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Adaptor-related protein complex 2, beta 1 subunit

beta-adaptin, beta2-adaptin, BAM22
The protein encoded by this gene is one of two large chain components of the assembly protein complex 2, which serves to link clathrin to receptors in coated vesicles. The encoded protein is found on the cytoplasmic face of coated vesicles in the plasma membrane. Two transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: p15, beta2, V1a, CAN, IRBP
Papers on beta-adaptin
Upregulation of pronociceptive mediators and downregulation of opioid peptide by adrenomedullin following chronic exposure to morphine in rats.
Hong et al., Fuzhou, China. In Neuroscience, 2014
administration of morphine for 6 days increased the expression of nNOS in the spinal dorsal horn and DRG neurons but decreased expression of the endogenous opioid peptide bovine adrenal medulla 22 (BAM22) in small- and medium-sized neurons in DRG.
Triphenylmethane dye activation of beta-arrestin.
Caron et al., Durham, United States. In Biochemistry, 2013
In the presence of these compounds, G protein signaling is inhibited, ERK and GSK3β signaling are preserved, and the recruitment of the beta2-adaptin, AP2 adaptor complex to clathrin as well as transferrin internalization is reduced.
Microextraction by packed sorbent and liquid chromatography-tandem mass spectrometry as a tool for quantification of peptides in plasma samples: determination of sensory neuron-specific receptors agonist BAM8-22 and antagonist BAM22-8 in plasma samples.
Abdel-Rehim et al., Riyadh, Saudi Arabia. In Biomed Chromatogr, 2013
Additionally, the accuracy and precision for BAM22-8 ranged from -13 to 7.0% and from 3.0 to 12%, respectively.
Role of bovine adrenal medulla 22 (BAM22) in the pathogenesis of neuropathic pain in rats with spinal nerve ligation.
Hong et al., Fuzhou, China. In Eur J Pharmacol, 2012
The opioid peptide bovine adrenal medulla 22 (BAM22) is a cleavage product of proenkephalin and has been shown to be involved in inflammatory pain and morphine tolerance.
Proteomic analysis identifies dysfunction in cellular transport, energy, and protein metabolism in different brain regions of atypical frontotemporal lobar degeneration.
Bahn et al., Cambridge, United Kingdom. In J Proteome Res, 2012
A protein encoded by this locus was found to be differentially expressed in postmortem brains from patients with atypical frontotemporal lobar degeneration.
Blockade of adrenomedullin receptors reverses morphine tolerance and its neurochemical mechanisms.
Hong et al., Fuzhou, China. In Behav Brain Res, 2011
Interestingly, chronic administration of morphine reduced the expression of the endogenous opioid peptide bovine adrenal medulla 22 (BAM22) in small- and medium-sized neurons in DRG and this reduction was partially reversed by the administration of AM(22-52) (35.8 μg).
ARH cooperates with AP-1B in the exocytosis of LDLR in polarized epithelial cells.
Fölsch et al., Chicago, United States. In J Cell Biol, 2011
The conclude that in addition to its role in endocytosis, ARH cooperates with AP-1B in basolateral exocytosis of LDLR from recycling endosomes.
[Bovine adrenal medulla 22 attenuates hyperalgesia in the early phase of complete Freund's adjuvant-induced inflammation in rats].
Hong et al., Fuzhou, China. In Sheng Li Xue Bao, 2011
The present study investigated the effects of intrathecal (i.t.) application of bovine adrenal medulla 22 (BAM22), an endogenous opioid peptide potently activating opioid receptors and sensory neuron-specific receptor (SNSR), on a model of complete Freund's adjuvant (CFA)-induced inflammatory pain.
Pathological classification and molecular genetics of meningiomas.
Perry et al., Magdeburg, Germany. In J Neurooncol, 2010
Other chromosome 22q genes implicated include BAM22, BCR (breakpoint cluster region), and TIMP-1, the last of which is implicated in higher-grade meningiomas.
