BACKGROUND: Khellin is a naturally occurring furochromone which, when combined with artificial ultraviolet (UV) A or solar irradiation (KUVA), is reported to repigment vitiligo skin as effectively as PUVA photochemotherapy. The exact mechanism of KUVA-induced repigmentation is unknown. OBJECTIVES: The aim of this study was to test the effect of khellin and KUVA on proliferation and melanogenesis of normal human melanocytes and Mel-1 melanoma cells in vitro. METHODS: Cultured normal human melanocytes, Mel-1 melanoma cells and fibroblasts were treated with khellin, UVA and KUVA and the effect on proliferation determined by cell counting. The effect on melanogenesis was determined by a radiometric melanin formation assay. Changes in gene expression and protein synthesis were determined by Northern blot, reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blot analyses. RESULTS: Khellin stimulated proliferation of Mel-1 melanoma cells and melanocytes at concentrations between 1 nmol L-1 and
TY - JOUR. T1 - Establishment of a Kit-negative cell line of melanocyte precursors from mouse neural crest cells. AU - Kawa, Yoko. AU - Soma, Yoshinao. AU - Nakamura, Masayuki. AU - Ito, Masaru. AU - Kawakami, Tamihiro. AU - Baba, Takako. AU - Sibahara, Kuniko. AU - Ohsumi, Kayoko. AU - Ooka, Shiho. AU - Watabe, Hidenori. AU - Ono, Hirotake. AU - Hosaka, Eri. AU - Kimura, Satoko. AU - Kushimoto, Tsuneto. AU - Mizoguchi, Masako. PY - 2005/6. Y1 - 2005/6. N2 - We previously established a mouse neural crest cell line named NCCmelb4, which is positive for Kit and negative for tyrosinase. NCCmelb4 cells were useful to study the effects of extrinsic factors such as retinoic acids and vitamin D3 on melanocyte differentiation, but in order to study the development of melanocytes from multipotent neural crest cells, cell lines of melanocyte progenitors in earlier developmental stages are needed. In the present study, we established an immortal cell line named NCC-melb4M5 that was derived from NCCmelb4 ...
Neural crest cells are multipotent progenitor cells that originate from the dorsal neural tube at the border of the neural plate and the lateral epidermis to give rise to various tissues, including the skeletal elements of the face and head, dorsal root and sympathetic ganglia, the glial cells of the peripheral and enteric nervous systems, and melanocytes (Baker and Bronner-Fraser, 1997; Knecht and Bronner-Fraser, 2002; Le Douarin et al., 2004; Selleck et al., 1993; Trainor, 2005). Neural crest-derived melanocytes originate as non-pigmented precursors called melanoblasts, which migrate along characteristic pathways to various destinations, such as the dermis and epidermis, the inner ear and the choroids of the eye (Crane and Trainor, 2006; Dupin and Le Douarin, 2003; Sauka-Spengler and Bronner-Fraser, 2006; Steel and Barkway, 1989). The development of mature pigment-producing melanocytes from their neural crest precursors is a complex process involving melanoblast specification, proliferation, ...
Vitiligo is an autoimmune condition characterized by loss of epidermal melanocytes. High frequencies of melanocyte-reactive cytotoxic T cells in the peripheral blood of vitiligo patients and the observed correlation between perilesional T-cell infiltration and melanocyte loss in situ suggest the important role of cellular autoimmunity in the pathogenesis of this disease. We isolated T cells from both perilesional and nonlesional skin biopsies obtained from five vitiligo patients, then cloned and analyzed their profile of cytokine production after short-term, nonspecific expansion in vitro. Perilesional T-cell clones (TCC) derived from patients with vitiligo exhibited a predominant Type-1-like cytokine secretion profile, whereas the degree of Type-1 polarization in uninvolved skin-derived TCC correlated with the process of microscopically observed melanocyte destruction in situ. Detailed analysis of broad spectrum of cytokines produced by perilesional- and nonlesional-derived CD4+ and CD8+ TCC confirmed
TY - JOUR. T1 - Identification of a novel peptide derived from the melanocyte‐specific gp100 antigen as the dominant epitope recognized by an HLA‐A2.1‐restricted anti‐melanoma CTL line. AU - Barker, Alexander B.H.. AU - Schreurs, Marco W.J.. AU - Tafazzul, Gaalda. AU - De Boer, Annemiek J.. AU - Kawakami, Yutaka. AU - Adema, Gosse J.. AU - Figdor, Carl G.. N1 - Copyright: Copyright 2016 Elsevier B.V., All rights reserved.. PY - 1995/7/4. Y1 - 1995/7/4. N2 - Cytotoxic T lymphocytes (CTL) reactive with human melanoma tumor cells occasionally display cross‐reactivity with normal melanocytes. Previously, we identified the melanocyte lineage‐specific antigen gp100 that is expressed by both melanoma cells and normal melanocytes, as a target antigen for tumor‐infiltrating lymphocytes derived from a melanoma patient (TIL 1200). Here, we demonstrate that the oligoclonal HLA‐A2.1‐restricted TIL 1200 line is reactive with 2 distinct peptides derived from the gpl00 protein. Apart from the ...
Piebaldism is a rare autosomal dominant disorder of melanocyte development. Common characteristics include a congenital white forelock, scattered normal pigmented and hypo pigmented macules and a triangular shaped
The transfer of melanin from melanocytes to keratinocytes is a crucial process underlying maintenance of skin pigmentation and photoprotection against UV damage. Here, we present evidence supporting coupled exocytosis of the melanin core, or melanocore, by melanocytes and subsequent endocytosis by keratinocytes as a predominant mechanism of melanin transfer. Electron microscopy analysis of human skin samples revealed three lines of evidence supporting this: (1) the presence of melanocores in the extracellular space; (2) within keratinocytes, melanin was surrounded by a single membrane; and (3) this membrane lacked the melanosomal membrane protein tyrosinase-related protein 1 (TYRP1). Moreover, co-culture of melanocytes and keratinocytes suggests that melanin exocytosis is specifically induced by keratinocytes. Furthermore, depletion of Rab11b, but not Rab27a, caused a marked decrease in both keratinocyte-stimulated melanin exocytosis and transfer to keratinocytes. Thus, we propose that the predominant
The terminal differentiation of melanocytes is associated with the transcriptional activation of genes responsible for pigment production such as tyrosinase. Pigment cell-specific transcription factors, such as Mitf, as well as specific proximal and distal regulatory elements (DRE) are implicated in the tight control of tyrosinase expression during development and adulthood. Proper tyrosinase expression in melanocytes depends upon the presence of a DRE that is located at -15 kb and provides enhancer activity via a central element termed core-enhancer. In this report, we show that the transcription factors Sox10, Mitf and USF-1 are able to activate the core-enhancer in luciferase reporter assays. Comparative sequence analysis identified evolutionarily motifs resembling Sox10 binding sites that were required for full enhancer activity in melanoma cells and in tyrosinase::lacZ transgenic mice. Sox10 was able to bind the DRE in vitro and mutation of the conserved motifs abolished the enhancer ...
Fig. 1. Cytokine-ELISA of culture supernatants from malignant melanoma cell lines and melanocyte cultures. The melanoma cell lines MV3, BLM (highly metastatic, marked by **) and IF6, 530 (low metastatic potential, marked by ∗) were kept for 24 h under hypoxia, followed by an additional 24 h of reoxygenation. Parallel cultures kept under normoxia for 24 and 48 h were used as control. A, ANG; B, VEGF; and C, Gro-α, cytokine production was determined by solid phase ELISA; bars, SD. D, ANG, VEGF, and Gro-α production in two melanocyte cultures, which were kept under the same conditions. Values (pg/106 cells) are given as means of three independent experiments for each cytokine; bars, SD. Differences concerning ANG induction levels between highly aggressive and low aggressive cell lines were statistically significant (P ≤ 0.05), whereas differences between baseline levels were not statistically significant.. ...
