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

Prohibitin 2

p22, BAP, REA, MYPT1
This gene encodes a resident endoplasmic reticulum (ER), N-linked glycoprotein with an N-terminal ER targeting sequence, 2 putative N-glycosylation sites, and a C-terminal ER retention signal. This protein functions as a nucleotide exchange factor for another unfolded protein response protein. Mutations in this gene have been associated with Marinesco-Sjogren syndrome. Alternate transcriptional splice variants have been characterized. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: HAD, CAN, V1a, Rhodopsin, Ros
Papers using p22 antibodies
Biomarkers for epithelial-mesenchymal transitions
Krupitza G et al., In British Journal of Cancer, 2008
... rabbit Akt antibody, monoclonal rabbit antibody ROCK-1 (C8F7), polyclonal rabbit ILK1 antibody, and polyclonal rabbit MYPT1 antibody were from Cell Signaling (Danvers, MA, USA) ...
Experimental infection of lactating bovine mammary glands with Streptococcus uberis in quarters colonized by Corynebacterium bovis
Oliver Stephen P. et al., In Veterinary Medicine International, 1986
... 37°C water bath, plated onto trypticase soy agar plate supplemented with 5% defibrinated sheep blood (BAP, Becton Dickinson and Company, Franklin Lakes, ...
Papers on p22
Multiple copy number variants in a pediatric patient with Hb H disease and intellectual disability.
Varela et al., Buenos Aires, Argentina. In Am J Med Genet A, Feb 2016
44,798,701-45,334,537) x1 and arr[hg19]Chr17(17q25.3; 80,544,855-81,057,996) x1) and a terminal duplication (arr[hg19]Chr7(7p22.3-p22.2;
Endothelium-Independent Effect of Fisetin on the Agonist-Induced Regulation of Vascular Contractility.
La et al., Taegu, South Korea. In Biomol Ther (seoul), Jan 2016
Furthermore, fisetin significantly inhibited fluoride-induced increases in pMYPT1 levels and phorbol ester-induced increases in pERK1/2 levels suggesting the mechanism involving the inhibition of Rho-kinase activity and the subsequent phosphorylation of MYPT1 and MEK activity and the subsequent phosphorylation of ERK1/2.
Abnormal myosin phosphatase targeting subunit 1 phosphorylation and actin polymerization contribute to impaired myogenic regulation of cerebral arterial diameter in the type 2 diabetic Goto-Kakizaki rat.
Cole et al., Calgary, Canada. In J Cereb Blood Flow Metab, Jan 2016
Pressure-dependent myogenic constriction, LC20, and myosin phosphatase targeting subunit 1 phosphorylation and actin polymerization were suppressed in both pre-diabetic Goto-Kakizaki and diabetic (18-20 weeks) Goto-Kakizaki rats, whereas RhoA, ROK2, and MYPT1 expression were unaffected.
Mechanisms Involved in Thromboxane A2 -induced Vasoconstriction of Rat Intracavernous Small Penile Arteries.
Simonsen et al., Århus, Denmark. In Basic Clin Pharmacol Toxicol, Jan 2016
Rat intracavernous penile arteries were mounted for isometric tension and intracellular calcium ([Ca(2+) ]i ) recording and corpus cavernosum for measurements of MYPT1 phosphorylation.
Calcium Sensitization Mechanisms in Gastrointestinal Smooth Muscles.
Perrino, Reno, United States. In J Neurogastroenterol Motil, Jan 2016
Inhibiting myosin light chain phosphatase activity with CPI-17 and MYPT1 phosphorylation is considered to be the primary mechanism underlying myofilament Ca(2+) sensitization.
Disturbance of Bcl-2, Bax, Caspase-3, Ki-67 and C-myc expression in acute and subchronic exposure to benzo(a)pyrene in cervix.
Kong et al., Xi'an, China. In Acta Histochem, Jan 2016
Benzo(a)pyrene (BaP) is one of the most potent tobacco smoke carcinogens in tobacco smoke.
Chronic Granulomatous Disease: clinical, molecular and therapeutic aspects.
Finocchi et al., Roma, Italy. In Pediatr Allergy Immunol, Jan 2016
CGD is a genetically heterogeneous disease with an X-linked recessive (XR-CGD) form caused by mutations in the CYBB gene encoding the gp91(phox) protein, and an autosomal recessive (AR-CGD) form caused by mutations in the CYBA, NCF1, NCF2 or NCF4 genes encoding p22(phox) , p47(phox) , p67(phox) and p40(phox) , respectively.
A self-encoded capsid derivative restricts Ty1 retrotransposition in Saccharomyces.
Purzycka et al., Athens, United States. In Curr Genet, Jan 2016
We discovered a novel truncated form of the Saccharomyces Ty1 retrotransposon capsid protein, dubbed p22 that inhibits virus-like particle (VLP) assembly and function.