Molecular basis for association of PIPKI gamma-p90 with clathrin adaptor AP-2.
Haucke et al., Berlin, Germany. In J Biol Chem, 2010
multiple interactions between PIPKI gamma-p90 and AP-2 lead to spatiotemporally controlled PI(4,5)P(2) synthesis during clathrin-mediated synaptic vesicle endocytosis
Alternate pathways preserve tumor necrosis factor-alpha production after nuclear factor-kappaB inhibition in neonatal cerebral hypoxia-ischemia.
Kavelaars et al., Utrecht, Netherlands. In Stroke, 2009
Our data indicate that the switch to JNK/AP-1 activation preserves HI-induced TNF-alpha expression and thereby might contribute to the neuroprotective effect of TAT-NBD possibly through a TNF-R2 dependent mechanism.
Immunohistochemical detection of EGFR, fibrillin-2, P-cadherin and AP2beta as biomarkers for rhabdomyosarcoma diagnostics.
Schäfer et al., Zürich, Switzerland. In Histopathology, 2009
EGFR, fibrillin-2, P-cadherin and AP2beta as biomarkers for rhabdomyosarcoma diagnostics.
[Cytogenetic alterations in meningioma tumors and their impact on disease outcome].
Maíllo et al., Salamanca, Spain. In Med Clin (barc), 2007
Accordingly, while the presence of monosomy 22/22q-, associated with mutation of the NF2, BAM22, RRP22, GAR22, MN1, SMARCB1, CLH22 and/or LARGE genes, is associated with neoplasic transformation, other alterations such us monosomy 14, del(1p), different chromosomal abnormalities localized at 9p, 10q and 17q and complex karyotypes are frequently related to tumor progression.
[Oxidative stress, beta-amyloide peptide and Alzheimer's disease].
Mas-Oliva et al., Mexico. In Gac Med Mex, 2006
We have also demonstrated that the process of protein translation of molecules implicated in the mechanism of endocytosis through the scavenger receptor, such as the case of beta-adaptin, is arrested in microglial cells treated with beta-amyloid.
Molecular genetics of meningiomas.
Jensen et al., Salt Lake City, United States. In Neurosurg Focus, 2005
This discrepancy supports the theory that a second tumor suppressor gene exists on chromosome 22, and the authors introduce several possible gene candidates, including BAM22, LARGE, INI1, and MN1 genes.
Non-opioid actions of opioid peptides.
Benyhe et al., Szeged, Hungary. In Life Sci, 2004
Peptides exhibiting non-opioid effects include beta-endorphin, dynorphin A, nociceptin/OFQ, endomorphins, hemorphins and a number of Proenkephalin A derived peptides, such as Met-enkephalin, Met-enkephalin-Arg-Phe (MERF) and bovine adrenal medullary peptide (BAM22).
Evolving concepts in G protein-coupled receptor endocytosis: the role in receptor desensitization and signaling.
Ferguson, London, Canada. In Pharmacol Rev, 2001
beta-Arrestin-dependent endocytosis of GPCRs involves the direct interaction of the carboxyl-terminal tail domain of beta-arrestins with both beta-adaptin and clathrin.
Beta-NAP, a cerebellar degeneration antigen, is a neuron-specific vesicle coat protein.
Darnell et al., New York City, United States. In Cell, 1995
We have identified a target antigen in autoimmune cerebellar degeneration, beta-NAP, that is closely related to the beta-adaptin and beta-COP coat proteins.
Beta-COP, a 110 kd protein associated with non-clathrin-coated vesicles and the Golgi complex, shows homology to beta-adaptin.
Kreis et al., Heidelberg, Germany. In Cell, 1991
beta-COP shows significant homology to beta-adaptin.
A coat subunit of Golgi-derived non-clathrin-coated vesicles with homology to the clathrin-coated vesicle coat protein beta-adaptin.
Wieland et al., Stanford, United States. In Nature, 1991
Four high-molecular-weight proteins form the main subunits of the coat of Golgi-derived (non-clathrin) coated vesicles.
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