Vitiligo is a chronic disease that causes loss of melanocyte and pigment of the skin. Traditional treatments for vitiligo including topical corticosteroids and phototherapy lead to limited clinical effects. Autologous melanocyte transplantation is another way to treat vitiligo. However, the effect is largely affected by whether cultivated melanocytes are successfully uptaken by vitiliginous skin. The aim of this study is to survey the self-assembly on biomaterials and functional analysis. In the long run, this study may provide a better way for treatment of vitiligo ...
The skin has two layers - the epidermis and the dermis. Melanocytes are special cells present in the bottom of the epidermis which make a pigment called melanin. The melanin is passed to the nearby skin cells, which colours the skin and protects them from the suns rays. Melanin causes the skin to tan in fair-skinned people. Dark-skinned people have more active melanocytes. The melanocytes are stimulated to make more melanin when exposed to sunlight.. Areas of skin with patches of vitiligo have no or very few melanocytes. The melanocytes are either damaged or destroyed in the body. Therefore, melanin cannot be made and the colour of the skin is lost. It is not known why the melanocytes go from affected areas of skin. They may be destroyed by the immune system or self-destruct for reasons not yet known. It is thought to be an autoimmune condition. This means that your own immune system (which normally protects your body from infections) causes damage. In the case of vitiligo, it destroys your ...
Previous work has demonstrated that two key melanocyte-specific elements termed the MSEu and MSEi play critical roles in the expression of the melanocyte-specific tyrosinase-related protein 1 (TRP-1) promoter. Both the MSEu and MSEi, located at position -237 and at the initiator, respectively, bind a melanocyte-specific factor termed MSF but are also recognized by a previously uncharacterized repressor, since mutations affecting either of these elements result in strong up-regulation of TRP-1 promoter activity in melanoma cells. Here we demonstrate that repression mediated by the MSEu and MSEi also operates in melanocytes. We also report that both the MSEu and MSEi are recognized by the brachyury-related transcription factor Tbx2, a member of the recently described T-box family, and that Tbx2 is expressed in melanocyte and melanoblast cell lines but not in melanoblast precursor cells. Although Tbx2 and MSF each recognize the TRP-1 MSEu and MSEi motifs, it is binding by Tbx-2, not binding by MSF, that
TY - JOUR. T1 - Basic fibroblast growth factor and ultraviolet B transform melanocytes in human skin. AU - Berking, Carola. AU - Takemoto, Richelle. AU - Satyamoorthy, Kapaettu. AU - Elenitsas, Rosalie. AU - Herlyn, Meenhard. PY - 2001. Y1 - 2001. N2 - Ultraviolet (UV) light is an epidemiological risk factor for melanoma, but its specific contribution to melanoma induction is not known. The first critical step of melanoma development, ie, the uncontrolled proliferation of melanocytes, may be induced by a combination of UV damage and an imbalance of growth factor production by cells in the immediate area of the melanocyte. Among several candidates, basic fibroblast growth factor (bFGF) is the major autocrine growth factor in melanoma and associated with tumor progression. Overexpression of bFGF via adenoviral gene transfer in human skin xenografted to severe combined immunodeficiency mice led to black-pigmented macules within 3 weeks of treatment. Immunofluorescence analysis demonstrated ...
Hyperpigmentation is a term used to describe a typically harmless condition of the skin in which certain areas are noticeably darker than the rest of the skin. Hyperpigmentation occurs when the body produces an excess of pigment called melanin. Although hyperpigmentation is not harmful to the body, it can be anxiety producing for those who have it because it is an obvious, visible condition of the skin. When melanocytes, or melanin-producing cells in the bottom layer of the skins epidermis, do not function properly, hyperpigmentation can occur. A high concentration of melanocytes or hyperactive melanocytes can be a factor. The many causes of hyperpigmentation include skin inflammation, acne, too much sun exposure, genetics, hormone changes or imbalances, and medications, to name a few. Although there is no true cure for hyperpigmentation, the overall appearance of the skin can be dramatically improved by the use of lightening techniques to even out the skin to a certain degree. It is important ...
A key link between amino acid catabolism and immune regulation in cancer is the augmented tryptophan (Trp) catabolism through the kynurenine pathway (KP), a metabolic route induced by interferon-γ (IFN-γ) and related to poor prognosis in melanomas. Besides its role in cancer, IFN-γ plays a key role in the control of pigmentation homeostasis. Here we measured KP metabolites in human melanoma lines and skin melanocytes and fibroblasts in response to IFN-γ. In general, IFN-γ affected KP in skin cells more than in melanoma cells, supporting IFN-γ roles in skin physiology and that of stromal cells in modulating the tumor microenvironment. ...
During progression of melanoma, malignant melanocytes can be reprogrammed into mesenchymal-like cells through a process similar to epithelial-mesenchymal transition (EMT), which is associated with downregulation of the junctional protein E-cadherin and acquisition of a migratory phenotype. Recent evidence supports a role for SLUG, a transcriptional repressor of E-cadherin, as a melanocyte lineage transcription factor that predisposes to melanoma metastasis. However, the signals responsible for SLUG expression in melanoma are unclear and its role in the invasive phenotype is not fully elucidated. Here, we report that SLUG expression and activation is driven by SPARC (also known as osteonectin), a secreted extracellular matrix-associated factor that promotes EMT-like changes. Ectopic expression or knockdown of SPARC resulted in increased or reduced expression of SLUG, respectively. SLUG increase occurred concomitantly with SPARC-mediated downregulation of E-cadherin and P-cadherin, and induction ...
Protein target information for Microphthalmia-associated transcription factor (human). Find diseases associated with this biological target and compounds tested against it in bioassay experiments.
De pigmentation of the skin refers to the absence of melanin in skin cells. The skin is made up of special cells called melanocytes. Melanocytes are also known as stem cells because the cells that produce melanin in the skin. Melanin is the role of protecting cells from the skin cells and tissues of the sun acts as a sunscreen and pigment-producing cells. Pigment cells are the pigment of the skin. They are present in the skin in three different colors (black, yellow and dark brown ...
In order to facilitate understanding of pigment cell biology, we developed a method to concomitantly purify melanocytes, iridophores, and retinal pigmented epithelium from zebrafish, and analyzed their transcriptomes. Comparing expression data from these cell types and whole embryos allowed us to reveal gene expression co-enrichment in melanocytes and retinal pigmented epithelium, as well as in melanocytes and iridophores. We found 214 genes co-enriched in melanocytes and retinal pigmented epithelium, indicating the shared functions of melanin-producing cells. We found 62 genes significantly co-enriched in melanocytes and iridophores, illustrative of their shared developmental origins from the neural crest. This is also the first analysis of the iridophore transcriptome. Gene expression analysis for iridophores revealed extensive enrichment of specific enzymes to coordinate production of their guanine-based reflective pigment. We speculate the coordinated upregulation of specific enzymes from ...
