RIII and SMAD1/5 activation to induce p27.
Up-regulation of the mitotic checkpoint component Mad1 causes chromosomal instability and resistance to microtubule poisons.
Weaver et al., Madison, United States. In Proc Natl Acad Sci U S A, 2012
These results suggest that levels of Mad1 must be tightly regulated to prevent aneuploidy and transformation and that Mad1 up-regulation may promote tumors and cause resistance to current therapies.
Transforming growth factor β inhibits bone morphogenetic protein-induced transcription through novel phosphorylated Smad1/5-Smad3 complexes.
Hill et al., London, United Kingdom. In Mol Cell Biol, 2012
TGF-beta induces the formation of complexes comprising phosphorylated Smad1/5 and Smad3, which bind to BMP-responsive elements in vitro and in vivo and mediate TGF-beta-induced transcriptional repression.
R-Smad competition controls activin receptor output in Drosophila.
O'Connor et al., Minneapolis, United States. In Plos One, 2011
Data show that dSmad2 directly influences Baboon's phosphorylation of Mad.
A crucial role for bone morphogenetic protein-Smad1 signalling in the DNA damage response.
Li et al., Singapore, Singapore. In Nat Commun, 2011
BMP-Smad1 signalling participates in the DNA damage response via the Atm-p53 pathway.
Activation of BMP-Smad1/5/8 signaling promotes survival of retinal ganglion cells after damage in vivo.
Reh et al., Seattle, United States. In Plos One, 2011
Activation of BMP-Smad1/5/8 signaling promotes survival of retinal ganglion cells after damage in vivo.
Lineage regulators direct BMP and Wnt pathways to cell-specific programs during differentiation and regeneration.
Zon et al., Boston, United States. In Cell, 2011
Both SMAD1 and TCF7L2 co-occupy sites with master regulators adjacent to hematopoietic genes.
Autoantibodies associated with diseases of the CNS: new developments and future challenges.
Waters et al., Oxford, United Kingdom. In Lancet Neurol, 2011
Antibodies to components of voltage-gated potassium channel complexes (VGKCs), NMDA receptors (NMDARs), AMPA receptors (AMPARs), GABA type B receptors (GABA(B)Rs), and glycine receptors (GlyRs) can be identified in patients and are associated with various clinical presentations, such as limbic encephalitis and complex and diffuse encephalopathies.
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