Norovirus mechanisms of immune antagonism.
Karst et al., Gainesville, United States. In Curr Opin Virol, Jan 2016
In this review, we discuss these emerging strategies used by noroviruses to subvert the immune response, including the actions of two nonstructural proteins (p48 and p22) to impair cellular protein trafficking and secretory pathways; the ability of the VF1 protein to inhibit cytokine induction; and the ability of the minor structural protein VP2 to regulate antigen presentation.
[Identification of genetic defects in a Chinese pedigree with factor XIII deficiency: case report and literature review].
Wang et al., Shanghai, China. In Zhonghua Xue Ye Xue Za Zhi, Oct 2015
METHODS: The activity levels of F XIII (F XIII:C)of proband and family members were measured by clot solubility test and REA-chrom F XIII kit.
Deregulated expression of EVI1 defines a poor prognostic subset of MLL-rearranged acute myeloid leukemias: a study of the German-Austrian Acute Myeloid Leukemia Study Group and the Dutch-Belgian-Swiss HOVON/SAKK Cooperative Group.
Delwel et al., Ulm, Germany. In J Clin Oncol, 2013
RESULTS: We divided 286 MLL-rearranged AMLs into three subgroups: t(9;11)(p22;q23) (44.8%), t(6;11)(q27;q23) (14.7%), and t(v;11q23) (40.5%).
Uterine development and fertility are dependent on gene dosage of the nuclear receptor coregulator REA.
Katzenellenbogen et al., Urbana, United States. In Endocrinology, 2012
Optimal uterine development and functional activities require the normal gene dosage of REA, with partial or complete deletion resulting in hyperresponsiveness or underresponsiveness to hormone and subfertility or infertility, respectively.
Site-specific phosphorylation of protein phosphatase 1 regulatory subunit 12A stimulated or suppressed by insulin.
Yi et al., Detroit, United States. In J Proteomics, 2012
Site-specific phosphorylation of protein phosphatase 1 regulatory subunit 12A stimulated or suppressed by insulin.
Subpixel colocalization reveals amyloid precursor protein-dependent kinesin-1 and dynein association with axonal vesicles.
Goldstein et al., San Diego, United States. In Proc Natl Acad Sci U S A, 2012
Data show that amyloid precursor protein (APP) levels are well-correlated with the amount of the light chain of kinesin-1 (KLC1).
LATS1/WARTS phosphorylates MYPT1 to counteract PLK1 and regulate mammalian mitotic progression.
Kuninaka et al., Tokyo, Japan. In J Cell Biol, 2012
It found deoxyribonucleic acid (DNA) damage-induced LATS1 activation caused PLK1 suppression via the phosphorylation of MYPT1 S445.
Mitochondrial dysfunction and adipogenic reduction by prohibitin silencing in 3T3-L1 cells.
Thompson et al., Atlanta, United States. In Plos One, 2011
PHB1 and PHB2 are critical mediators in promoting 3T3-L1 adipocyte differentiation and may be the potential targets for obesity therapies
Genome-wide association study identifies a susceptibility locus for schizophrenia in Han Chinese at 11p11.2.
Zhang et al., Beijing, China. In Nat Genet, 2011
We identified two susceptibility loci for schizophrenia at 6p21-p22.1 (rs1233710 in an intron of ZKSCAN4, P(combined) = 4.76 × 10(-11), odds ratio (OR) = 0.79; rs1635 in an exon of NKAPL, P(combined) = 6.91 × 10(-12), OR = 0.78; rs2142731 in an intron of PGBD1, P(combined) = 5.14 × 10(-10), OR = 0.79) and 11p11.2
Genome-wide association study identifies five new schizophrenia loci.
Schizophrenia Psychiatric Genome-Wide Association Study (GWAS) Consortium, Boston, United States. In Nat Genet, 2011
and two of which have been previously implicated (6p21.32-p22.1 and 18q21.2).
Residual NADPH oxidase and survival in chronic granulomatous disease.
Gallin et al., Frederick, United States. In N Engl J Med, 2011
Chronic granulomatous disease is caused by missense, nonsense, frameshift, splice, or deletion mutations in the genes for p22(phox), p40(phox), p47(phox), p67(phox) (autosomal chronic granulomatous disease), or gp91(phox) (X-linked chronic granulomatous disease), which result in variable production of neutrophil-derived ROIs.
Riboflavin kinase couples TNF receptor 1 to NADPH oxidase.
Krönke et al., Köln, Germany. In Nature, 2009
In mouse and human cells, RFK binds to both the TNFR1-death domain and to p22(phox), the common subunit of NADPH oxidase isoforms.
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