In a study reported in Clinical Cancer Research, Bartlett and colleagues found that melanoma metastases exhibit site-specific antigen heterogeneity that correlates with T-cell infiltration.. A total of 3,086 metastatic tumors involving various anatomic sites were assessed for a panel of melanocyte differentiation antigens, which revealed a site-specific pattern of antigen expression that was highest in the brain, intermediate in soft tissues/lymph nodes, and lowest in visceral metastases. Hierarchical clustering analysis supported the finding of a phylogenetically determined pattern of antigen expression varying by anatomic site of the metastases. Expression of the melanocyte differentiation antigen tyrosinase was more frequently lost in metastatic sites other than the brain and was correlated with endogenous CD8-positive and CD4-positive T-cell infiltrates.. The investigators concluded, Site-specific antigen heterogeneity represents a novel attribute for human melanoma metastases that should ...
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Abstract: : Purpose: Isolation of adult human cells able to produce neurons is of particular interest to have an in vitro model of human neurogenesis and to provide cells for neural tissue repair. Several eye tissues have as origin the neuroectoderm: the retina including RPE cells, the iris, and the melanocytes located in the choroids and the sclera. Previous observations in the sixties suggest that some eye melanoma might generate neurons. In this study we investigate the possibility of generating neurons in vitro from human eye-derived melanocytes. Methods: Eyes from deceased donors constitute our tissue source. During dissection, melanocytes are scratched off the sclera to produce high melanocyte density cultures. Cells were plated in the presence of EGF and FBS. Results: After one week in growth medium, melanocytes proliferated in clusters generating a monolayer of pigmented and non-pigmented cells. The first step of growth took one month. Cells were transferred on laminin substrate to ...
Transfer of the melanocyte-specific and lysosome-related organelle, the melanosome, from melanocytes to keratinocytes is crucial for the protection of the skin against harmful ultraviolet radiation (UVR)--our main physiological cutaneous stressor. However, this commonplace event remains a most enigmatic process despite several early hypotheses. Recently, we and others have proposed a role for filopodia in melanin transfer, although conclusive experimental proof remained elusive. Using known filopodial markers (MyoX/Cdc42) and the filopodial disrupter, low-dose cytochalasin-B, we demonstrate here a requirement for filopodia in melanosome transfer from melanocytes to keratinocytes and also, unexpectedly, between keratinocytes. Melanin distribution throughout the skin represents the key phenotypic event in skin pigmentation. Melanocyte filopodia were also necessary for UVR-stimulated melanosome transfer, as this was also inhibited by MyoX knockdown and low-dose cytochalasin-B. Knockdown of ...
Vitiligo is a chronic depigmentation skin disease, vitiligo patients should pay special attention to it in their daily life. Diet restrictions are quite important for vitiligo patients. There are several diet attentions Id like to introduce
Vitiligo treatment in Delhi has seen many new changes over the last few years. Vitiligo surgery has come up in a big was with non cultured Melanocytes cell suspension giving a new hope for patients of Vitiligo who were resistant to medical treatment. Vitiligo is a skin disease where de-pigmentation of the skin occurs due…
Since tumor progression is dependent on the ability of malignant cells to interact with the extracellular matrix, molecules on the cell surface which mediate cell-substratum interactions are likely to be important regulators of tumor invasion and metastasis. The purpose of this study was to examine the distribution of one such group of cell adhesion receptors, the integrins, in benign and malignant lesions of human melanocytes. The distribution of integrin adhesion receptors was defined on cells in culture derived from normal and malignant melanocytes and in tissue sections from benign to increasingly malignant melanocytic lesions using a panel of monoclonal antibodies against specific integrin subunits. Cells in culture expressed a large variety of integrins, including all of the previously characterized members of the β1 subfamily plus the αv/β3 vitronectin receptor. The expression of integrins was similar in cells cultured from either benign or malignant lesions. In contrast, consistent ...
Using an ultrafast femtosecond laser, researchers at Tufts University in Medford, Mass., were able to label, draw patterns on, and remove individual melanocytes cells from a species of frog tadpole (Xenopus) without damaging surrounding cells and tissues. Melanocytes are the cells responsible for skin pigment; they also are descendants of a specific type of stem cell that has regenerative potential and other characteristics similar to some cancer cells.. By precisely marking and ablating these cells, the researchers were able to track how melanocytes migrated and regenerated within a live organism. The researchers hope this technique will enable new avenues of research in wound repair, regenerative medicine, and cancer studies. The new method could also be used to study how certain organisms respond to spinal cord damage and how they are able to regenerate portions of their spinal cords.. According to the researchers, femtosecond lasers have already become important tools in biological studies ...
Increased pigmentation of the skin from UV is thought to help minimize the damage from UV, said NCI Director John E. Niederhuber, M.D. This research on SOX9 not only gives us important insights into the intricate mechanism our body uses to protect itself from ultraviolet rays, but also into cellular pathways that might contribute to the origins and spread of melanoma.. After showing that melanocytes in normal human skin express SOX9 under normal conditions, the investigators exposed normal human melanocytes to UV radiation, and compared the levels of SOX9 between radiated and non-radiated cells. They found that levels of SOX9 increased within two hours after UV exposure, and continued to increase until eight hours after exposure.. The investigators next attempted to pinpoint the cellular mechanisms responsible for the increased levels of SOX9 after UV exposure. They chose to examine a cell-signaling pathway, called the cAMP pathway, that is known contribute to the regulation of human ...
Purpose: In this study, we assessed the specific role of BRAF(V600E) signaling in modulating the expression of immune regulatory genes in melanoma, in addition to analyzing downstream induction of immune suppression by primary human melanoma tumor-associated fibroblasts (TAF).. Experimental Design: Primary human melanocytes and melanoma cell lines were transduced to express WT or V600E forms of BRAF, followed by gene expression analysis. The BRAF(V600E) inhibitor vemurafenib was used to confirm targets in BRAF(V600E)-positive melanoma cell lines and in tumors from melanoma patients undergoing inhibitor treatment. TAF lines generated from melanoma patient biopsies were tested for their ability to inhibit the function of tumor antigen-specific T cells, before and following treatment with BRAF(V600E)-upregulated immune modulators. Transcriptional analysis of treated TAFs was conducted to identify potential mediators of T-cell suppression.. Results: Expression of BRAF(V600E) induced transcription of ...
Vitiligo. Vitiligo is a form of leukoderma, or loss of skin pigmentation. Vitiligo affects at least 1% of the worlds population, and about half of people with this skin disorder experience some pigment loss before the age of 20. About one third of all Vitiligo patients report that other family members also have the condition. Vitiligo develops as white spots in the skin that vary in size and location. The spots occur when melanocytes are destroyed and melanin can no longer be produced. Melanocytes normally occur throughout the skin, and in the hair follicles, mouth, eyes, and some parts of the central nervous system. With Vitiligo, pigment cells can be lost in any of these areas.. Severe trauma such as burns can also destroy pigment cells, resulting in leukoderma. Stretch marks, acne scars, post-surgical and traumatic scars can also produce a similar loss of pigment.. Until recently the only treatments available included UV phototherapy and topical or injected corticosteroids. And while none of ...
1-Hydroquinone HQ causes reversible inhibition of cellular metabolism by affecting both DNA and RNA synthesis. The cytotoxic effects of HQ are not limited to melanocytes, but the dose required to inhibit cellular metabolism is much higher for nonmelanotic cells than for melanocytes. Thus, HQ can be considered a potent melanocyte cytotoxic agent with relatively high melanocyte-specific cytotoxicity. HQ is also a poor substrate of tyrosinase, thereby competing for tyrosine oxidation in active melanocytes. Contact dermatitis occurs in a small number of patients and responds promptly to topical steroids. An uncommon, yet important, adverse effect of HQ is exogenous ochronosis. This disorder is characterized by progressive sooty darkening of the skin area exposed to HQ. Histologically, degeneration of collagen and elastic fibers occurs. This degeneration is followed by the appearance of characteristic ochronotic deposits consisting of crescent-shaped, ochre-colored fibers in the dermis.hydroquinone ...
