Creld2 Antibodies

Protein disulfide isomerase Creld2 (Creld2)

May regulate transportation of alpha4-beta2 neuronal acetylcholine receptor. .

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Gene Information

Mouse
Gene Name:	Creld2
Uniprot:	Q9CYA0
Entrez:	76737

Family

Belongs to:
CRELD family

Alternative Names

CRELD2; cysteine-rich with EGF-like domain protein 2; cysteine-rich with EGF-like domains 2; DKFZp667O055; MGC11256

Molecular Weight

Mass (kDA):
38.22 kDA

Genomic Context

Mouse
Location:	15|15 E3
Sequence:	15;

Diseases

• Osteochondrodysplasias
• Physiological Stress
• Endoplasmic Reticulum Stress
• Neoplasms
• Metaphyseal Chondrodysplasia
• Multiple Epiphyseal Dysplasia
• Adenocarcinoma
• Malignant Neoplasm Of Prostate
• Neuroblastoma
• Cell Transformation, Neoplastic
• Dysplasia

• Metaphyseal Chondrodysplasia, Schmid Type
• Prostatic Neoplasms
• Malignant Neoplasms
• Neoplasms, Hormone-dependent
• Hypertrophy
• Dwarfism

Pathways

• Secretion
• Transport
• Methylation
• Glycosylation
• Dna Methylation
• Cell Growth

• Chondrocyte Proliferation

PTMs

• Glycosylation

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/Creld2

Boster Bio: Best Uses Of The CRELD2 Marker

This article will discuss key topics concerning the use and history of gene infographics. It will also include information about the CRELD2 marker and its potential applications in the field. If you're interested in learning more about Steven Boster, check out his bio.

High-affinity primary antibodies

In this study, we used a polyclonal antibody to CRELD2 that is Myc/His-tagged to characterize the subcellular localization of CRELD2. We used monoclonal antimyc antibodies to detect Myc tagged CRELD2, as well as anti-CRELD2 clonal antibodies to detect CRELD2 untagged. We then made secondary antibodies against these markers with FITC or rhodamine-conjugated anti-mouse IgG. Finally, we used immunofluorescence microscopy (IFM) to identify the specific antibodies.

KD is a measure of the affinity of monoclonal antibodies to a given drug ligand. This value is generally measured as the ratio between the off-rate and the on-rate of the peptide spots printed on the microarray. The KD value is defined as the ratio of the experimentally measured on and off-rates of the peptide spots. The affinity of an antibody is determined by its KD.

In this study, antibodies specific for hen egg white lysozyme represented different stages of affinity maturation. The increase in affinity was correlated to the number of somatic mutants, despite the fact there was no increase in buried area. The enhanced affinity was linked to an increase at the VH–HEL interface in shape complementarity. The evolution of heme binding proteins is closely related to affinity maturation of hen eggs white lysozyme.

CRELD2 a novel secretory glycoprotein that is controlled sar1 & GRP78. Secretion plays a significant role in the protein's C terminus. We used a monoclonal anti-mouse antibody that recognizes this protein to determine its exact function. However, this antibody cannot be used in COS7 cells. These cells require a culture medium that is rich in fetal bovine serum.

A similar approach is used to generate antibodies for anti-influenza virus. CRELD2 markers allow us to identify antibodies containing the CRELD2 marker. High-affinity antibodies containing the CRELD2 marker have a higher affinity than those expressing it as a soluble IgG. CRELD2 markers have been shown to increase affinity by as much as 2,000-fold.

History

The CRELD2 marker is a novel ER stress response gene. It is a 50 kDa, secretory glycoprotein that is positively regulated and controlled by ATF6, an ER stress master regulator. Overexpression of CRELD2 increases secretion, and its overexpression is associated with the overexpression of the Ig binding protein (IgB) and the MANF gene.

CRELD2 was first detected in mice at the beginning of NS and was found in 3 ml urine from C321R-mutants. CRELD2 production by podocytes increases under ER stress. The CRELD2 marker wasn't detected in the urine of Tg-WT and WT mice.

After bilateral kidney damage, urinary CRELD2 levels were detected within 3 hours. CRELD2 expression levels were highest in the proximal tubes. It peaked at 24 hours, then declined until it completely resolved 15 days after ischemia. It was discovered that the CRELD2 concentration had disappeared completely from the glomeruli within 15 days of ischemia. It was also found that mice with 30 minutes of bilateral ischemia exhibited urinary CRELD2 excretion within three hours after reperfusion.

Acute kidney injuries often cause an elevation in the CRELD2 marker. AKI is severe when urine CRELD2 levels are elevated. High urinary levels of CRELD2 in the urine have been linked with AKI as well as increased infection rates and recurrent blood infections. These findings suggest that patients who have high levels of CRELD2 should have renal transplantation before they can receive hemodialysis.

CRELD2 may be detected in urine and used as a high-throughput method to detect ER Stress. Targeted therapies for patients with rare genetic variants or ER stress may be possible by early detection of CRELD2 markers in urine. This marker will provide a valuable tool in clinical trials. It is also associated with ER stress, making it an important biomarker for disease progression in this condition.

Gene infographics

Boster has created a series infographics about the CRELD2 gene that explain its role in our health. Each infographic contains basic information about each gene and includes all known mouse and human genes. The site also offers a handy gene search tool that will allow you to find the gene that interests you. Here are some highlights from the infographics.