Effect of a cholecystokinin tetrapeptide analogue on opioid reception under acute and chronic morphine administration

Effects of a modified CCK-4, a tetrapeptide fragment of cholecystokinin, on opioid reception and cAMP level were studied. The modified CCK-4 changed the ligand binding of the opioid receptors of μ-and δ-types in vitro. In vivo, it prevented changes in opioid reception caused by an acute morphine administration or by morphine withdrawal after its long-term administration. The CCK-4 analogue did not exert any effect in the state of intoxication after a long-term administration of morphine or even promoted the morphine effect. The injection of the CCK-4 analogue alone or together with morphine changed the forskolin-stimulated level of cAMP. These changes depended on the brain structure and the duration of the administration of morphine and the CCK-4 analogue.     

Distinct isocomplexes of the TRAPP trafficking factor coexist inside human cells

The transport protein particle (TRAPP) complex is required for proper vesicular transport from the ER to the Golgi. The composition of yeast TRAPP is well characterized, but the organization of mammalian TRAPP complex remains elusive. Using a tandem affinity purification (TAP) approach, we provide first experimental proof for the association of NIBP (NIK/IKKβ binding protein) with Bet3 and find two human paralogs of Trs33 (A and B) associated with Bet3. Interaction studies and gel filtration analysis reveal that both proteins are part of human TRAPP and might mark two distinct isocomplexes that exert different functions in the regulation of ER-to-Golgi traffic.

Structured summary

MINT-6784845:

Bet3 (uniprotkb:O43617) physically interacts (MI:0218) with Trs33B (uniprotkb:Q86SZ2) by anti bait coimmunoprecipitation (MI:0006)

MINT-6785053:

Trs33B (uniprotkb:Q86SZ2) physically interacts (MI:0218) with Bet3 (uniprotkb:O43617) and Sedl (uniprotkb:O14582) by anti bait coimmunoprecipitation (MI:0006)

MINT-6784856:

Bet3 (uniprotkb:O43617) physically interacts (MI:0218) with Trs33A2 (uniprotkb:O75865-2) by anti bait coimmunoprecipitation (MI:0006)

MINT-6785038:

Trs33A1 (uniprotkb:O75865-2) physically interacts (MI:0218) with Sedl (uniprotkb:O14582) and Bet3 (uniprotkb:O43617) by anti bait coimmunoprecipitation (MI:0006)

MINT-6784879:

Bet3 (uniprotkb:O43617) physically interacts (MI:0218) with NIBP (uniprotkb:Q96Q05) by tandem affinity purification (MI:0676)

MINT-6785068:

Trs33B (uniprotkb:Q86SZ2), Trs33A2 (uniprotkb:O75865-2) and Bet3 (uniprotkb:O43617) colocalize (MI:0403) by molecular sieving (MI:0071)

MINT-6785415:

Bet3 (uniprotkb:O43617) physically interacts (MI:0218) with Trs33A1 (uniprotkb:O75865) by anti bait coimmunoprecipitation (MI:0006)

     

Selective separation procedure for determination of ribosomal proteins L7 and L12.

An electrophoretic procedure for the selective separation and determination of the closely similar ribosomal proteins L7 and L12 (which are specifically involved in the GTPase reactions of the ribosome) from the total protein mixture extracted from unwashed ribosomes is described. In this procedure, which takes advantage of their unusually low isoelectric points. L7 and L12 (and a few other acidic proteins) migrate into gel asanions, while the bulk of ribosomal proteins which are basic remain behind. The positions of L7 and L12 were determined with authentic, pure proteins. It was further determined by means of 2-dimensional gel electrophoresis that no other protein components present in unwashed ribosomes comigrate with the bands of L7 and L12.     

Frequency of genetic polymorphisms of ADAM33 and their association with allergic rhinitis among Jordanians

Allergic rhinitis is a chronic inflammatory disease that is assumed to be due to an interaction between different genetic and/or environmental factors. A disintegrin and metalloprotease domain 33 (ADAM33) has been extensively studied as a susceptibility gene in asthma and has been linked to bronchial hyper-responsiveness. In this study, we investigated the association between ADAM33 single nucleotide polymorphisms and the incidence of allergic rhinitis among the Jordanian population. We conducted a case–control association study on 120 adult individuals diagnosed with allergic rhinitis and 128 normal healthy controls. 8 single-nucleotide polymorphisms in ADAM33 were genotyped using PCR-RFLP method. No significant differences in the allelic frequencies of all SNPs tested between AR patients and the control volunteers were found, although S2 C/G SNP showed a tendency toward significance with P = 0.06. On the genotype level significant association were found in the following genotypes: T1 AA, T1 AG, T2 GG, T2 AG, T + 1 GG, T + 1 AG, V4 CG, S2 CC, S2 CG, Q-1AA. Seven haplotypes were present only within AR patients and eight haplotypes were completely absent from the AR patients. Three haplotypes exhibited significant association with AR P ≤ 0.05, two of them were present only in AR patients. In conclusion, the polymorphisms in the ADAM33 gene are associated with susceptibility to AR in the Jordanian population. Furthermore, the haplotype of the tested SNPs were also associated with the risk of AR.