Our research goals are to discover innovative and effective treatments for melanoma by targeting innate pathways that occur during normal melanocyte development and stem cell maintenance. We find that the normal molecular processes that regulate cellular differentiation, homeostasis, growth, and migration of adult and embryonic melanocytes are corrupted during melanoma tumorigenesis, progression, and metastasis. The discovery of these molecular pathways and knowledge on how they function will reveal new targets for future melanoma therapies.. ...
The purpose of this study is to evaluate the hypothesis that, in patients with stable vitiligo unresponsive to conventional treatments including traditional phototherapy and/or topical steroids, the application of a non-cultured autologous hair follicle outer-root-sheath melanocytes suspension in the area affected by the disease followed by targeted ultraviolet B (UVB) phototherapy can lead to a significant skin repigmentation. To assess the effect of the proposed treatment, a within-subject controlled study involving selected symmetric lesion areas localized to the back of the hands will be conducted ...
Man: Just For Men. Shell love the way you look. Flanagan: So why does it happen?. Dr. Jennifer Chwalek: The process of hair changing from darker color to white or gray with age is mainly due to genetics. It can be inherited from either parent. The color of our hair is determined by the form of hair pigment that we have. The pigment is actually produced along the hair shaft, and there are two main forms of hair pigment. Theres eumelanin and pheomelanin. Eumelanin is what we see in brunettes and darker-haired people, and pheomelanin is what we see in blonds and redheads. The cells in our hair bulb produce a little bit of hydrogen peroxide, which is a metabolic byproduct, and typically theres an enzyme called catalase that breaks this down to water and oxygen. But as we age, theres declining levels of catalase, and this allows the build-up of hydrogen peroxide in the hair bulb, which damages and destroys the melanocytes, or the pigment-producing cells, of our hair.. Flanagan: So I wanted you to ...
TY - JOUR. T1 - Store-operated Ca2+ entry (SOCE) regulates melanoma proliferation and cell migration. AU - Umemura, Masanari. AU - Baljinnyam, Erdene. AU - Feske, Stefan. AU - De Lorenzo, Mariana S.. AU - Xie, Lai Hua. AU - Feng, Xianfeng. AU - Oda, Kayoko. AU - Makino, Ayako. AU - Fujita, Takayuki. AU - Yokoyama, Utako. AU - Iwatsubo, Mizuka. AU - Chen, Suzie. AU - Goydos, James S.. AU - Ishikawa, Yoshihiro. AU - Iwatsubo, Kousaku. PY - 2014/2/21. Y1 - 2014/2/21. N2 - Store-operated Ca2+ entry (SOCE) is a major mechanism of Ca 2+ import from extracellular to intracellular space, involving detection of Ca2+ store depletion in endoplasmic reticulum (ER) by stromal interaction molecule (STIM) proteins, which then translocate to plasma membrane and activate Orai Ca2+ channels there. We found that STIM1 and Orai1 isoforms were abundantly expressed in human melanoma tissues and multiple melanoma/melanocyte cell lines. We confirmed that these cell lines exhibited SOCE, which was inhibited by knockdown ...
The expression of genes encoding antioxidant and/or phase 2 detoxifying enzymes can be enhanced in response to various environmental stresses. The main transcription factor involved in this response is nuclear factor erythroid 2-related factor 2 (Nrf2). Nrf2 activity is negatively regulated by the protein Kelch-like-Ech-associated-protein 1 (Keap1). While the roles of Nrf2 and phase 2 genes in chemoprevention of carcinogenesis have been well described; only few studies have dealt with their role in skin cancer. Normal human keratinocytes (NHK) and melanocytes (NHM) were treated by chemical inducers of the Nrf2 pathway or by small interfering RNAs (siRNA) used to knock down Keap1 mRNA. The above treatments resulted in significant stimulation of NQO-1 (NADPH-Quinone-Oxidoreductase 1) gene expression. GCL (gamma-Glutamyl-cysteinyl-ligase) gene was also induced but interestingly increased mRNA encoding the catalytic, heavy subunit GCLC was mainly stimulated in NHK, whereas the mRNA encoding the ...
By now, youve been told to keep track of your moles and have a dermatologist look at them regularly. And rightfully so: 30% of all melanomas begin as a mole, and 90% of moles have cancer-causing properties. However, despite that huge number, most moles wont become malignant, and up until a few years ago, scientists werent sure why. University of Michigan researchers pinpointed the prevention in a cell structure called endoplasmic reticulum, responsible for cells protein production. ER senses activity in melanocytes (the pigment cells) and essentially puts them in check. When amino acids start to build up, ER puts the cells in suspended animation by slowing or unfolding the protein, and tumor creation is suppressed. In the case of moles, melanocytes can stay this way for 20 to 40 years or even your whole life, said Maria Soengas, PhD, of the Multidisciplinary Melanoma Clinic. For most of us, just holding cells in an arrested state is sufficient to prevent the development of cancer. ...
Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor ...
Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor ...
undergraduate co-author. Huang, C-c, Monte, A. CANCEROUS CELL GROWTH INHIBITING COMPOUNDS. (melanoma treatments) U.S. Patent No. US 10,550,095 B2:, U.S. Patent and Trademark Office, Date Issued: February 4, 2020.. Martinson, K.,* Stueven, N.*, Monte, A., Huang, C-C. A Novel Stilbene-Like Compound That Reduces Melanin Through Inhibiting Melanocyte Differentiation and Proliferation without Inhibiting Tyrosinase. Cosmetics, 2018, 5(45) 1-14.. Steuven, N. A.*, Schlaeger, N. M.*, Monte, A. P., Huang, S.-P. L., Huang, C.-c. A novel stilbene-like compound that inhibits melanoma growth by regulating melanocyte differentiation and proliferation. Toxicology and Applied Pharmacology, 2017, 337, 30-38.. Schwan, W. R., Polanowski, R., Dunman, P. M., Medina-Bielski, S.*, Lane, M.*, Rott, M. A., Lipker, L.*, Wescott, A.*, Monte, A. P., Cook, J. M., Baumann, D., Tiruveedhula, V. V. N. Phani B., Witzigmann, C. M., Mikel, C.*, Rahman, M. T. Identification of Staphylococcus aureus cellular pathways affected ...
TY - JOUR. T1 - Informatic selection of a neural crest-melanocyte cDNA set for microarray analysis. AU - Loftus, S. K.. AU - Chen, Y.. AU - Gooden, G.. AU - Ryan, J. F.. AU - Birznieks, G.. AU - Hilliard, M.. AU - Baxevanis, A. D.. AU - Bittner, M.. AU - Meltzer, P.. AU - Trent, J.. AU - Pavan, W.. N1 - Copyright: Copyright 2015 Elsevier B.V., All rights reserved.. PY - 1999/8/3. Y1 - 1999/8/3. N2 - With cDNA microarrays, it is now possible to compare the expression of many genes simultaneously. To maximize the likelihood of finding genes whose expression is altered under the experimental conditions, it would be advantageous to be able to select clones for tissue-appropriate cDNA sets. We have taken advantage of the extensive sequence information in the dbEST expressed sequence tag (EST) database to identify a neural crest-derived melanocyte cDNA set for microarray analysis. Analysis of characterized genes with dbEST identified one library that contained ESTs representing 21 neural ...
