 Hi, my name is Mio Akim. I'm an assistant professor of research in UTI TV, University of Texas of Rio Grande Valley. My name is Liza Morales. I'm a research associate also with UT Rio Grande Valley. We're part of the School of Medicine. It's a new, actually medical school that was founded in 2015. We're very excited about our new medical school. Dr. Kim, she is in the Department of Biomedical Sciences and currently I'm actually in with the South Texas Diabetes and Obesity Institute. I have questions. Why you chose to conduct this research? When I joined Kim's lab in 2014, over the 2015, at this time he has already have a previous data for TCPTP nuclear translocation in C.K. Kaisen Genesis. In his grant, he want to promote his data. He want to find a mechanism of translocation. So how does it work in a nucleus or the cytosome? At the time, I think it's a very big story because TCPTP has known to be in localized nucleus in other cell lines, not skin cells. So if I found this mechanism, so we could know, we could develop the role of TCPTP in nucleus or the skin Kaisen Genesis. So it's a very interesting, so I started that study. Yes, so in general, the phosphotyrosine signaling, you know, it's involved in a lot of different cellular processes and so kinases, which usually are responsible for phosphorylating proteins and activating them, they've been very well studied within different types of cancers and things like that. But we're actually now trying to look at the counterpart to kinases, which is protein tyrosine phosphatases. And TCPTP is, as one of them, as Dr. Kim mentioned, our primary investigator, Dr. Deshinkan, had found that STAT 3, it's a major transcription factor, very critical to the development of skin cancer. He found that TCPTP was one of the major phosphatases to regulate STAT 3. And so, again, as Dr. Kim mentioned, we're delving into TCPTP and its regulation of STAT 3 and found, you know, that TCPTP has potential as a tumor suppressor. And this mechanism that we talk about in the paper, again, as she mentioned, TCPTP is actually more known because of its nuclear localization sites to be found within the nucleus of most cells. And what this mechanism is actually showing is that within keratinocytes, specifically skin cells, it's actually located within the cytoplasm, and then you expose it to a stress such as UVB radiation, and it can actually be translocated into the nucleus where then it acts upon, you know, for example, STAT 3. Yeah, actually, this finding is a tip of the iceberg because of titration phosphatase, it has several phosphatase, phosphorylation sites, so we have already have mutant types, so we want to develop that function in nuclear translocation, other experimental stress. Is it possible I want to find a look for different mechanism in skin calcium genesis and cell apoptosis? Because the TCPTP can have many other substrates other than STAT 3, so there's a potential that it's regulating, you know, many different saline pathways which, you know, are activated by transcription factors or other substrates within the nucleus, and, you know, how are those pathways involved in different aspects of skin cancer development, or even within the keratinocytes themselves, Dr. Candice in our lab has shown, you know, that TCPTP is important for a kerosene type of survival and proliferation and differentiation. So, another question, what you found to be the most challenging or rewarding aspect of the world research? In my case, transfection, because of skin and primary keratinocytes, it's a very difficult to be transfected by using general method, transfection method, so we need many times to find the condition, and then maybe as a writing part, we have to appeal to your previous research researchers. Yes, because as we mentioned, you know, TCPTP is more known to be already within the nucleus, so this was kind of new data showing that there's a potential that it's actually within the cytoplasm, and then there's a specific mechanism for in cells where it's translocated to the nucleus to be activated or triggered and to perform its regulatory activities. In my case, when I started this work, so is it possible to use previous data? So, I'm a little bit confused because the transfection problem, because of the transfection problem, I have difficulties to elucidate this data because the TCPTP localized the boundary in the nucleus membrane. So, you know, the skin is a very sensitive tissue, so the cells, when I stress a little bit, nuclear translocation is very faster and easier, so the time transfection condition is very difficult, but when I found this finding, I realized it is starting to restart, so I'm so very happy. Again, actually, and then also too, as you see in the paper, the data show that this mechanism is actually very critical for TCPTP activity, because if you have, you know, a mutation that affects the target site that allows for the translocation by AKT and 1433 sigma, you lose this nuclear translocation and it affects TCPTP-mediated regulation of receptors. But research, you would like to see that in the picture as a response to your finding or what research you will be doing yourself in the picture. Right before I mentioned, I have several mutant types for TCPTP, so I want to find a novel mechanism of TCPTP in nuclear translocation and, you know, I want to find a substrate for TCPTP, which will work together with TCPTP in skin cancer genesis. That is my next project. And overall, part of the reason our PI wanted to study at our particular university, we're located in South Texas. Being in South Texas, you know, there's a lot of exposure to UV sunlight, these types of things. So we're in a good region where it's an area for, you know, potential for skin cancer. And so these projects can all lead to, you know, identifying, you know, a novel, new target, developing therapies for prevention and treatment