ATP11C Antibodies

Phospholipid-transporting ATPase IG (ATP11C)

Catalytic component of a P4-ATPase flippase complex which catalyzes the hydrolysis of ATP coupled to the transport of aminophospholipids from the outer to the inner leaflet of various membranes and ensures the maintenance of asymmetric distribution of phospholipids. In the cell membrane of erythrocytes, it's required to keep phosphatidylserine (PS) from the inner leaflet preventing its exposure on the surface.

This asymmetric distribution is vital for the survival of erythrocytes in circulation since externalized PS is a phagocytic signal for splenic macrophages (PubMed:26944472). Phospholipid translocation appears also to be implicated in vesicle formation and in uptake of lipid signaling molecules (By similarity).

Gene Information

Human
Gene Name:	ATP11C
Uniprot:	Q8NB49
Entrez:	286410

Family

Belongs to:
cation transport ATPase (P-type) (TC 3.A.3) family

Alternative Names

ATPase IQ; ATPase, class VI, type 11C; ATPIGprobable phospholipid-transporting ATPase IG; ATPIQATPase class VI type 11C; EC 3.6.3; EC 3.6.3.1; phospholipid-transporting ATPase IG

Molecular Weight

Mass (kDA):
129.477 kDA

Genomic Context

Human
Location:	Xq27.1
Sequence:	X; NC_000023.11 (139726346..139933083, complement)

Tissue Specificity

Widely expressed.

Subcellular Localizations

Cell membrane; Multi-pass membrane protein. Endoplasmic reticulum membrane. Efficient exit from the endoplasmic reticulum requires the presence of TMEM30A. Some cell membrane localization observed in the presence of TMEM30B.

Diseases

• Hypoparathyroidism
• Genetic Diseases, X-linked
• Hyperbilirubinemia
• Congenital Absence
• Liver Diseases
• Intrahepatic Cholestasis
• Anemia
• Liver Carcinoma
• Chromosome Inversion
• Hyperbilirubinemia, Hereditary

• Carcinoma
• Cholestasis
• Lymphopenia
• Loss Of Chromosome X

Pathways

• Transport
• Golgi Localization
• Parturition
• Cell Development
• Phospholipid Transport
• Protein Transport
• Phospholipid Translocation

• Localization

PTMs

• Phosphoprotein

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/ATP11C

Best Uses of the ATP11C Marker

In this article, you will learn about ATP11C, an enzyme that is crucial for B cell differentiation. This enzyme bypasses the membrane staining step and is mapped to Xq27.1 locus. After learning about this enzyme, you will learn how to clean the ATP11C Marker. Continue reading to find out more about the best uses ATP11C.

ATP11C is an enzyme critical for B cell differentiation

The function of ATP11C is crucial for the differentiation of B cells, and its mutated form is responsible for hepatic cholestasis. It is an ubiquitously expressed P4 ATPase. It is involved with antigen and cytokine receptor signals. B cells lacking this enzyme can develop abnormal cell differentiation. This condition could eventually lead hepatocellular carcinoma.

The transition from pro-B to pre-B cells requires signaling from the IL-7 receptor, and the rearrangement of immunoglobulin heavy chain genes is essential for this process. Deficiency of ATP11C causes a lack in differentiation in both sexes and reduced production of B cells. Mutant mice show normal numbers and quality of pro-B cell and NK cells, but lack the ATP11C.

In UPS-1 cells, exogenous expression of ATP11C rescues PS-flipping activity. UPS-1 cells were infected with an empty retrovirus vector or a recombinant virus encoding HA-tagged ATP11C(WT). The cells were then treated using NBD-PS. The residual fluorescence could be measured by flow cytometry.

Mutant ATP11C mice have lower B cell proliferation and a decreased production of IL-7, a signaling protein that inhibits pro-B cell proliferation. ATP11C deficient mutant mice had higher numbers than wild-type mice of pre-B-cells. Mutant mice also had higher rates of mutant pro–B cells and IL-7 resistance pre-Bs cells.

Phospholipid transport is directly connected to the function of B-cells. However, our understanding of the process is still incomplete. We still don't understand exactly how the B cell differentiation process works. However, our understanding of the process depends on the discovery and implementation of a missing step. This missing step is ATP11C. This discovery will enable us to better understand the process and function of B cell differentiation.

Mice lacking ATP11C had normal spleens, but a lower number of mature B cell. The percentage of mature B cells was less than 10% in Atp11camb/0 mice. The number of follicular B cells was normal, but there was a lack of mature B cells. This result did not have a significant effect as marginal cells compensated for the absence of ATP11C.

It bypasses the pre-BCR signaling step

BCR activation depends on the ability to bypass the pre-BCR step. This enzyme regulates both the positive and negative aspects of the signaling process. The gene LYN controls ITIM activity. This enzyme has a unique immunoregulatory function. It can also propagate inhibitory signs in certain configurations. BCR activation can also be affected by inhibitory ITAMs.

Pro-B cell proliferation is dependent on the IL-7 receptor. Pro-B cell proliferation was lower in mice without the ATP11C genetic gene than in wild-type mice. In addition, pro-B cell DNA content in wild-type and mutant mice was lower than that of wild-type mice. These results show that the ATP11C mutation inhibits B cell differentiation and prevents it from working correctly.

In a previous study it was discovered that ATP11C required Ig-gene rearrangement to pro-B cells. In mutant mice, the absence of ATP11C caused a decrease in PS flippase activity. However, other members of ATP11C were implicated in B cell cloning as well as genetic studies of yeast. The yeast P4ATPases can regulate protein trafficking, and this could have indirect effects on PS flippase activity.

These subcompartments are crucial for B cell development. However, we don't know much about their function. Despite the importance ATP11c plays in B cell differentiation, there are not many genetic tools available to study these processes. However, it could be a new drug target in the treatment for B cell malignancies. This gene has also shown a link to hepatocellular carcinoma in men.

It skips the membrane staining step

To simulate stained cell surfaces, a new technique uses a stain network. This technique can run at 1.5 mm2/s on a consumer-grade desktop with two GPUs. This approach offers significant advantages over traditional CycleGAN-based methods. It can also avoid the need to do destructive sectioning or biopsies. This new technique will help you save time and effort.

A histological examination of stained tissue is the best way for diagnosing various diseases. The tissue's constituents are revealed by examining it under a microscope. The histological staining stage is an important part of the pathology workflow. It provides contrast and chromatic distinction between tissue constituents. This step allows the pathologist to determine the presence of disease or infection.

For training the virtual staining network, image patches measuring 256 x256 pixels were used. The images were restained by chemically destaining or restaining the steps. The training network used a YCbCr color space as the input and ground truth. The network can accurately predict the presence or absence of a stained cell and can even replace manual staining.