Vitiligo is a stubborn skin disease which make the patients suffered a lot. Vitiligo patients need to have a more comprehensive understanding about the health cares for their vitiligo and search for a treatment earlier. There are 5 daily he
A fundamental event in the development and progression of malignant melanoma is the de-regulation of cancer-relevant transcription factors. We recently showed that c-Jun is a main regulator of melanoma progression and, thus, is the most important member of the AP-1 transcription factor family in this disease. Surprisingly, no cancer-related specific c-Jun target genes in melanoma were described in the literature, so far. Therefore, we focused on pre-existing ChIP-Seq data (Encyclopedia of DNA Elements) of 3 different non-melanoma cell lines to screen direct c-Jun target genes. Here, a specific c-Jun antibody to immunoprecipitate the associated promoter DNA was used. Consequently, we identified 44 direct c-Jun targets and a detailed analysis of 6 selected genes confirmed their deregulation in malignant melanoma. The identified genes were differentially regulated comparing 4 melanoma cell lines and normal human melanocytes and we confirmed their c-Jun dependency. Direct interaction between c-Jun ...
|p|Melanocyte stimulating hormone release inhibiting factor,(C|sub|13|/sub|H|sub|24|/sub|N|sub|4|/sub|O|sub|3|/sub|), a tri-peptide with the sequence H2N-Pro-Leu-Gly-amide, MW= 284.35. Melanocyte-inhibiting factor (also known as Pro-Leu-Gly-NH|sub|2|/sub|
Rashighi, Medhi; and Harris, John E., Melanocytes in psoriasis: convicted culprit or bullied bystander (2016). UMass Metabolic Network Publications. 47 ...
KIT encodes the mast/stem cell growth factor tyrosine kinase receptor. The heterozygous W mouse phenotype is similar to the human piebald trait, also caused by a KIT mutation, which is characterized by a congenital white hair forelock and ventral and extremity depigmentation (Fleischman et al. 1991). Mutations in coding or regulation of KIT have been characterized in additional species as causative of defects in pigmentation and hearing (Haase et al. 2007; Ruan et al. 2005; Spritz and Beighton 1998). Cable et al. (1995) have demonstrated that mutations in Kit do not prevent early melanoblast migration or differentiation in mice white spotting mutants but severely affect melanoblast survival during embryonic development.. Cairns et al. (2003) described murine cell type-specific DNase I hypersensitive sites that delineated Kit regulatory regions in primordial germ cells, hematopoietic stem cells, and melanoblasts. Genomic regions defined by the hypersensitive sites, once engineered into transgenic ...
Vitiligo (or leukoderma) is the patchy loss of skin pigmentation due to an auto-immune attack by the bodys own immune system on skin melanocytes. It frequently begins in late adulthood, with patches of unpigmented skin appearing on extremities. The patches may grow or remain constant in size. Occasional small areas may repigment as they are recolonised by melanocytes.
TY - JOUR. T1 - Microphthalmia-associated transcription factor (MITF) locus lacks linkage to human vitiligo or osteopetrosis. T2 - An evaluation. AU - Tripathi, Ram K.. AU - Flanders, Dean J.. AU - Young, Terri L.. AU - Oetting, William S.. AU - Ramaiah, Abburi. AU - King, Richard A.. AU - Boissy, Raymond E.. AU - Nordlund, James J.. N1 - Copyright: Copyright 2017 Elsevier B.V., All rights reserved.. PY - 1999/6. Y1 - 1999/6. N2 - The microphthalmia-associated transcription factor (MITF) locus has been mapped to human chromosome 3p12-p14.1, and encodes a basic helix-loop-helix zipper (bHLH-ZIP) protein homologous to a number of transcription factors. Numerous mutations at the mouse microphthalmia (mi) locus have been described, and all have reduced or absent pigmentation of the eyes, ears, and/or pelage, with some genotypes exhibiting small or absent eyes and osteopetrosis. The mivit/vit mutation at the mouse mi locus produces a postnatal depigmentation that resembles human vitiligo. The mice ...
Our hair color depends on a set of specialized stem cells called melanocyte stem cells, and every time a new hair grows, these melanocyte stem cells have to divide in two and make a new melanocyte, [or] pigment cells, explains Melissa Harris, assistant professor of biology at the University of Alabama at Birmingham. These pigment cells stay in the base of your hair and their job is to produce pigment. These melanocytes reach out skinny arms, called dendritic processes, that shuttle the pigment to the hair shaft as it grows. So if all your melanocyte stem cells disappear, so do your melanocytes and so does your hair pigment. Thus - gray hair.. ...
Recent progress in the structural identification of human melanoma antigens recognized by autologous cytotoxic T cells has led to the recognition of a new melanocyte differentiation antigen, Melan-A(MART-1). To determine the properties of the Melan-A gene product, Melan-A recombinant protein was produced in Escherichia coli and used to generate mouse monoclonal antibodies (mAbs). Two prototype mAbs, A103 and A355, were selected for detailed study. Immunoblotting results with A103 showed a 20-22-kDa doublet In Melan-A mRNA positive melanoma cell lines and no reactivity with Melan-A mRNA-negative cell lines. A355, in addition to the 20-22-kDa doublet, recognized several other protein species in Melan-A mRNA-positive cell lines. Immunocytochemical assays on cultured melanoma cells showed specific and uniform cytoplasmic staining in Melan-A mRNA-positive cell lines. Immunohistochemical analysis of normal human tissues with both mAbs showed staining of adult melanocytes and no reactivity with the ...
Autoimmune dermatoses targeting melanocytes have gained attention in human medicine due to their progressive nature and the social impact suffered by affected individuals. In veterinary medicine, vitiligo and the uveodermatological syndrome are the two autoimmune diseases that are known to affect skin melanocytes. In the first part of this article, we will review the signalment, clinical signs, histopathology and the treatment outcome of vitiligo in dogs, cats and horses; where pertinent, we compare the animal diseases to their human homologue. In a similar fashion, the information on the uveodermatological syndrome in dogs is reviewed and, where relevant, it is compared to the Vogt-Koyanagi-Harada (VKH) syndrome in humans. Canine, feline and equine vitiligo have many features that mirror their human counterparts. The most effective treatment and outcome of vitiligo in animals remain unclear. The canine uveodermatological syndrome resembles the incomplete VKH variant in humans; for affected individuals,
TY - JOUR. T1 - Profile of vitiligo patients and distribution of narrowband-UVB therapy at dr. Cipto Mangunkusumo General Hospital. AU - Suseno, Lili Surachmiati. AU - Sukma, Putu Martha Gerynda. AU - Rihatmadja, Rahadi. AU - Agustin, Triana. AU - Rahmayunita, Githa. AU - Novianto, Endi. PY - 2018. Y1 - 2018. N2 - Background: Vitiligo is a disease marked by depigmented macules. Prevalence of vitiligo varies between 0.1- 2.3% worldwide. The objectives of this study are to identify the socio-demographic profile of vitiligo patients and distribution of narrowband-UVB given as a treatment modality. However, in Indonesia, including at dr. Cipto Mangunkusumo General Hospital, there has not been any study on the profile of vitiligo patients. Therefore, a preliminary study on the patients profile would be very useful for healthcare providers in calculating the need for narrowband-UVB equipment and evaluation of its current use. Method: A retrospective descriptive study, using secondary data obtained ...
