Goat IgM ELISA Set (DEIA641)

Regulatory status: For research use only, not for use in diagnostic procedures.

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Size
1000T
Sample
serum, plasma
Species Reactivity
Goat
Intended Use
Enzyme linked immunosorbent assay (ELISA) for the detection of Goat IgM in serum or plasma.
Contents of Kit
1. Affinity purified Goat IgM Coating Antibody, 1 mL
2. Goat Reference Serum, 0.1 mL
3. HRP Conjugated Goat IgM Detection Antibody, 0.1 mL
Storage
Store kit at 2-8°C or -20°C upon arrival up to the expiration date. Avoid multiple freeze/thaw cycles. For more detailed information, please download the following document on our website.

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References


Chronic wounds alter the proteome profile in skin mucus of farmed gilthead seabream

BMC GENOMICS

Authors: Cordero, Hector; Brinchmann, Monica F.; Cuesta, Alberto; Esteban, Maria A.

Background: Skin and its mucus are known to be the first barrier of defence against any external stressors. In fish, skin wounds frequently appear as a result of intensive culture and also some diseases have skin ulcers as external clinical signs. However, there is no information about the changes produced by the wounds in the mucosae. In the present paper, we have studied the alterations in the proteome map of skin mucus of gilthead seabream during healing of experimentally produced chronic wounds by 2-DE followed by LC-MS/MS. The corresponding gene expression changes of some identified skin proteins were also investigated through qPCR. Results: Our study has successfully identified 21 differentially expressed proteins involved in immunity and stress processes as well as other metabolic and structural proteins and revealed, for the first time, that all are downregulated in the skin mucus of wounded seabream specimens. At transcript level, we found that four of nine markers (ighm, gst3, actb and krt1) were downregulated after causing the wounds while the rest of them remained unaltered in the wounded fish. Finally, ELISA analysis revealed that IgM levels were significantly lower in wounded fish compared to the control fish. Conclusions: Our study revealed a decreased-expression at protein and for some transcripts at mRNA levels in wounded fish, which could affect the functionality of these molecules, and therefore, delay the wound healing process and increase the susceptibility to any infection after wounds in the skin of gilthead seabream.

Genetic Approaches for Definitive Diagnosis of Agammaglobulinemia in Consanguineous Families

JOURNAL OF CLINICAL IMMUNOLOGY

Authors: Ben-Ali, Meriem; Kechout, Nadia; Mekki, Najla; Yang, Jing; Chan, Koon Wing; Barakat, Abdelhamid; Aadam, Zahra; Gamara, Jouda; Gargouri, Lamia; Largueche, Beya; BelHadj-Hmida, Nabil; Nedri, Amel; Ben Ameur, Houcine; Mellouli, Fethi; Boukari, Rachida; Bejaoui, Mohamed; Bousfiha, Aziz; Ben-Mustapha, Imen; Lau, Yu-Lung; Barbouche, Mohamed-Ridha

Autosomal recessive agammaglobulinemia (ARA) is a primary immunodeficiency characterized by absent peripheral B cells, severe hypogammaglobulinemia, and absent BTK gene mutations. In ARA, mutations occur in genes encoding the pre-B cell receptor (pre-BCR) or downstream signaling proteins. In this work, we used candidate gene and whole-exome sequencing to investigate the molecular basis of ARA in 6 patients from 4 consanguineous North-African families. Sanger sequencing of candidate genes encoding the pre-BCR components (Iota G Eta Mu, CD79A, CD79B, IGLL1, and VPREB1) was initially performed and determined the genetic defect in five patients. Two novel mutations in IGHM (p.Val378Alafs*1 and p.Ile184Serfs*21) were identified in three patients from two unrelated kindred and a novel nonsense mutation was identified in CD79A (p.Trp66*) in two siblings from a third kindred. Whole-exome sequencing (WES) was performed on the sixth patient who harbored a homozygous stop mutation at position 407 in the RAG2 gene (p.Glu407*). We concluded that conventional gene sequencing, especially when multiple genes are involved in the defect as is the case in ARA, is costly and time-consuming, resulting in delayed diagnosis that contributes to increased morbidity and mortality. In addition, it fails to identify the involvement of novel and unsuspected gene defects when the phenotype of the patients is atypical. WES has the potential to provide a rapid and more accurate genetic diagnosis in ARA, which is crucial for the treatment of the patients.

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