CSNK1A1 Antibodies

Casein kinase I isoform alpha (CSNK1A1)

It can phosphorylate a large number of proteins. Participates in Wnt signaling.

Phosphorylates CTNNB1 at'Ser-45'. May phosphorylate PER1 and PER2.

Gene Information

Human
Gene Name:	CSNK1A1
Uniprot:	P48729
Entrez:	1452

Family

Belongs to:
protein kinase superfamily

Alternative Names

Casein Kinase 1 alpha; casein kinase 1, alpha 1; casein kinase I isoform alpha; CK1CKI-alpha; CSNK1A1; down-regulated in lung cancer; EC 2.7.11.1; HLCDGP1; PRO2975

Molecular Weight

Mass (kDA):
38.915 kDA

Genomic Context

Human
Location:	5q32
Sequence:	5; NC_000005.10 (149492982..149551439, complement)

Subcellular Localizations

Cytoplasm. Cytoplasm, cytoskeleton, microtubule organizing center, centrosome. Chromosome, centromere, kinetochore. Nucleus speckle. Cytoplasm, cytoskeleton, cilium basal body. Localizes to the centrosome in interphase cells, and to kinetochore fibers during mitosis. Also recruited to the keratin cytoskeleton (PubMed:23902688).

Diseases

• Malignant Neoplasms
• Neoplasms
• Neoplasm Metastasis
• Malignant Neoplasm Of Lung
• Malignant Paraganglionic Neoplasm
• Malignant Neoplasm Of Breast
• Carcinoma
• Cell Invasion
• Lung Neoplasms
• Non-small Cell Lung Carcinoma
• Adenoma
• Malnutrition
• Metastatic Malignant Neoplasm To The Lymph Node

• Melanoma
• Hypoxia
• Neoplasm Invasiveness
• Dysplasia
• Multiple Myeloma
• Loss Of Chromosome 5q
• Myelodysplastic Syndrome With Isolated Del(5q)

Interacting Proteins

• CARD11
• CRBN
• LRRK2
• MALT1
• MDM2

• MDM4
• RIPK1

Pathways

• Senescence
• Regulation Of Macroautophagy
• Macroautophagy
• Cell Cycle
• Cell Motility
• Cellular Senescence
• Cellular Homeostasis
• Atp/adp Exchange

• Pathogenesis
• Catabolic Process

PTMs

• Phosphorylation

Research Areas

• Protein Kinase
• Wnt Signaling Pathway

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/CSNK1A1

Best Uses Of The CSNK1A1 Marker

CSNK1A1 RNAi marker blocks UVRAG K29 ubiquitination. This marker also acts as an activator of ZRANB1 DUB activity. The marker has other useful features that are discussed in this article. CSNK1A1 can be used with SDS-PAGE and is not toxic. Its greatest use is in molecular biology. It is compatible with SDS-PAGE and is accessible to all scientists, regardless of whether they are a molecular biologist or biotech engineer, or an expert in cell biology.

CSNK1A1 blocks UVRAG K29 and K33-linked Ubiquitination

We have established that CSNK1A1 blocks UVRAG K29 and/or phosphorylation via SMURF1. Particularly, UVRAG is ubiquitinated through the chains K29 and SMURF1. By inhibiting SMURF1 blocked the ubiquitination process of UVRAG.

CSNK1A1 regulates autophagosome maturation via phosphorylating S522 via UVRAG. Lysosomal degradation is also facilitated by reducing UVRAG phosphorylation. Additionally UVRAG ubiquitination, phosphorylation and UVRAG are key to controlling HCC cell growth and function.

The autophagy mechanism involves the regulation of UVRAG by ubiquitination. UVRAG is not subject to proteolytic ubiquitylation by SMURF1 or HECT E3 Ligase. Counterbalancing modifications on UVRAG, which include direct deubiquitylation via ZRANB1, affect autophagic flux. CSNK1A1 can inhibit UVRAG and also block the autophagic functions of SuFu, a tumor suppressor proteins. SuFu plays a crucial role in Hedgehog signaling which is essential for cerebon aevelopment and tumorigenesis.

Additionally, CSNK1A1 hinders RNF8 E3 ligase, which is responsible for the ubiquitylation of core H2A-type histones. In addition, CSNK1A1 inhibits UVRAG K33-linked ubiquitination. This protein could be useful in anticancer therapies.

Numerous studies have shown that CUL4-mediated nonproteolytic-ubiquitylation CENP- (K124) is a key player in roles in DNA replication and DDR. Two new studies have expanded the significance of the SPOP complex in maintaining DNA integrity. They identified the CUL3/SPOP compound, which promotes nondegradative polyubiquitination Geminin. This protein also hinders interactions between the mini-chromosome maintenance compound (MLKP1) and DNA replication over-firing.

The potential for metastatic growth of breast carcinoma cells is enhanced by the suppression of ubiquitylation mediated by RNF26 via CSNK1A1. For metastatic cancers aependent on TGF-b, therapeutic targeting of CUL4/AMBRA1-mediated SMAD4 Ubiquitylation must also be investigated. The CSNK1A1 inhibitor also blocks UVRAG K33-linked tumor ubiquitination.