TY - JOUR. T1 - GILT accelerates autoimmunity to the melanoma antigen tyrosinase-related protein 1. AU - Rausch, Matthew P.. AU - Irvine, Kari R.. AU - Antony, Paul A.. AU - Restifo, Nicholas P.. AU - Cresswell, Peter. AU - Hastings, K. Taraszka. PY - 2010/9/1. Y1 - 2010/9/1. N2 - Melanocyte differentiation Ags, including tyrosinase-related protein (TRP) 1, are relevant to both autoimmune skin depigmentation (vitiligo) and tumor immunity, because they are expressed by both benign melanocytes and many malignant melanomas. Melanoma patients generate CD4+ T cells that specifically recognize these proteins. TRP1 contains internal disulfide bonds and is presented by MHC class II molecules. γ-IFN-inducible lysosomal thiol reductase (GILT) facilitates the generation of class II-binding peptides by the endocytic reduction of protein disulfide bonds. We show in this study that GILT is required for efficient MHC class II-restricted processing of a TRP1 epitope in vitro and accelerates the onset of ...
Antigen Background Tyrosinase-related protein-1 (TRP-1) is a member of a family of proteins which are involved in melanin biosynthesis. The catalytic function of TRP-1 has not been fully resolved but the enzyme appears to be important in the oxidation of 5,6-dihydroxyindole-2-carboxylic acid to form a high molecular weight pigmented biopolymer. In mammals, there are two basic types of melanin, the brown-black eumelanin and the reddish-yellow phaeomelanin. The concentrations of each are variable and are not related to skin type. In skin exposed to suberythemal doses of UVB, an increase in the number of melanocytes expressing TRP-1 and TRP-2 is reported with no increase in the number of tyrosinase-expressing melanocytes. In normal, untreated skin the number of melanocytes that express either TRP-1, TRP-2 or tyrosinase are similar irrespective of skin type. TRP-1 is also reported to be expressed in more than 50 percent of choroidal melanocytes in the adult eye.. ...
I read with interest the recent report by Snyder et al[1] describing melasma associated with the application of a topical estrogen cream. The development of melasma is multifactorial and female sex hormones have been implicated in the pathogenesis of this condition.[2] Estrogen receptor expression is increased in melasma lesions.[3] Also, melanogenesis of cultured human melanocytes can be stimulated by estrogens and inhibited by estrogen antagonists.[4]. The induction of melasma with a topical estrogen raises the possibility that the treatment of this condition could be facilitated by the use of a topical anti-estrogen. I recently proposed a novel topical approach for the treatment of melasma that utilized an anti-estrogen, such as a selective estrogen receptor modulator (tamoxifen or raloxifene) or an aromatase inhibitor (anastrozole or tetrozole or exemestane).[5] The topical agent would also include a vascular endothelial growth factor inhibitor (bevacizumab) that would be directed toward ...
Abstract: : Purpose:We reported that patients with Vogt-Koyanagi-Harada (VKH) disease had immune responses specific to human melanocyte antigens, tyrosinase and gp100. This study was aimed at analyzing whether lymphocytes of patients with VKH disease have a cross-reaction between melanocyte peptides and virus antigens. Methods:The subjects of this study were patients with VKH disease and patients with other uveitis in 1989-2001at our hospital. We searched molecular mimicry between tyrosinase450-462, gp10044-59 and exogenous antigen, such as virus, using database screening. Then, crossreactivity to melanocyte peptides and virus antigen were examined by lymphocyte proliferation assay. The seroprevalence of various viruses in patients with VKH disease (n=109) was examined by complement fixation test. In order to examine if the virus infection in VKH patients were latent, genomic DNA of virus was measured by quantitative PCR using samples from serum, cerebro-spinal fluid, and aqueous humor. All ...
2Division of Basic Sciences, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892-4472 USA. Wnt1 signaling has been implicated as one factor involved in neural crest-derived melanocyte (NC-M) development. Mice deficient for both Wnt1 and Wnt3a have a marked deficiency in trunk neural crest derivatives including NC-Ms (1). We have used cell lineage-directed gene targeting of Wnt signaling genes to examine the effects of Wnt signaling in mouse neural crest development. Gene expression was directed to cell-lineages by infection with subgroup A avian leukosis virus vectors (RCAS) (2) in lines of transgenic mice that express the retrovirus receptor tv-a (2). Transgenic mice with tva in either nestin expressing neural precuror cells (line Ntva) or dopachrome tautomerase (DCT) expressing melanoblasts (line DCTtva) were analyzed. We over-stimulated Wnt signaling in two ways: directed gene transfer of Wnt1 to Ntva+ cells and transfer of b-catenin to DCTtva+ NC-M precursor ...
Vitilox® Pigmentation Cream, Melanocytes, Melanin, Vitiligo Treatment, Vitiligo Pigmentation Cream, Vitiligo face treatment, Melanin stimul
The LIM and SH3 protein 1 (LASP1) is a focal adhesion protein. Its expression is increased in many malignant tumors. However, little is known about the physiological role of the protein. In the present study, we investigated the expression and function of LASP1 in normal skin, melanocytic nevi and malignant melanoma. In normal skin, a distinct LASP1 expression is visible only in the basal epidermal layer while in nevi LASP1 protein is detected in all melanocytes. Melanoma exhibit no increase in LASP1 mRNA compared to normal skin. In melanocytes, the protein is bound to dynamin and mainly localized at late melanosomes along the edges and at the tips of the cell. Knockdown of LASP1 results in increased melanin concentration in the cells. Collectively, we identified LASP1 as a hitherto unknown protein in melanocytes and as novel partner of dynamin in the physiological process of membrane constriction and melanosome vesicle release.
Vertebrate pigment cells are derived from neural crest, a tissue that also forms most of the peripheral nervous system and a variety of ectomesenchymal cell types. Formation of pigment cells from multipotential neural crest cells involves a number of common developmental processes. Pigment cells must be specified; their migration, proliferation, and survival must be controlled and they must differentiate to the final pigment cell type. We previously reported a large set of embryonic mutations that affect pigment cell development from neural crest (R. N. Kelsh et al., 1996, Development 123, 369-389). Based on distinctions in pigment cell appearance between mutants, we proposed hypotheses as to the process of pigment cell development affected by each mutation. Here we describe the cloning and expression of an early zebrafish melanoblast marker, dopachrome tautomerase. We used this marker to test predictions about melanoblast number and pattern in mutant embryos, including embryos homozygous for ...
Endothelin receptor b (Ednrb) and its ligand Endothelin 3 (Edn3) have been implicated in melanoma. Several studies have shown an upregulation of EDNRB and EDN3 at both the protein and mRNA levels, as melanoma becomes more aggressive. This study investigated the putative role played by Edn3 over-expression in melanoma progression and angiogenesis in vivo. We crossed Tg(Grm1)Epv transgenic mice that aberrantly express metabotropic glutamate receptor1 under the Dopachrome tautomerase promoter, leading to spontaneous melanocytic lesions in the ears and tails that do not metastasize, with transgenics that overexpress Edn3 under the Keratin 5 promoter (K5-Edn3) or overexpress Ednrb in melanocytes (Tg(Ednrb)1Lk). In both the Tg(Grm1)Epv/K5-Edn3 and Tg(Grm1)Epv/Tg(Ednrb)1Lk mice, tumors appeared earlier and grew significantly larger and faster when compared to Tg(Grm1)Epv mice. Approximately eighty-one percent of Tg(Grm1)Epv/ K5-Edn3 mice and 76% of Tg(Grm1)Epv/Tg(Ednrb)1Lk mice had pigmented lesions in distant
Melanoma in situ is the very earliest stage of a skin cancer called melanoma. In situ is Latin for in space. It means that the cancer cells have not had the opportunity to spread to anywhere else in the body.. About 7,000 people in the UK are diagnosed with melanoma each year. The word melanoma comes from the Greek word melas, meaning black. Melanin is the pigment that gives the skin its natural colour. Melanin is made in the skin by pigment cells called melanocytes. After our skin is exposed to sunlight, the melanocytes make more melanin, and so the skin becomes darker.. Melanocytes sometimes grow together in harmless groups or clusters, which are known as moles. Most people have between 10 and 50 moles and often they are darker than the surrounding skin.. Melanomas can arise in or near to a mole but can also appear on skin that looks normal. They develop when the skin pigment cells (melanocytes) become cancerous and multiply in an uncontrolled way. They can then invade the skin around ...
