Srcin1 Antibodies

SRC kinase signaling inhibitor 1 (Srcin1)

Acts as a negative regulator of SRC by sparking CSK which inhibits SRC activity and downstream signaling, resulting in impaired cell spreading and migration. Regulates dendritic spine morphology.

Involved in calcium-dependent exocytosis. May play a role in neurotransmitter release or synapse maintenance (By similarity).

Gene Information

Mouse
Gene Name:	Srcin1
Uniprot:	Q9QWI6
Entrez:	56013

Family

Belongs to:
SRCIN1 family

Alternative Names

KIAA1684P140; p130Cas-associated protein; p140CapSNAP25-interacting protein; SNIPSNAP-25-interacting protein; SRC kinase signaling inhibitor 1

Molecular Weight

Mass (kDA):
134.859 kDA

Genomic Context

Mouse
Location:	11|11 D
Sequence:	11;

Tissue Specificity

Expressed predominantly in central nervous system with high levels detected in cortex, cerebellum, midbrain and spinal cord (at protein level). Also expressed in testis and epithelial-rich tissues such as mammary gland, lung and kidney.

Diseases

• Malignant Neoplasms
• Neoplasms
• Tumor Progression
• Metaplastic Cell Transformation
• Tissue Adhesions
• Neoplasm Invasiveness

PTMs

• Methylation

• Phosphoprotein

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/Srcin1

The Best Uses of the SRCIN1 Marker

This article will introduce Steven Boster to you, the man behind SRCIN1's molecule. Learn more about his clinical experience, research, and opinions regarding the SRCIN1 indicator. This biomarker is truly unique. This genetic marker is currently the most widely used in clinical diagnosis for ovarian cancer. We'll also be discussing some of its key uses.

History of Steven Boster

His history with Steve Boster can be traced back as far as 1993, when he created his first product, which was a kit to detect antibodies. Steven Boster was the most prolific primary antibody developer in China by the late 90s. Boster developed proprietary ELISA platforms based on his trade secrets that delivered high-sensitivity ELISA products.

His research

The SRCIN1 gene encodes a protein that contains two highly charged coiled-coil domains. It is believed to play an essential part in cancer progression. His research revealed that miRNAs target the gene and suppress its growth. p140Cap is one of several miRNAs implicated in cancer. These molecules suppress the expression of p140Cap, a gene that he hopes to target to improve cancer detection and treatment.

To identify the putative miR-373 binding sites, his lab used the 3'UTR region of SRCIN1. The genome of SKN-2 (2) cells was amplified with the plasmid containing the wild type SRCIN1 (and the mutated SRCIN1) plasmid. The mutated and wild type 3'UTRs of SRCIN1 were then subcloned into psiCHECK2 luciferase Vector, respectively. All constructs have been confirmed by DNA sequencing.

His studies have shown that patients with a high level of p140Cap expression are more likely to survive. This gene is linked to higher survival rates, especially among ERBB2-positive patients with breast cancer. His research on SRCIN1 highlights, interestingly, the importance of this gene and its post-transcriptional control in cancer. SRCIN1 plays a crucial role in the regulation and expression of the tumor interactome.

SRCIN1 functions as a target of miR-373. It has been implicated also in the growth and metastasis NB cell growth. Furthermore, the SRCIN1 gene is highly conserved in mammals. Its expression may be a reliable marker of cancer. The next step in SRCIN1 testing is to create new drugs. If it's successful, it could become a new treatment option to treat NSCLC.

His clinical experience

The SRCIN1 marker is a biomarker that could be a useful addition to the NB patient cohort stratification. This biomarker is found in the human neonatal adrenal medulla which is the primary site for NB onset in more than 30% of patients. Its expression in tumors can help determine if the treatment is working as expected or if additional testing may be necessary.

His opinions on SRCIN1

We report in this study that SRCIN1 overexpression inhibits HepG2 cell proliferation. This finding has some caveats. SRCIN1 can also be overexpressed, which can inhibit the growth and development of other cell types. This will be explained in the context SRCIN1 and Cancer. Let's get on to the important conclusions and questions that were raised during the study.

We first examined the effects of SRCIN1 overexpression on the epithelial-mesenchymal transition in HepG2 cells. The observed phenotypes were increased invasiveness, increased mobility, resistance to apoptosis, production of extracellular matrix components, and increased resistance to migratory. Western blot also measured the levels of vimentin, N-cadherin (E-cadherin), and N-cadherin protein. Next, we determined the mRNA levels of N-cadherin and Snail using qRT-PCR.

The 3'UTR of SRCIN1 contains putative miR-373 binding sites. To validate this finding, we amplified the 3'UTR of the gene from the genome of SK-N-BE(2) cells. After cloning, we introduced the mutations using site-directed molecular mutagenesis (SDM) We analyzed the gene expression levels in both wild-type and mutated SRCIN1 cells by Western blot.

SRCIN1 is a tumor suppressor for human liver cancer. It inhibits HepG2 and EMT cell proliferation. MiR-32 regulates SRCIN1, and overexpression promoted HepG2-cell proliferation. Our data indicate that SRCIN1 is an important target in the fight against liver cancer. How can we stop SRCIN1 from causing cancer?