This compound also targets GNRh2 and poly(A)-binding protein 1 (PABC1) A protein that is responsible for the replication of DNA. This protein functions as a translocation molecule in the nucleus. Additionally, the activity of GNRh2 has been linked to the hypothalamic axis.

It triggers ZRANB1 DUB activity.

In vitro, the researchers examined the effects of CSNK1A1's mutation on ZRANB1 DUB activity using an assay in which the mutant protein is expressed with CSNK1A1. The T35A mutation T209A blocked CSNK1A1 activating ZRANB1 which is crucial for activating the process of ubiquitination. We also found that the T35A S209A mutant inhibited CSNK1A's activation by UVRAG. Additionally, we discovered that the mutant protein was not active for UVRAG-mediated ubiquitination inhibition which could explain the absence of CSNK1A.

The marker CSNK1A1 phosphorylates ZRANB1 between the Thr35 and Ser209 and Ser209, which activates its deubiquitinating function. It is associated with poor prognosis for HCC patients. UVRAG ubiquitination plays a role in regulating autophagosome maturation. The UVRAG ubiquitination triggers the CSNNK1A1 marker, and the levels of UVRAG S522 phosphorylation correlate well with prognosis.

Incredibly, the CSNK1A1 molecule increases the rate of tumor growth in human cancer cells. It promotes cell division, inhibits cellular immune as well as activation of the inflammatory response, and also aids in the progression of tumors in human cancer cells. Additionally, a role for CSNK1A1 in cancer stem cell self-renewal is likely to be discovered through targeting the HECTH9-HK2 signaling pathway.

The CSNK1A1 gene is located on chromosome 5q32 and is expressed in foun aifferent spliced transcript variants. Each one aiffers in the length and kinase aomain, and flag-UVRAG cells were used to transfect. The tests were conducted using immunoprecipitation phosphatase-l-PPase and other methods.

CSNK1A1 is an E3 ligase that is localized to ER. RNF26 acts as an instrument for perinuclear position of endosomes. It ubiquitylates p62/sequestosome 1 (SQSTM1) scaffold protein and recruits adapters to the membrane of vesicles. The resulting traps stay in the perinuclear space and targeted vesicles recover mobility and are released to allow for rapid microtubule-based transport to the cell outside.

It boosts the phosphorylation process of nuclear FOXO3A

The FOXO family of transcription factors that includes forkhead box O (FOXO) has many advantages, including the suppression and extension of growth. The CK1 alpha-mediated phosphorylation of nuclear FOXO3A protein regulates the stability of the CK1a protein which is then stabilized by a PI3K/AKT effector axis.

As a member of the Forkhead box family, FOXM1 is essential for cell proliferative and Apoptosis. A rise in FOXM1 expression has been linked to the progression and aevelopment of cervical cancer. Recent biochemical and functional studies have confirmed FOXM1's role in oncogenesis. FOXM1 blocks p27 expression, that has anti-proliferative qualities.

Active AMPK blocks FOXM1 expression in cervical cancer cells. The feedback loop is not clear. A FOXM1 inhibitor, thiostrepton, reduced the expression of FOXM1 without altering the activity of AMPK. Similar results were observed when the endogenous FOXM1 protein was eliminated. In this study the inhibition of FOXM1 was affected by a aifferent method.

Besides regulating insulin, CSNK1A1 also protects mammalian neurons from glucose toxicity. It slows down aging and protects neurons against proteotoxicity. These properties make CSNK1A1 an attractive treatment for aging-related illnesses. It can be used to treat a wide range of age-related diseases like Alzheimer's and Parkinson's.

Researchers also found that CSNK1A1 impedes Smad1 signaling. This may be a contributory factor to the progression and aevelopment of diabetic nephropathy. It also plays a role in the aevelopment of other diseases including lupus cancer and aiabetes. It also blocks Col4 and ASM. However, the results are not conclusive. Further research is needed.

It is a kinome RNAi marker

CSNK1A1 has been implicated in many types of cancers. It is responsible for the regulation of apoptosis in erythrocytes, influences cytosolic Ca2+ activity, promotes homolog pairing, and is a regulator of genome organization. CSNK1A1 in Drosophila is responsible for the degrading of chromosome-associated protein H2, which regulates its activity.

The CSNK1A1 gene is part of the CK1 family. It is located on chromosomes 5q32. There are foun variants of this gene that can be alternatively spliced. Each variant aiffers due to a 12-amino-acid "L" insert within the kinase aomain. The CSNK1A1 protein has the conserved PVGKRKR. This is an attribute of vertebrates, and could serve as a signal for nuclear localization. The kinase-related domain includes Ile12 and Ala282 as two regions with high expression of CSNK1A1.

A study using H929 cell lines using a specific siRNA targeting the CSNK1A1 gene revealed that it was significantly decreased after transiently transfected with shRNA. The shRNA 6044 of H929 was used to transduce H929 cell lines, and to inhibit CK1a. After transduction using CK1a siRNA as well as LC3B-II and p62 expression levels were also reduced. These results suggest that CSNK1A1 is a potential drug target for anti-cancer drugs.

The absence of CK1a causes intestinal hyperplasia, which blocks the apoptosis pathway. It is involved in cancers caused by RAS such as colon and functions as a negative regulator for prostate and liposarcoma. It also helps in the treatment of skin cancers caused by ultraviolet. Autophagy is also increased when CK1a is eliminated.