Melanoma in situ is the very earliest stage of a skin cancer called melanoma. In situ is Latin for in space. It means that the cancer cells have not had the opportunity to spread to anywhere else in the body.. About 7,000 people in the UK are diagnosed with melanoma each year. The word melanoma comes from the Greek word melas, meaning black. Melanin is the pigment that gives the skin its natural colour. Melanin is made in the skin by pigment cells called melanocytes. After our skin is exposed to sunlight, the melanocytes make more melanin, and so the skin becomes darker.. Melanocytes sometimes grow together in harmless groups or clusters, which are known as moles. Most people have between 10 and 50 moles and often they are darker than the surrounding skin.. Melanomas can arise in or near to a mole but can also appear on skin that looks normal. They develop when the skin pigment cells (melanocytes) become cancerous and multiply in an uncontrolled way. They can then invade the skin around ...
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As is known to all, vitiligo is a kind of very stubborn skin disease, that vitiligo patients should pay attention to take a shower? How to take a shower is beneficial to the health of patients with vitiligo? This is a lot of patients issues of concern, to this, huahai vitiligo hospital experts point out that, in the bath, patients should pay attention to the following: ...
Most melanomas harbor oncogenic BRAFV600 mutations, which constitutively activate the MAPK pathway. Although MAPK pathway inhibitors show clinical benefit in BRAFV600-mutant melanoma, it remains incompletely understood why 10% to 20% of patients fail to respond. Here, we show that RAF inhibitor-sensitive and inhibitor-resistant BRAFV600-mutant melanomas display distinct transcriptional profiles. Whereas most drug-sensitive cell lines and patient biopsies showed high expression and activity of the melanocytic lineage transcription factor MITF, intrinsically resistant cell lines and biopsies displayed low MITF expression but higher levels of NF-κB signaling and the receptor tyrosine kinase AXL. In vitro, these MITF-low/NF-κB-high melanomas were resistant to inhibition of RAF and MEK, singly or in combination, and ERK. Moreover, in cell lines, NF-κB activation antagonized MITF expression and induced both resistance marker genes and drug resistance. Thus, distinct cell states characterized by ...
Pigment-producing (Animal-type) Melanoma Pigment-producing (Animal-type) Melanoma Images https://www.webpathology.com/image.asp?case=1026&n=33
Bachem offers H-4406 Melanocyte Protein PMEL 17 (44-59) (human, bovine, mouse) for your research. Find all specific details here. Find product specific information including available pack sizes, CAS, detailed description and references here.
The conversion of melanocytes into cutaneous melanoma is basically dictated by the consequences of solar ultraviolet radiation (UVR). to secure a more accurate family portrait of the consequences of solar UVR over the melanocytes within this framework, we utilized the technique of Laser beam Catch Microdissection (LCM). This system allowed melanocytes from your skin of individual volunteers to become obtained pursuing their contact with simulated UVR (ssUVR), this is the UVA and UVB rays of sunshine. This novel strategy has allowed us to discover new evidence recommending that UVR can differentially have an effect on the circuitry of miRNAs in the melanocytes of people with a brief history of melanoma in comparison with those of healthful individuals. Strategies and Components Research individuals Eight healthful fair-skinned females between your age range of 31 and 38, and with Fitzpatrick epidermis types of I or II [13], had been signed up for this scholarly research. None of these acquired a ...
What are moles?. Moles are also called nevi. They are very common. Almost any person has a few moles scattered around their body. Usually, people with lighter skin have more moles. It is normal to have 10 to 40 moles on your skin. So, when do you have to search for mole removal in Sydney NSW?. First, lets learn more about moles. They are skin growth composed of cells called melanocytes, producing pigment or color. Melanocytes can also cause moles to darken once teenage years arrive, during pregnancy or after sun exposure.. One mole can show up anywhere on a persons skin, from the face to the feet. Sometimes they show up alone; sometimes, in groups. For most people, moles are acquired in the first 20 years of life. Often, they are brown. They can also be black or blue, even flesh-colored. Most moles are tiny and cannot cause harm or pain, unless they are bumped on something or rubbed.. When should I be worried?. Usually, moles are smaller than a pencil eraser and black or brown in color. If ...
The Vitiligo is a plural disease often presents after suffering strong impressions or in the presence of a situation of stress. This condition is triggered in genetically predisposed individuals a neural response (neurochemistry) which destroys the melanocytes showed the presence of an excess of free radicals in the areas of depigmentation phase when melanin becomes toxic to the cells that produced them. Taking antioxidant vitamins and minerals are highly recommended to enhance treatment Melagenina Plus.. The toxins are accumulated in the liver and all those bodies responsible for their elimination, and this leads to remain undifferentiated melanocytes in the basal layer as a result of lack of blood flow, leading to the melanocytes lose their functions and remain in the basal cells as undifferentiated (ie no function to produce melanin which becomes progressive depigmentation of the skin), and this coupled with the inability to acquire keratinocytes retain little melanin that is produced. Such ...
Styes and chalazia are usually harmless and rarely affect your eyeball or your eyesight. Common I started eaking out I told my husband I needed a pregnancy test and I am having a girl this whose had a girl/boy felt at It should go away in a couple of days. Pores On Tongue Skin For Tanning Prone Best Lotion patient Comments: really raw honey acne care vichy salicylic hydrating lotion acid Staph Infection - Length Symptoms Lasted.. Vitiligo is a skin disorder that causes the pigment-producing cells does apple cider vinegar help sore muscles for skin tree prone tea to die (melanocytes). large acne-like blisters on face neck and bacterial pnemonias and these pimple-like blisters on my face neck Severe skin rash (Kaletra Im going to ice my lip now My cold sore always flare up after I have dental work done only on the right side of Cold sores are the worst. The WebMD Symptom Checker is designed to help you understand what your medical symptoms could mean Family & Pregnancy; Pregnancy; Newborn & ...
VAMP7 has been implicated in melanosome biogenesis (Tamura et al., 2011; Jani et al., 2015), but the pathways by which it is directed toward and recycled from melanosomes were unknown. Here, we show that VAMP7 functions during melanosome biogenesis primarily as a v-SNARE in BLOC-1-dependent tubular transport from endosomes to melanosomes and thereby promotes melanosomal delivery of BLOC-1-dependent cargoes such as TYRP1. Importantly, our analyses of VAMP7 dynamics revealed a previously undocumented SNARE retrieval pathway from maturing melanosomes. This pathway employs membrane tubules that emerge from melanosomes at sites enriched in RAB38 and VARP and that require the RAB32/38 GEF BLOC-3 for their formation. The resulting model (Fig. 10 e) has important implications for RAB32/38, BLOC-3, and VAMP7 function in the biogenesis of other LROs and in the etiology of the most common forms of HPS.. Cargoes are delivered to melanosomes by two distinct pathways that emerge from early endosomes: one that ...
BACKGROUND: Vitiligo is a chronic skin disorder. White macules caused by melanocyte destruction is a characteristic finding that cosmetically disturbing. Until recently, pathogenesis of vitiligo is still unclear. The role of homocysteine in vitiligo is mentioned in previous studies thus it is probable that it can be a biomarker to determine vitiligo severity. AIM: To determine correlation between serum homocysteine and vitiligo area Scoring Index (VASI). SUBJECT AND METHOD: This was a cross-sectional analytic study which involved 30 vitiligo patients that were diagnosed by clinical and Woods lamp examinations then VASI score was determined and same numbers of control ...
Uppsala University, Medicinska vetenskapsområdet, Faculty of Medicine, Department of Medical Sciences. (Dermatology and Venereology) ...
Why the interest in such an obscure cell? There is not a lot of information in the literature.. I am a clinician with a special interest in melanoma and, as such, you are continually struck by the potential aggressive and lethal nature of invasive melanoma and its resistance to therapeutics. There are some striking differences in behaviour between melanoma and its non-melanoma skin cancer relatives. Obviously, the melanocyte as the cell of origin, rather than the keratinocyte, and inevitably the neural crest origin of the melanocyte.. The Satellite cell, its close relative the Schwann cell, the melanocyte and its malignant offspring the melanoma cell, all share this Neural crest cell origin.. During evolutionary development, aspects of the Neural crest began to appear in early chordate species and eventually reached full expression in vertebrates. Protochordates were thin transparent sessile filter-feeders sitting in burrows on the sea floor but with evolutionary development grew in size, became ...
Group of melanocytic lesions which all appear blue in colour due to the optical effects of light reflecting off melanin deep in the dermis. The blue nevus, a benign, usually solitary lesion, represents a localized proliferation of dermal melanocytes. It presents as a dark blue to black, moderately firm, rounded, sharply defined nodular tumour composed of spindle-shaped melanocytes with slender cytoplasmic processes, occurring often in association with melanin-laden macrophages in a sclerotic dermis.. ...
In this report, we show that in normal melanocytes Rab27a colocalizes with melanosomes and myosin-V. In melanocytes from a GS patient, we observed a lack of Rab27a expression that coincides with the absence of melanosome accumulation at the dendrite tips. Sequencing of Rab27a cDNA from this patient revealed a deletion of five nucleotides in the terminal exon. This deletion leads to a frameshift, a conversion Q172N, and the appearance of a premature termination codon in 173 (Menasché et al. 2000). At the protein level, the termination codon in 173 implies that 49 COOH-terminal amino acids are deleted in the mutant form of Rab27a. This deletion involves the hypervariable domain of Rab GTPases that contains a geranylgeranylation motif (CXC) and structural elements that determine the association of Rab proteins with their specific target vesicles. In choroideremia, impairment of Rab27a geranylgeranylation results in a decreased expression of the protein (Seabra et al. 1993). Thus, the mistargeting ...
Vitiligo is a condition in which you develop white patches of skin over various parts of your body. It is a result of the loss of melanin, the pigmenting component in the upper layer of your skin. In the course of vitiligo, the melanin producing cells in your skin, the melanocytes, are destroyed, melanin production ceases and your skin may become depigmented. Vitiligo is caused by an autoimmune reaction, or an attack on your melanocytes by your bodys own immune system.
Vitiligo is a common dermatological disorder of chronic depigmentation which is phenotypically characterized by white macules on the skin caused as a result of the systematic destruction of functional melanocytes. This review provides an overview of vitiligo, its etiopathogenesis and disease management, and also discusses the scope of network-interaction studies and polypharmacological studies in understanding vitiligo disease module. A narrative review of the relevant published literatures known to the authors that comprehensively discussed about vitiligo and its implications was conducted. Emerging evidence underlines the existing connection between deregulated miRNA function and vitiligo pathogenesis. It has also been linked with autoimmunity for the cause of melanocyte death in susceptible individuals. Alteration of genetic factors involved in immune responses and melanogenesis along with environmental factors are central to disease manifestation. Screening methods as such are not available for
Title:Role of Genetics and Epigenetics in Mucosal, Uveal, and Cutaneous Melanomagenesis. VOLUME: 16 ISSUE: 5. Author(s):Mario Venza, Maria Visalli, Concetta Beninati, Carmelo Biondo, Diana Teti and Isabella Venza. Affiliation:Department of Clinical and Experimental Medicine, Azienda Policlinico Universitario G. Martino, Torre Biologica, 4° piano, via Consolare Valeria, 1, 98125, Messina, Italy.. Keywords:Cutaneous melanoma, epigenetics, genetics, mucosal melanoma, uveal melanoma.. Abstract:Melanoma prevalently occurs on parts of the body that have been overexposed to the sun. However, it can also originate in the nervous system, eye and mucous membranes. Melanoma has been thought for a long time to arise through a series of genetic mechanisms involving numerous irreversible changes within the human genome. However, recently, epimutations have attracted considerable attention owing to their high prevalence rate and reversible nature. These observations opened up new perspectives in the use of ...
Dark spots is medically termed as hyperpigmentation ,which occurs when the skin is exposed to sun. It causes increase in production of melanocyte cells, causing darkening of skin or black spots. In few cases, it can also be a sign of aging. There are unlimited cosmetics options available in the market to conceal these spots…
TYRP1 (tyrosinase-related protein 1), Authors: Kunal Ray, Mainak Sengupta, Sampurna Ghosh. Published in: Atlas Genet Cytogenet Oncol Haematol.
Insane in the Chromatophores from Backyard Brains on Vimeo.. The folks at Backyard Brains, a DIY-neurobiology project, made these pigment-producing cells in a dead squid pulse to the base beats of Cypress Hills Insane in the Brain. Go watch that thing right now.. Done? Wowed? Prepare to be more wowed: They did it by exploiting the fact that electrical current is key to both the actions of cells and the playing of mp3s. These pigmented cells, called chromatophores, are surrounded by muscle cells, and its by flexing these muscles that the squid reveals its colorful spots. By hooked up the nerve that sends the flexing orders to the wire of a set of earbuds, they got these amazing results.. Heres their description of how music made the muscles pulse:. ...
Dermatologic disease, although seldom life threatening, can be extremely disfiguring and interfere with the quality of life. In addition, as opposed to other organs, just the aging of skin and its adnexal structure the hair follicle can result in cosmetic concerns that affect most of us. The articles in this dermatology Review Series demonstrate recent progress in understanding the cell biology and molecular pathophysiology of the epidermis and hair follicles, which harbor keratinocyte and melanocyte stem cells. They reveal a dynamic relationship between research and clinical care: knowledge of dermatologic disease has facilitated the understanding of the biology of the epidermis and, in turn, progress in basic science has informed our understanding of disease. This type of synergy is a profound strength of clinical research of the type that the JCI is dedicated to publishing. ...
Immunohistochemistry has become one of the most reliable techniques to study the expression of different molecules throughout very specific regions, especially in neuroscience. In this compilation, the authors begin by explaining how to perform excellent immunohistochemistry to obtain high quality images, and more importantly, how to automatically analyze these images.. In immunohistochemistry, it is also essential to be able to guarantee analytical reproducibility. By involving experienced observers, data consistency may be improved by increasing interobserver concordance.. Immunohistochemistry has value in melanoma diagnostics, allowing for the distinguishing of malignant melanocytes from benignant ones. This technique also has prognostic relevance in detecting tumor infiltrating lymphocytes and microvascular metastases, discerning the lymphatics from the blood vessels ...